Student Cerebellum and BG NS II 2024 PDF

The Basal Ganglia and Cerebellu m Remember the big picture… Basal Ganglia Basal = Ganglia = Caudate + Putamen = Striatum Globus Pallidus (internal and external) Subthalamic Nucleus (STN) Substantia nigra = Thalamus Inputs to Basal Ganglia Cerebral Cortex Substantia Nigra of M...

The Basal Ganglia and Cerebellu m Remember the big picture… Basal Ganglia Basal = Ganglia = Caudate + Putamen = Striatum Globus Pallidus (internal and external) Subthalamic Nucleus (STN) Substantia nigra = Thalamus Inputs to Basal Ganglia Cerebral Cortex Substantia Nigra of Midbrain Outputs: Superior colliculus Thalamus A) Direct Pathway B) Indirect Pathway BOX 18B Basal Ganglia Loops and Non-Motor Brain Functions 2 Major Hypokinetic types of BG Disorders Hyperkinetic General Movement Problems Associated with Basal Ganglia Movement Disorders Tremor Tics Chorea Ballismus Dystonia Dyskinesia Hemiballismus Akinesia Athetosis Bradykinesia Hyperkinetic Disorders Hyperkinetic Disorders: TREMOR: involuntary movements involving both the agonist and antagonist resulting in rhythmic or alternating movements of a joint Resting tremor Associated with Parkinson’s Disease VS. Intention tremor – caused by cerebellar lesion Occurs with action, particularly reaching Hyperkinetic Disorders: DYSTONIA: sustained involuntary contractions of agonist and antagonist muscles of a particular body segment Causes abnormal posturing or twisting movements Dystonia video Hyperkinetic Disorders: ATHETOSIS: slow, involuntary, writhing, twisting, “wormlike” movements Frequently more in distal UEs Athetosis video Hyperkinetic Disorders: HEMIBALLISMUS: large amplitude sudden, violent, flailing motions of the arm and leg of one side of the body Primarily axial and proximal musculature Hemiballismus video Hyperkinetic Disorders: TICS: abrupt, repetitive movements or vocalizations Tourette’s Disorder Tourette's video Hyperkinetic Disorders: CHOREA: involuntary, rapid, irregular, jerky movements Involves multiple joints Most apparent in UEs Hyperkinetic Disorders: Huntington’s Disease aka Huntington’s Chorea Signs: Dementia and CHOREA Hereditary and progressive Onset 40-50 years Death approximately 15 years after onset Treatment: anticonvulsants, antipsychotics Chorea video  Figure 19-15 Horizontal sections of cortex illustrating (a) normal size of caudate nucleus in people without HD and (b) atrophy of the head of the caudate nucleus and enlargement of the anterior horn of the lateral ventricle as manifested in people with Huntington's disease (HD). Medical Management of HD Hereditary condition Presents typically at ages 35-55 Progression of symptoms from hyperkinetic to eventual rigidity at end of life; includes changes in affect and cognition, with eventual dementia Treatment: Genetic counseling Pharmacological once unwanted movements begin Examination and Intervention in HD United Huntington's Disease Rating Scale (UHDRS) Assessment of activities of daily living Tests of strength, tone, and gait Mental state and psychological status assessment People with HD are underserved in rehabilitation Hypokinetic Disorders Hypokinetic Disorders AKINESIA: Inability to initiate movement; associated with fixed postures; freezing phenomenon BRADYKINESIA: decreased amplitude and velocity of voluntary movement RIGIDITY: increase in muscle tone causing resistance to PROM Lead pipe: uniform, constant resistance Cogwheel: series of brief catches Hypokinetic Disorder – Parkinson’s Disease Incidence 1 in 100 people over age 70 Affects men and women equally Typically develops after age 65 10-15% diagnosed before age 50 Etiology Cause is unknown Strong support for environmental cause (more prevalent in industrial and agricultural countries) Genetic link in people diagnosed before 50 Parkinson’s Disease Pathology Death of dopamine-producing cells in substantia nigra Death of cells occurs long before onset of symptoms 80% of dopamine-producing cells die before signs of disease appear Figure 19-12 Substantia nigra of the midbrain. In the normal condition, the substantia nigra pars compacta is seen as a black pigmented area. In the midbrain of people with PD, there is a loss of the black pigmented cells in substantia nigra pars compacta and, therefore, a loss of dopamine (DA) production. Hypokinetic Disorder – Parkinson’s Disease Cardinal Signs: Tremor PD tremor Rigidity Cogwheel Lead pipe Akinesia Bradykinesia Freezing Postural Instability Loss of postural reflexes Parkinson’s Disease Other Symptoms Forward flexed posture Masked face Decreased volume of speech Increased speed of speech Monotone speech Festinating gait Demonstration of gait Decreased arm swing Difficulty with initiation and termination Micrographia Autonomic Parkinson’s Disease Medical Management Medication Levodopa – helps balance dopaminergic and cholinergic neurons Surgery Pallidotomy Deep Brain Stimulation (DBS) Parkinson’s Disease Medical Management - Medication Levodopa – helps balance dopaminergic and cholinergic neurons by replacing dopamine Helps reduce signs of the disease Challenges with Levodopa Side effects: psychosis, hallucinations, DYSKINESIA or DYSTONIA On/Off phenomenon: periods of normal movement and periods of immobility https://youtu.be/3-wrNhyVTNE May relate to time of day or time of dosage Tolerance: over time, the response to L-dopa decreases Parkinson’s Disease Medical Management - DBS Deep Brain Stimulation (DBS) Implantation of electrodes into BG Location depends on symptoms Continuous high-frequency e-stim inhibits firing of overactive thalamic neurons DBS on/off Parkinson’s Disease Subjective Measure Parkinson’s Disease Questionnaire (PDQ-39) Measures participation 8 domains Mobility ADLs Emotions Stigma Social support Cognition Communication Bodily discomfort Cerebellu m Cerebellum – The Great Comparator ERROR CORRECTION Integrates: executive commands + sensory feedback = moment-to- moment adjustment of behavior Outputs to circuits of UMNs An organ of agility (movement of the mind and body) Coordination of ongoing multi-jointed movement Coordination of ongoing sequential cognitive processes 3 Basic Parts/Components of Cerebellum Component Anatomy Connections Gray Matter Cerebellar Folia Cortex Deep Nuclei Floor of 4th ventricle White Matter Peduncles Middle (largest) Incoming from pons Superior Outgoing Inferior Incoming from spinal cord and brainstem Outgoing Terminology Used to Discuss the Cerebellum LOBES LONGITUDINAL ZONES FUNCTIONAL REGIONS Flocculonodular Vermis Vestibulocerebellum Anterior Intermediate/Paravermis Spinocerebellum Posterior Lateral Pontocerebellum  3 Major Functional Divisions Division Anatomy Connections & Nuclei Function Peduncles Spinocerebellum Medial strip of Input from spinal Interposed Movements of vermis and cord (through arms/legs hemispheres inferior peduncle) Some cranial movement Cerebrocerebellu Lateral To/from cerebral Dentate Skilled m hemispheres cortex (through movements of superior and distal middle peduncle) extremities, especially when there is a goal directed plan Vestibulocerebell Flocculus + Connects to Fastigial Calibrating and um nodulus vestibular nuclei governing in brainstem vestibular motor (through inferior output peduncle) Cerebellar Circuitry: Inputs From Cortex Cortex -> Pons -> Decussation -> Contralateral Cerebellar Cortex and Nuclei Therefore, cortex can only communicate with cerebellum indirectly From Sensory System From Brainstem Inferior olive of medulla Clinical Connections 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 FIGURE 19.9 Neurons and circuits of the cerebellum (Part 1) FIGURE 19.10 Excitatory and inhibitory connections in the cerebellar cortex and deep cerebellar nuclei (Part 1) FIGURE 19.10 Excitatory and inhibitory connections in the cerebellar cortex and deep cerebellar nuclei (Part 2) Motor Learning and Plasticity Works by modifying the strength of the inhibition of the cortical inhibitory loop Causes weakended input from the cerebellar cortex Motor learning is a stronger input to the cerebellar deep nuclei which allows the cerebellum to have more influence over UMN circuits Figure 19-9 Finger-to-nose test. (a) The accuracy of performance of an individual with an intact cerebellum. (b) The dysmetria of an individual with cerebellar dysfunction. The trajectory is wavy instead of straight (dysmetria) and is offset from the nose. Clinical Connection: Medulloblastoma Highly malignant tumor occurring predominantly in children ages 4–8 Symptoms of listlessness, vomiting, headaches, and falling Increased intracranial pressure causes papilledema Clinical Connection: 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, hypotonia, asthenia, asynergia, and ataxia Differentiating Cerebellar From Somatosensory Ataxia Not all ataxia is caused by cerebellar lesions. To differentiate between somatosensory and cerebellar ataxia, movement coordination should be compared with eyes open and eyes closed. Copyright © 2018 by Elsevier, Inc. All rights reserved. 54 Medical Intervention In general intervention is complicated and prognosis of restoration of normal function is poor  Clinical Diagnoses https://youtu.be/17ch1guvoLA (PD) https://youtu.be/m6SxJUjJGlc (HD) Bring it all together. Motor control of the body is primarily controlled by cortical signals sent to LMNs This relationship is modulated by the inputs of the basal ganglia and cerebellum Learning requires error Questions? Reflection.