Anatomy and Function of the Basal Ganglia Flashcards
L9 and L10
1
Q
Give an overview of Basal Ganglia anatomy
A
- Lentiform nucleus
- Putamen
- Globus pallidus
- Corpus striatum
- Caudate nucleus
- Putamen
- Pallidum
- globus pallidus internal + external
- Neostriatum = dorsal striatum
- Caudate
- Putamen
2
Q
Explain how the basal ganglia interfaces with the cortex
A
- the striatum and pallidum form the basal ganglia which transmits information to the thalamus
- the thalamus interfaces with the cerebral cortex which feedback to the Basal Ganglia
- There are 4 basal ganglia loops, two motor, and two-non-motor
- Motor
- Oculomotor
- Prefrontal
- Limbic
3
Q
Explain the Loops in the basal ganglia
A
- each have a Cortical Input –>
- motor, premotor somatosensory cortex
- posterior parietal, prefrontal cortex
- Dorsolateral prefrontal cortex
- Amygdala, hippocampus, orbitofrontal, anterior cingulate, temporal cortex
- striatum –>
- putamen
- body of the caudate
- anterior caudate
- ventral striatum
- pallidum –>
- lateral, globus pallidus, internal segment
- Globus pallidus, internal segment, substantia nigra pars reticulata (x2)
- ventral pallidum
- thalamus –>
- ventral lateral and lateral anterior nuclei
- mediodorsal and ventral anterior nuclei (x2)
- Mediodorsal nucleus
- then back to the cortex
4
Q
Explain the Direct pathway
A
- promotes movement
- provides a disnihibtory effect
5
Q
Explain the indirect/ hyper-direct pathway
A
6
Q
Give an overview of how the basal ganglia pathways work
A
- Inhibitory signals are the release of GABA
- Excitatory signals are the release of Glutamate
- Cortex –> striatum is excitatory
- Striatum outputs –> inhibitory
- Thalamus –> cortex is excitatory
- The inhibition of thalamus prevents movement
- Reducing inhibition of thalamus facilitates movement
7
Q
How is the input from the cortex modulated by the Striatum?
A
- Controlled by DA and ACh
- 2 populations of specialised dopamine receptors D1 and D2 medium spiny neurons
- D1: use G-proteins that increase cAMP - enhance the excitatory input from the cortex
- D2: use G-proteins that decrease cAMP - suppress the excitatory input from the cortex
- There are Striatum interneurons that use ACh
- this opposes the action of DA, tipping the pathway towards prevention of movement
- the release of Dopamine tips pathway towards the promotion of movement
8
Q
Explain the basal ganglia syndrome Hemiballismus
A
- it is a hyperkinertic movement disorder that causes ballistic involuntary movements of the limbs
- caused by damage to the subthalamic nucleus
- stroke in the STN is the most common cause
9
Q
Give a description of Tic disorders
A
- Brief repetitive stereotypes movements with a premonitory urge.
- Simple: like blinking, coughing
- Complex: jumping or twirling
- Plus: motor disorder
- Coprolalia: swearing - rare
- Reduced by distraction and concentration
- Worse with anxiety or fatigue.
- 50% have ADHD
- 33.3% have OCD
- Up to 50% have anxiety
- Tourette syndrome is the more severe expression of a spectrum of tic disorders,
10
Q
What is this an MRI of?
A
Subthalamic Nucleus Stroke
- can cause Hemiballismus
11
Q
Explain the action Prefrontal (cognitive loop) in the basal ganglia and its presentation in Parkinson’s Disease (PD)
A
- Pre-frontal cortex (dorso-lateral) → Caudate → Anterior Putamen → Globus Pallidus →Ventral anterior (VA) thalamic nucleus →Prefrontal cortex.
- Role in forward planning of complex motor intentions (volition).
- Therefore when a motor task becomes automatic, the motor loop of the basal ganglia takes over.
- PD patients have impairment of working memory
- Activation of the supplementary motor area on intended movements – Barietschaft potential which can be recorded Neurophysiologically and useful for assessing patients with a functional neurological disorder.
12
Q
Explain the action of the Limbic loop in the basal ganglia and it’s presentation in Parkinsons Disease (PD)
A
- Inferior prefrontal cortex → Nucleus Accumbens → Ventral Pallidum → Medio-dorsal nucleus of the thalamus → Inferior frontal cortex.
- Role in the visible expression of emotion. E.g smiling, showing aggression.
- This may explain why PD patiends have facial masking.
13
Q
Explain the action of the Oculomotor loop in the basal ganglia and its presentation in Parkinson’s Disease (PD)
A
- Frontal eye field and parietal cortex → Caudate nucleus → Substantia Nigra (Pr) → VA nucleus of thalamus → Frontal eye field and parietal cortex
- Ocular fixation is held by tonic activity (repetitive impulses) in the SN (Pr)
- When a saccade (voluntary movement) is made, the superior colliculus is disinhibited by the activated oculomotor loop.
- The superior colliculus neurons cause the eyes to make a rapid movement to a new target. The Sn(Pr) then resume tonic activity holding the visual gaze in that position.
- In PD: loss of dopamine neurons in the SN (Pr) means there is less disinhibition of the superior colliculus neurons resulting in slow eye movement (ocular hypokinesia).
14
Q
What is Chorea and when would choreiform movements present?
A
- Jerky, brief, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next. patient appears fidgety, restless
- Can present when
- there is a pathology in the STN
- Huntington’s disease
- Neuroleptic drugs
15
Q
Explain what Huntington’s Disease is
A
- autosomal dominant degenerative disease
- CAG trinucleotide repeat on chromosome 4
- the longer the repeat sequence the earlier the onset- seems to ‘anticipate’ with each generation
- Cognitive presentation
- inability to make a decision and multitask, slowness of thought
- Behavioural presentaion
- irritability, depression, apathy, anxiety, delusions
- Physical presentation
- Chorea, motor persistence, dystonia, eye movements
25
Q
What is the pathophysiology of Parkinson’s Disease?
A
- Decreased dopamine input leads to reduced activation of direct pathway and reduced inhibition of the indirect pathway
- leads to reduced movements
