Basal Ganglia Physio

imissyou419's version from 2017-01-29 17:59

Section 1

Question Answer
3 areas of cerebral cortex that interact with motor cortex in production of movementsparietal cortex (body image), premotor cortex, supplementary motor cortex (receives info from basal ganglia, parallel to motor cortex receiving info from cerebellum)
6 features of basal ganglia circuits KNOW THESE1. there are at least 4 separate circuits (loops) from cerebral cortex, through the basal ganglia, back to cerebral cortex.
2. there are 2 inputs to caudate/putamen (from cerebral cortex and substantia nigra pas compacta).
3. the major NT in the caudate/putamen are dopamine (can be excitatory or inhibitory), Ach, glutamate.
4. from the caudate/putamen to the internal globus pallidus, there is a direct and indirect pathway.
5. GABA is the inhibitory NT.
6. One major output is from the internal globus pallidus to the thalamus (inhibitory)
What are the 4 loops through the basal ganglia and their functions and the disorders resulting from lesions1. Motor: limb, face movements. [Parkinsons, Huntingtons]
2. Oculomotor: eye movements [fewer, slower saccades].
3. Limbic: emotion [irritability, depression].
4. Cognition: planning, working memory, attention [absent minded, reasoning ability, dementia, tourettes, OCD]
What is a possible function of the basal ganglia for motor loops?exerts continuous inhibition which prevents unwanted movements. (a lot of things send from cerebellum to cerebral cortex) When a movement is to be made, the basal ganglia select neural programs by releasing them from inhibition

Section 2

Question Answer
Parkinson's Disease PathologyDegeneration of dopamine neurons in the substantia nigra pars compacta. Changes balance of activity in direct and indirect pathways
6 Features of Parkinson's Disease1. Rigidity (lead pipe, NOT spasticity i.e. flexors and extensors, not velocity dependent),
2. RESTING tremor (pill rolling, stops during movement),
3. Akinesia (poverty of movement, no spontaneous movement).
4. Bradykinesia (slowed movement)
5. Dementia (involvement of frontal cortex, cognitive loop).
6. Shuffling gate, mask-like face, flexed posture
What happens in akinesia?INCREASE IN TONIC DISCHARGE IN NEURONS OF INTERNAL GLOBUS PALLIDUS, Results in increased inhibition at thalamus and decreased excitation in the motor cortex (when motor instructions come from cerebellum, motor cortex hyperpolarized)
4 Treatment for Parkinson's Disease (no cure)1. Lesion in the internal globus pallidus. Improvement in specific motor signs depending on lesion position.
2. High frequency electrical stimulation (deep brain stim) of the internal globus pallidus or subthalamic nucleus stimulus driven entrainment of motor cortex neurons normalizes their pathological firing patterns.
3. L-dopa, change balance b/w dopamine and acetylcholine i.e. increase dopamine, decrease Ach (anticholinergics). Too little dopamine causes akinesia, too much causes dyskinesia (involuntary movements).
4. Stem cell or fetal dopamine cells injection into neostriatum
What happens if you have too much dopamine?dyskinesia (abnormal involuntary movements)
What happens if you have too little dopamine?akinesia
What has a protective effect against PD?caffeine
Huntington's Chorea PathologyDegeneration of neurons in caudate and putamen. Associated with repeats of Huntingtin gene. Causes abnormal protein folding and cell death
What are the first signs of Huntington's?absentmindedness, irritability, depression, fidgeting, clumsiness, sudden falls then uncontrolled movements, speech becomes incomprehensible, cognitive functions deteriorate, eventually total disability and death; no treatment available
What happens in chorea?DECREASE IN TONIC DISCHARGE IN NEURONS OF INTERNAL GLOBUS PALLIDUS, less inhibition to thalamus so increased excitation at motor cortex (depolarized so random signal can come in and will fire resulting in dyskinesia)
6 Features of Huntington's1. Heritability.
2. Chorea (motor loop).
3. other movement disorders (e.g. slurred speech).
4. dementia (limbic, cognitive loops)
5. death
6. No treatment
What is the cause?
Violent movement of 1 limb due to lesion in subthalamic nucleus
Tourette's syndromeinappropriate utterances, tics (brief, repetitive involuntary movements such as eye blinks, head tosses, facial grimaces), though to be result of excessive activity of the cognitive (prefrontal) basal ganglia circulatory/motor loops
MPTP drugdepletes the brain dopamine levels so these people developed Parkinson-like symptoms overnight (rigidity, resting tremor, severe akinesia) [they named it Hysterical paralysis]
What are the 2 positive outcomes of MPTP drug1. produces animal model of Parkinson's.
2. Parkinson might be related to environmental toxin (pesticide), current view is that both genetic + environmental factors are involved