deck_3168577 Flashcards
Describe the cerebellum
Highly folded and convolutedGrey matter cortexWhite matter core
What are the three functional zones of the cerebellum?
VestibulocerebellumSpinocerebellumCerebrocerebellum
Describe the vestibulocerebellum
Input from vestibular system- balance and ocular reflexes
Describe the spinocerebellum
Input from spinocerebellar tract- unconcious proprioception and error correction
Describe the cerebrocerebellum
Input from contralateral cerebral cortex- fine motor control- movement planning- motor learning
What are some general signs that are associated with cerebellar dysfunction?
Incoordination of movementAtaxic gaitAtaxic, dysarthritic speechAbnormal eye movementsHyptonia
Define dysmetria
Inability to control smooth and accurate targeted movements- jerky movements- overshooting target- finger-nose or heel-shin test
Describe ataxic gait
Staggering gait, may become wide-based later on- mild cases may only be seen when getting the patient to walk heel to toe
What kind of abnormal eye movements do you see with cerebellar dysfunction?
coarse nystagmus- more pronounced when looking towards side of lesion
Describe the rebound phenomenon
Push down on outstretched arms of the Pt the abruptly release. Arms will rebound upwards further than expected.
Define the basal ganglia
A collection of subcortical nuclei
What structures make up the basal ganglia?
Caudate nucleusPutamenGlobus pallidusSubstantia nigraSubthalamic nucleus
What is the neostriatum?
Made up from the caudate nucleus and the putamen
What id the lenticular nucleus?
The putamen and the globus pallidus
What is the role of the basal ganglia?
Regulates the amplitude and velocity of the planned movement, particularly in relation to the use of proprioceptive information.
What does the basal ganglia do at rest?
Actively inhibits movement
Describe the process of what the basal ganglia does at rest.
- Cerebral cortex does not stimulate striatum- Globus pallidus interna inhibits the thalamus- Thalamus cannot stimulate the cerebral cortex- Less stimulation of the cerebral cortex gives less movement
What does the direct pathway of the basal ganglia do?
Amplifies planned movements
Describe the process of the direct pathway of the basal ganglia
- Cerebral cortex stimulates the striatum- Striatum inhibits the globus pallidus interna- GPi inhibition removes thalamus inhibition- Thalamus stimulate the cerebral cortex and increases stimulus of movements via upper motor neurones
What does the indirect pathway of the basal ganglia do?
Dampens down planned movements- takes longer than direct pathway, so acts after it
Describe the process of the indirect pathway of the basal ganglia
- Cerebral cortex stimulates striatum- Striatum inhibits globus pallidus externa- GPe removes inhibition from the subthalamic nucleus- Subthalamic nucleus stimulates the GPi- GPi stimulates inhibition of the thalamus- Thalamus cannot stimulate the cerebral cortex- Lees stimulation leads to less movement due to less stimulation of UMNs form the cerebral cortex
What does the substantia nigra compacta do?
Amplifies direct and inhibits indirect basal ganglia pathways. Causes an increases amplification of movements.
How does the substantia nigra compacta bring about its action?
- Dopaminergic neurones form the SNC act on the striatum- D1 = increase GPi inhibition- D2 = decrease GPe inhibition
What types of movement will be generated in basal ganglia dysfunction?
HypokineticHyperkinetic
Describe Parkinson’s Disease
Hypokinetic disorderDue to progressive degeneration of dopaminergic neurones that run between the substantial nigra and the striatum
What are the symptoms that are seen in Parkinsons?
- tremor at rest2. hypertonia3. bradykinesiaParkinsonian gait - stooped posture, with shuffling steps and pedestal turning
When do symptoms of Parkinson’s disease appear?
Older then 60 yearsOnce 75-80% of dopaminergic neurones have degeneratedWill have had the disease for a number of years before symptoms appear
What changes occur in the basal ganglia in Parkinson s disease?
- Death of dopaminergic neurones in substantia nigra- Less dopamine at D1 receptors (increase inhibition of thalamus)- Less dopamine at D2 receptors (increased inhibition of thalamus)- Suppression of direct pathway0- Amplification of indirect pathway- Increase thalamus inhibition which leads to less stimulation of the cerebral cortex- Less output leads to hypokinesia
Describe Huntington’s Chorea
Autosomal dominant genetic diseaseCauses jerky, involuntary movements as well as the progressive development of psychiatric and cognitiv symptoms.
What causes Huntingtons?
Gene mutation in Huntingtin protein. Causes aggreagates adn leads to cell death.
What changes are seen in Huntingtons?
Neuronal loss in the caudate nucleusReduction in GABA and AchLoss os inhibitor synaptic transmission which leads to decreased thalamic inhibtion and therefore an increase in stimulation of movement via the cerebral cortex.
What happens with sympathetic innervation to the bladder?
Stimulation by the hypogastric nerve (T10-L2) will cause:- detrusor relaxation (NA at B3)- contraction of internal urethral sphincter (NA at A1)
What happens with parasympathetic innervation to the bladder?
Stimulation by the pelvic nerve (S2-S4) releases ACh which acts on M3 receptors to cause contraction of the detrusor muscle.
What stimulates the change form the sympathetic to parasympathetic stimulation?
Activation of afferent stretch receptors (S2-S4) once the bladder reaches 400ml
How does micturition occur?
Removal of sympathetic stimulation causes relaxation of internal urethral sphincter whilst increase parasympathetic stimulation causes contraction of the detrusor muscle. The brain then makes the conscious decision to urinate, which stimulates relaxation of the external urethral sphincter via the pudendal nerve (S2-S4).
How does the brain bring about urination?
Brain micturition centre stimulate the spinal micturition centre to increase the parasympathetic stimulation.
Describe pure pyramidal UMN signs
Loss of spinal cord excitation by the motor cortex (corticospinal and corticobulbar)- hypotonia- loss of fractionation of finger movementsVERY RAREunlikely to sever only one tract
Describe extra-pyramidal UMN signs
Extrapyramidal tracts are responsible for mediation descending inhibition of LMN- hypertonia due to inability to mediate movement by descending inhibition.
