Physiology 1.05 - Motor, Cerebellum, Basal Ganglia (Vico Advento's Conflicted Copy 2014-05-23)

November 1, 2017 | Author: Jessica Compuesto | Category: Cerebellum, Cerebral Cortex, Spinal Cord, Basal Ganglia, Motor Neuron
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Motor, Cerebellum, Basal Ganglia...




JULY 16, 2013



Motor Function  Motor Cortex  Basal Ganglia  Brain Stem Motor Areas II. Postural Adjustments  Enables us to do our distal movements because our posture is maintained  Prior to movement  During movement III. Physiological and Pathophysiological Mechanism  ↓ Muscle Strength  ↓ and ↑ Muscle tone  ↓ Reflexes Requirement for voluntary movement 1. Sensory Information - Consolidation by limbic association area 2. Motor Impulse 3. Muscle recruitment 4. Postural Reflexive movement HIERARCHY OF MOTOR 1. Limbic lobe and PFC 2. Association areas (posterior parietal cortex  visuospatial) 3. Subcortical Basal Ganglia and Thalamus  stimulated in influencing the cortex in selecting the muscle groups that are intended for the movement. Cerebellum and cortex are involved in planning and adjusting the timing and sequence of movement. 4. Brainstem Reticular Formation & Cerebellum (Pontine reticular formation) 5. Areas 4 & 6, 3,1,2 origin of Corticospinal tracts and Corticobulbar o From cortex to medulla o The discharge of the corticospinal tract neuron will be beginning 100 msecs prior to the actual movement. So during that time, they are firing at a frequency that is proportional to the force exerted in a movement – meaning if a person is carrying a 1kg of load, that person is lifting it up with 1kg of force compared with carrying a 50kg load generating a 50kg of force. At the same time they are changing the firing rate prior to the limb movement through the cerebellum in its autocorrective function

o Upper motor neurons to motor neurons Corticobulbar tracts o Represents the brainstem o Upper motor neurons to spinal cord Strong or Weak Movement / Fast or Slow  Done through gradation of force via increase in frequency 1. Temporal Summation  If you want to carry small load, only low frequency firing (example: carrying a small notebook)  In heavier load, there would be high frequency firing (example: carrying a heavier book) 2. Spatial Summation  Recruitment of muscle fibers – CST neurons  In carrying heavy load, more cells are recruited  In carrying small load, only once cell firing  Therefore, an increase in number of motor units recruited firing , increase in tension produced in individual muscle = stronger or faster movement Force generated by the muscle with maximal intensity / stimulus = 1.82g  force generated by all muscle fibers  all muscle fibers are contracting Compared to 5.95g  maximal tetanic force  highest frequency possible to create this force, increasing it further will produce same force If you (1)  number of Motor units recruited and/or (2)  frequency of firing rates → Tension produced in individual muscles → stronger and faster movements. You have more myosin-actin filaments involved CEREBRAL MOTOR AREAS

Corticospinal tracts o Will end at medial anterior TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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  Area 4: PRIMARY MOTOR AREA  in the first convolution of the frontal lobes anterior to the central sulcus (Precentral gyrus)  Synthesizes agonist into infinite variety of discrete patterns of movement  Gives the simplest motor programs compared with the secondary motor area (pre-motor area and association areas – basal ganglia and cerebellum) which gives more complicated motor programs  Distal muscles – skilled movements  was done by electrically stimulating the different areas of the motor cortex in human beings who were undergoing neurosurgical operations 

Contains Betz cells o Giant pyramidal cells o Gives rise to large myelinated fibers in the CST o Up to 70 m/sec

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Comprise 30% of corticospinal tract (CST) Lesions: Flaccid paralysis ( movements, re-appearance of grasp reflex o No purposeful movements Removal of Area Pyramidalis: o This area is essential for voluntary initiation of finely controlled movements, especially of the hands and fingers o Varying degrees of paralysis of the represented muscles

o Caudate nucleus(sublying) and adjacent Premotor and Supplementary motor areas are not damaged  gross postural and limb “fixation” movements can still occur  loss of voluntary control of discrete movements of the distal segments of the limbs, especially of the hands and fingers.  ability to control the fine movements is gone Lesions at adjacent areas to motor cortex o i.e. Basal ganglia o During stroke o muscle spasm almost invariably occurs in the afflicted muscle areas on the opposite side of the body o results mainly from damage to accessory pathways from the nonpyramidal portions of the motor cortex  normally inhibit the vestibular and reticular brain stem motor nuclei o disinhibition results to spontaneously active and cause  EXCESSIVE SPASTIC TONE Synapse with lamina of anterior horn (only one neuron synapse one lower motor neuron) Other neurons will be synapsing with inhibitory motor neurons Stretch Reflex - Has 2 types of neurons - First order neuron from muscle spindles, afferents synapse with α or γ motor neuron - The reflex would just continue in cycle without the inhibitory interneurons from corticospinal tracts synapsing with α or γ interneurons  SPASTICITY - Cutting off the CS tract will cause many neurons not to be stimulated (stimulation of α or γ interneurons= inhibition of reflex) to α or γ neurons, not all will cause inhibition

Lateral Corticospinal Tract  Origin: Area 4, Area 6, Area 3,1, and 2  Area 4 – 30%  Area 6 – 30%  60% motor cortical areas – a large part wil be coming from sensory areas 40%  Area 3,1,2 – not the only contributory sensory area to CST  Another contributory is Areas 5 and 7 – giving visuospatial information  30-90% of PFC will decussate and become lateral CST. Will decussate at the level of the pyramid until it reaches the spinal cord. Synapse with alpha and gamma motor neuron through interneuron connections so movement will be executed

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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To prevent spasticity – PFC will connect with Inhibitory interneuron – synapse with alpha and gamma so that reflex arc , inhibiting the stretch reflex PFC really does facilitate alpha and gamma motor unit Distal limb muscle for skilled movements by controlling the recruitment order and firing rate 55% PFC upper executive limb muscle – more skilled movements with upper extremities than the feet (exception is the armless pianist)

Corticobulbar Tract – upper motor neuron to the cranial nerves  Decussates before it reaches the cranial nerves  At the level of the cranial nerve to which they will synapse with, CBT decussates, and therefore, affecting the contralateral motor nuclei *From recording: Drawing explanation: This is the entire CBT. This 2 or 3 CBT supplies both cranial nerves, if this were the cortex, the majority will be going to the contralateral, 20-30% will go to the ipsilateral CN nucleus. About CN 7, the facial paralysis. If this is the CBT and this is the CN 7, what will happen to your face? A lower motor neuron lesion or cranial nerve nucleus lesion of the CN 7 will give you an ipsilateral facial paralysis. While the upper and lower motor fibers will be paralyzed. While if you have your same sided CBT lesion, more fiber going to the other side, therefore there will be contralateral. Bilateral – the upper muscle fibers are the ones who will get from the both CBT. Area 6: PRE-MOTOR AREA  Involves in planning your next movement  Spatially guided by the area 5 and 7 (posterior parietal cortex) – will give the pre-motor area the visuospatial information needed for movement  Lateral system: motor tract of the lateral cord, they are your lateral PFC and rubrospinal tract (originates in the red nucleus) – Lamina 9 (alpha and gamma here will be supplying the distal limb muscle)  Medial system: medial lamina - lamina 8 (supply proximal limb muscles and axial muscles – erector spinae and extensors that hold you upright)  To influence Pontine reticular spinal tract – synapse with lamina 8 and synapse with lower motor neuron, such that you will have distal movements that will give you skilled movements, then maintenance of posture  Lesions in area 6 – will give you mild weakness, spasticity, hypertonia, hyperreflexia, and awkwardness (inability to reach for visually identified target)

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Medial surface of area 6 entire body of SMA give bilateral tonic contraction of the limb or bilateral manual coordination (e.g. piano playing)  gross contralateral movement  Lesion: will not give paralysis but will impair bimanual coordination, impaired postural correction  Dancing example:  In spontaneous dancing -Area 4, area 312 are lighting up.  While if you are a member of a dance group and rehearsing for a particular routine, area 6 will also be lighting up because this is the area memorizing the dance steps (area of memorized movements) Area 6 Guided by visual clues through sensory input  Assoc. areas 5 &7  Visual spatial analysis and posterior parietal cortex (integrated somatosensory w/ visual) Neuronal response occurred in the PM area during movements guided by visual clues


Internally guided from memory (i.e. rehearsed dance steps)

Neuronal response occurred in SMA instead of PM area when the monkey performed movement sequence from its memory

Significance of Areas 5 and 7 on movements: - Lesion: difficulty in understanding Visuospatial information - Example: the monkey given a problem with visuospatial information. Food is under the podium of glass floor. In order to get it, the monkey should place his arm on the hole. - If with lesion in areas 5 and 7, will not be able to solve the problem. Even though it can see the food and the hole, it cannot analyze the visuospatial information. It perceives the hole as different, the food is different information, and it cannot add the two together, it cannot analyze the system, it cannot solve the problem. - So therefore, this apraxic animal will be sitting on its but until evening. It will not be able to get it. - So if you have this kind of patient, an apraxic child or individual, you have to solve the problem for that patient. - In the case of the monkey, you have to put the arm on the hole. Once it is inside the hole, it would be easy for it to get the food. - The next morning however, still being apraxic, the same problem will not be solved. So you have to repeat how to solve it for 22 times MOTOR TRACTS

SUPPLEMENTARY MOTOR AREA TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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The Lateral system gives you skilled movements together with the lateral CST – distal limbs. The interneurons will be ipsilaterally, meaning the lateral CST here will not be able to affect the contralateral anterior cord. The Medial system brought about by 4 posture-related tracts – pontine reticulospinal tract, lateral vestibulospinal tract, tectum spinal tract, anterior or ventral corticospinal tract – synapse with lamina 8 motor neuron and going to your proximal and axial muscles thereby contributing in the maintenance of posture. The interneuron here project bilaterally. Whenever you stand up or sit up, you will have bilateral contraction of your muscles.

Dynamic stretch reflex Stimulus: sudden stretch of muscle spindles cause: contraction of the polar ends by means of by means of gamma motor neurons This reflex is self-perpetuating – go on and on Inhibitory mechanism: 1. Cst - inhibitory interneuron inhibit alpha and gamma motor neuron 2. Inverse stretch – 1b will be synapsing with an inhibitory interneuron going to the agonist muscle and firing the antagonist muscle. 3. Renshaw cells – are inhibitory interneuron. Muscle tone Part of static gamma motor neuron that will cause the basal formation of the muscle You have spontaneous firing of the static gamma motor neuron, therefore, what will happen if these are not inhibited by the lateral CST, that muscle tone will also be affected. Therefore, you will have increased muscle tone. The mechanisms of increased muscle tone are: Any lesion of the upper motor neuron that decreases the inhibitory signals of the CST neurons on LMN affecting the stretch reflex Plus increase impulses thru the posture regulation tracts Increase firing of efferent alpha and gamma motor neuron, so basically every component of the reflex arc will increase in firing giving you the disinhibition of alpha and gamma motor neuron SPASTICITY  

The corticospinal tract is inhibitory to the stretch reflex. If this is lesioned, you will have spasticity. The basal ganglia, on the other hand, will not give you spasticity. It will give you hypertonia if you have a lesion in the basal ganglia, because it does not have a direct influence on the PFC, the thalamus does. The cerebellum has an inhibitory influence on the stretch reflex.

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The reticulospinal tract has a facilitatory influence on the stretch reflex. The medullary reticulospinal tract has an inhibitory effect on stretch reflex.

Mechanisms of Spasticity: 1. Removal of inhibitory influences on spinal stretch reflexes 2. Maintained activity of facilitatory influences Identifying Characteristics of Spasticity: - Exaggerated stretch reflex - Exaggerated DTR - Predilection for involvement of muscle groups: antigravity muscles (Leg extensors if you are upright and not lying down; Arm flexors)  HYPERTONIA


UPPER MOTOR NEURON Any of the descending fiber systems that can influence and modify the activity of the LMN

Descending impulses for: a. mediation of somatic motor activity b. control of muscle tone c. maintenance of posture and equilibrium d. suprasegmental control of reflex activity e. innervation of visceral and autonomic structures f. modification of sensory input Upper Motor Neuron (Corticospinal tract) + Eventual Lesions Disinhibition/Release from Inhibition signs: 1. Spasticity & Hypertonia develop gradually over weeks to months 2. Hyperactive Deep Tendon Reflex (Cord lesions 3. Hyperactive DTR +Hyperactive brainstem reflexes (Cerebral lesions) 4. Clasp-knife phenomenon Negative signs o Weakness of muscles Spinal cord injury longer than Cerebral Vascular Accidents Temporal Profile of UMN Lesion in Cerebral Hemisphere: IMMEDIATELY AFTER - Flaccid contralateral paralysis - DTR depressed. AFTER VARIABLE PERIODS - DTR reappear in an exaggerated form in the paralyzed limbs. - superficial abdominal reflexes and the cremasteric reflexes in the male, disappear on the side of the paralysis. AFTER A VARIABLE PERIOD - muscle tone in the affected limb gradually returns but is

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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Hypertonic/Spastic. - This increase of tone is not exhibited in all muscles in the affected limbs. Spasticity selectively involves the antigravity muscles - “flexor synergy” in the UE - “extensor synergy” in the LE - increased resistance to passive movement - hyperactive DTR and manifested as clonus. Clonus - is a manifestation of the exaggerated stretch reflex - contractions of one muscle group are sufficient to stretch antagonistic muscle groups and initiate myotactic responses in that muscle group. - tendency to perpetuate itself in a synchronous manner. Paralysis - May appear complete at the onset of an UMN lesion, - tends to become less severe in time - affected most: motor functions of those associated with fine, skilled movements - affected least: those with gross movements, and those which involve a whole limb. They also show considerable restitution. AFTER A PERIOD OF YEARS, some atrophy of disuse becomes evident. Temporal Profile of UMN Lesion in the Cord COMPLETE CORD TRANSECTION: IMMEDIATE EFFECTS of Complete SC Transection a. Somatic sensation b. Visceral sensation c. Motor function d. Muscle tone e. Reflex activity Period of Spinal Shock: 1- 6 WEEKS and averages about 3 WEEKS. - During this time of spinal shock, there is no evidence of neural activity below the level of the lesion. The termination of the period of Spinal Shock is heralded by the appearance of the Babinski sign! PERIOD OF RECOVERY OF NEURAL FXN AFTER PERIOD OF SPINAL SHOCK - sequence of events which make up the Period of Recovery of Neural Function varies in duration Minimal reflex activity Flexor spasms Alternate flexor and extensor spasms Predominant extensor spasms

3 – 6 weeks post-SCI (Spinal Cord Injury) 6 – 16 weeks post-SCI 16 weeks post-SCI 6 mos post-SCI

1. Minimal Reflex Activity - Characterized by weak flexor responses to painful stimuli which begin distally and progressively involve proximal muscle groups in the extremities

- Babinski sign can be obtained bilaterally - Muscles are flaccid and the DTR cannot be elicited 2. Flexor Muscle Spasms - Characterized by increasing tone in the flexor muscles and by stronger flexor responses to painful stimuli, which progressively involve more proximal muscle groups - Triple flexion response is first seen o flexion of LE at hip, knee and ankle in response to a mild painful stimulus o Mass reflex = most exaggerated form  due to the spread of afferent impulses form one segment to the next  dispersion of impulses in such a manner as to cause motor units to continue firing after the stimulus has been withdrawn 3. Alternate Flexor and Extensor Spasms - mass reflex becomes less severe ~ 4 months post-SCI - Extensor muscle tone gradually begins to increase. - both flexor and extensor muscle spasms occur - extensor muscle tone predominates eventually 4. Predominant Extensor Spasms - Extensor muscle tone may be so predominant - patient can momentarily support his weight in a standing position. 5. Examination of an SCI patient 1 year posttransection: a. Complete paralysis below the level of the lesion b. Loss of all sensation (somatic and visceral) below the level of the lesion c. Marked extensor muscle tone (spasticity) below the level of the lesion d. Hyperactive DTR below the level of the lesion e. Clonus in both LE f. Bilateral Babinski signs g. Bladder and bowel dysfunction - Paralysis of bowel and bladder, present from the time of spinal cord transection, - constitutes one of the major problems - reflex emptying of bowel and bladder can be established. h. Disturbance of sexual function *From recording: - If the CST is affected by spinal cord lesion: And that spinal cord undergoes spinal shock – (example: Christopher Reeve – sustained a C3 to C4 complete transection, he was unable to breathe because the phrenic nerve going to the diaphragm (between C3 to C5) is affected. He had to be sustained by a ventilator) - Spinal shock can be seen on your motor system in the following manner: 1-6 weeks no motor function at all (not able to move) in an average of 3 weeks Then, the beginning of the recovery of the motor nerves seen through the reemergence of the reflexes It is only after the first week that you will see the reemergence of reflexes. Prior to that, if you start assessing for reflexes, you will only get a score of zero

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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- In cerebral lesion: shorter period of flaccidity Example in hemorrhage, stroke affecting the motor tract, you will have zero function for only 12 hours. Before the th 12 hour, you should be monitoring for your patient for the reemergence of the motor functions. - In both spinal cord and cerebral lesion, when you say you have no motor function at all, you are flaccid. And then the beginning of the spasticity means you will have the reemergence of reflexes, then the flexor spasm, next is the extensor spasm until you get the full blown fixture of spasticity. Decreased muscle tone Can be either from lower motor neuron problem, anything that will disrupt the reflex arc, or cerebellar problem will give you hypotonia LOWER MOTOR NEURON Receives muscle spindle efferents (Ia) directly Indirectly influenced by afferents from GTO via the Internuncial neurons - Afferent input from stretch receptors (muscle spindle and GTO) activates ipsilateral cell groups in the SC - Afferent impulses from other sensory receptors are distributed by multi-synaptic circuits bilaterally in the SC - Under powerful indirect suprasegmental control provided by impulses transmitted via descending spinal systems - A lesion confined to one spinal segment will cause weakness, and not complete paralysis, in all muscles innervated by this segment. o Anterior horn cells that innervate a single muscle extend longitudinally through several spinal segments o Several cell columns exist at each spinal level Complete paralysis - Occurs only when the lesion involves the column of cells in several spinal segments that innervate a particular muscle, or the ventral root fibers that arise from these cells - Most appendicular muscles are innervated by fibers arising from parts of three spinal segments - Complete paralysis of a muscle resulting from a central lesion in the anterior horn indicates involvement of several spinal segments. -

Temporal Profile of Lower Motor Neuron Lesion: 1. Hypotonia, Flaccidity and Areflexia - occur almost immediately following a LMN lesion. 2. Muscle atrophy - develops gradually and becomes evident by 2 - 3 WEEKS - muscles may exhibit fasciculations o represent the discharge of muscle fibers innervated by nerve fibers arising from a single LMN

o occur asynchronously in different parts of various muscles and o due to a triggering of motor unit discharges that occur within the cell body of the motor neuron. 3. Fibrillations - small potentials of 1- 2 msec duration - occur irregularly and asynchronously in EMG of denervated muscle Abnormalities of REFLEXES: Hyporeflexia causes:  Anything that disrupts the reflex o Lower motor neuron o NMJ lesion o Muscle Hyperreflexia (reduce inhibition to the stretch reflex)  Upper motor neuron lesion  CST lesion Hypotonia  Anything that disrupts the reflex o Cerebellar o LMN o NMJ (transient) o Muscle Hypertonia  CST – at Cerebral cortex level, brainstem level or spinal cord level  CST is the long neuron that can be affected by tumor, blood vessel problem or any other problem, let’s say multiple sclerosis, you will have spasticity  Spasticity that will be seen 3-4 months after a spinal cord lesion or earlier if cerebral lesion  Basal ganglia – rigidity If you have weakness, you can either have upper or lower motor neuron problem. ABNORMALITY OF TONE HYPOTONIA HYPERTONIA Cerebellar lesion Area 6 lesion LMN lesion SMA lesion NMJ lesion BG lesion Muscle fibers lesion Spinal cord lesion Dec. MUSCLE POWER Weakness or paralysis

Inc. MUSCLE POWER Not produced by neurological lesions

HYPOFLEXIA LMN lesion NMJ lesion Muscle lesion


Question and Answer: Motor root lesion: flaccid paralysis Lateral corticospinal tract lesion: spastic paralysis

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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Lower motor neuron lesion: flaccidity, hypotonia, atrophy or hyporeflexia LIMBIC SYSTEM (Depression) ASSOCIATED SYSTEM (Apraxia)

Vestibular System Sensory of angular acceleration (semicircular canal); Sensory of linear acceleration (otoliths) ↓ (info about head kinematics) Vestibular nucleus and Cerebellum Vestibular apparatus – proprioceptor of the head Axis

BRAINSTEM (Spastic Paralysis) X Skeletal Muscular System (Flaccid Paralysis) POSTURAL CONTROL Posture: control of relative position of various parts of body w/ respect to egocentric reference

Around X Y

Feed forward Mechanisms prior to Pulling Rope

Around Y Z

Situation: Random guy pulling on a rope with an attached load Question: Here we have two types of muscles, the gastrocnemius and the biceps muscle. Which muscle should contract first in order to pull the load and remain standing? Answer: Gastrocnemius should contract first. If it were the biceps which contracted first, the person would just fall toward the load. Postural control ensures the maintenance of upright position while doing multiple skilled movements.

POSTURAL REFLEX ARC 1. Afferents (Sensory systems): 1) CN VIII, 2) proprioceptive SCT, 3) visual apparatus → these should be maintained to maintain posture a. Lesion on one of the three: Posture can still be maintained. b. Lesion on two: Poor posture; you may not be able get up at all. 2. Center: Brainstem integration, Cerebellar integration 3. Efferents: Posture regulating tracts of axial and proximal muscle a. Vestibulospinal tract b. Reticulospinal tract c. Anterior corticospinal tract d. Tectospinal tract

Location of axis Through the nose

Through the ears

Type of acceleration Linear



In the car moving forward; walking backwards Tilting the head


In the MRT


Pitching; Nodding “Yes” Through Linear Going up and the neck down the elevator Around Angular Moving head to Z say “No” *All these information regarding the movement of the head will be brought to the vestibular nucleus of CN VIII. 4 Nuclei of CN VIII (Upper Medulla, lower pons) [SLIM] 1. Superior 2. Lateral – origin of VST 3. Interior 4. Medial [2] Lateral Vestibular Nucleus (Deiter’s nuclei) - origin of VST - supply extensor muscles of the same side Lateral vestibular nucleus → VST → extensor MN (ipsilateral) → axial and proximal muscles of the same side + reciprocal inhibition of flexor MN Functions: - Postural adjustments of body during head angular or linear accelerations Example: You fall to your right → right CN VIII stimulated → right VST → trunk and limb muscles of the same side will extend to protect you [3] Medial vestibular Nuclei & - Vestibular nuclei & Medial Longitudinal Fasciculus - Ascending MLF  contralateral to CN VI (abduction of eye); ipsilateral to CN III (adduction of eye) - Descending MLF  Ipsilateral to spinal cord, upper part of cervical cord and mid thoracic [MEDIAL SYSTEM]

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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PHYSIOLOGY Functions: - Postural adjustments of angular accelerations


Example: Vestibulo-ocular reflex/Doll’s eye reflex: helps maintain eye movements in relation to the head → left CN VI → abduction of left Turn head to right eye→ eyes will turn to the left → Right MLF →right CN III → adduction of right eye → eyes will turn to the left Vestibular system: takes care of head movements in response to the eye movements; takes care of eye movements in response to head movements Reticulospinal Tract 1. Pontine RST – excitatory to extensor muscles of axial and proximal limb 2. Medullary RST – inhibitory stretch reflex Cerebral lesions: decrease cortical inhibition → spastic hemiplegia Excitatory-Inhibitory Antagonism Between Pontine and Medullary Reticular Nuclei

Red nucleus o located in the mesencephalon, functions in close association with the corticospinal tract o has close connections with the cerebellum o Receives: - Corticorubral tract Primary motor cortex  Red nucleus - Branching fibers from the corticospinal tract as it passes through the mesencephalon Synapses with Magnocellular portion below RN - Rubrospinal tract Red nucleus  Spinal cord Crosses to the opposite side in lower brain stem Runs anterior to CST into Lateral columns of the spinal cord Forms the LATERAL MOTOR SYSTEM with CST Termination: o terminate mostly on the interneurons of the intermediate areas of the cord gray matter o directly on anterior motor neurons Corticorubrospinal Tract o accessory route for transmission of relatively discrete signals o motor cortex  spinal cord o with destroyed CST, it can still causes discrete movements except for fine control of fingers and hands o Lesion: no wrist movements

Pontine Reticular Nuclei - EXCITATORY signals through pontine reticulospinal tract in the anterior - column of the cord - terminates at medial anterior motor neurons that excite the axial muscles (antigravity) - muscles of the vertebral column and the extensor - muscles of the limbs - receive strong excitatory signals from the vestibular nuclei and deep nuclei of cerebellum Lesion above pontine RST, below red nucleus → rubrospinal tract will have no effect on rigidity → decerebrate rigidity (upper & lower limbs affected)

Rubrospinal tract

Medullary Reticular Nuclei - INHIBITORY signals to the same antigravity - anterior motor neurons - through Medullary Reticulospinal tract (Lateral column) - prevents abnormal tension of antigravity muscles - Receives collaterals: 1. CST 2. RST 3. Other motor pathways

CEREBELLUM Basic Circuitry Inputs to cerebellum

Red Nucleus Serves as an Alternative Pathway Cortical Signals  Spinal Cord

Red nucleus → decussate to contralateral midbrain → lateral spinal cord → terminates on cervical spinal cord → control of functions in upper extremities Lesion above RN → decorticate rigidity (flexion abnormality) → upper extremities are flexed, lower extremities are extended (arms are flexed or bent inward the chest, hands clenched, legs extended, feet turned inward) Poorer prognosis: Decerebrate rigidity

1. Motor cortex gives intended movement pattern--also a planner of movements, also basal ganglia, cerebellum, and PPC 2. Visuospatial information proprioceptive information of spinal cord—the intended movement and planned movement All these going to the deep nuclei of cerebellum from pontine nuclei and inferior olivary nucleus

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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Deep Nuclei: Fastigial Vestibulocerebellum Globose Spinocerebellum Emboliform Dentate  Neocerebellum

2. Spinocerebellum or Paleocerebellum [POSTURE] - Inputs from limbs via SCT (superior and inferior peduncle)  Globus & Emboli) GE; From motor cortex  GE - Outputs to contralateral red nucleus, thalamus - Unconscious proprioceptive information from GE nuclei  to contralateral red nucleus, thalamus - Analyzes proprioceptive input to anticipate future positions of body parts  Muscle tone, posture - Compares actual movements with intended movements - In just 15-20 milliseconds, the cerebellum is able to predict and compare actual movements, etc. 3. Neocerebellum or cerebrocerebellum [COORDINATION] - Inputs from Cortical areas (esp. PFC)  Corticorubropontocerebellar tract  Dentate (D) - Ouputs to contralateral red nucleus thalamus, motor cortex (Dentato-rubro-thalamo-cortical pathway) - Coordinates planning of movements and muscle tone required for skilled movements (esp. planning and execution of complex spatial and temporal sequences of movements—includes speech) - Largest and receives input from cerebral cortex Cerebellar Functions     

Compare calculate timing, distance and pattern Corrects and anticipates error Coordinates learned movement and skilled movements Balances all sensory feedbackmore response Postural equilibrium

Cerebellar Divisions of Function Disorders of the Cerebellum

 Vestibulocerebellum or archicerebellum EQUILIBRIUM  Spinocerebellum or paleocerebellum  POSTURE or muscle tone  Neocerebellum or cerebrocerebellum  COORDINATION of skilled movements initiated at cortical levels 1. Vestibulocerebellum or archicerebellum [EQUILIBRIUM[] - Inputs from vestibular nuclei of brainstem; Reticular Formation (RF)  Fastigial nucleus (F) - Outputs mostly to ipsilateral vestiblar nucleus; contralateral to RF

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Truncal ataxia –dysfunction of spinocerebellum Limb ataxia Intention tremors Pendular jerks due to hypotonia Dysdiadochokinesia Decompostion of movement Dysmetria Cerebellar Lesions

Malcomparison  +/- lesion Miscalculation  Dysmetria, ataxia, past pointing Malcorrection  intention tremor, mystagmus Incoordination of learned movements Imbalance

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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PHYSIOLOGY    o o o o o 


BASAL GANGLIA Like the cerebellum, constitute another accessory motor system and always function in association with other systems of motor control Receive most of their input signals from the cerebral cortex itself and also return almost of their output back to the cortex On each side of the brain, consist of: Caudate nucleus Putamen Globus pallidus Substantia nigra Subthalamic Nucleus Almost all of the sensory nerve fibers connecting the cerebral cortex and the spinal cord pass through the space that lies between the caudate nucleus and the putamen called the internal capsule of the brain

When there is serious damage to the basal ganglia, the cortical system can no longer provide these patterns e.g. writing of letters of the alphabet becomes crude, as if learning for the first time how to write Neural Pathways of the Putamen Circuit  Execution of learned patterns of movement begin in the premotor and supplementary motor areas of the motor cortex and in the somatosensory areas of the sensory cortex  Next, they pass to the putamen, mainly bypassing the caudate nucleus, then to the internal portion of the globus pallidus, next to the ventroanterior and ventrolateral relay nuclei of the thalamus  Finally, they return to the cerebral primary motor cortex and to portions of the premotor and supplementary areas closely associated with the primary motor cortex The putamen circuit has its inputs mainly from those parts of the brain adjacent to the primary motor cortex but not much from the primary motor cortex itself. Its ouputs mainly go back to the primary motor cortex or closely associated premotor and supplementary cortex. 1. In close association with the primary putamen circuit are ancillary circuits with this pathway: From the putamen  Globus pallidus  subthalamus  Substantia nigra  Return to the motor cortex by way of the thalamus

EXECUTING PATTERNS OF MOTOR ACTIVITY – THE PUTAMEN CIRCUIT  The basal ganglia functions with the corticospinal system to control complex patterns of motor activity

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

Abnormal Function in the Putamen Circuit 1. Athetosis o Spontaneous and often continuous writhing movements of a hand, an arm, the neck, or the face Page 10 of 12



o Cause: Lesions in the globus pallidus 2. Hemiballismus o Flailing movements of an entire limb o Cause: Lesion in the subthalamus 3. Chorea o Flicking movements in the hands, face, and other parts of the body o Cause: Multiples small lesions in the putamen 4. Parkinson’s Disease o Extremely severe rigidity, akinesia, and tremors o Cause: Lesions of the substantia nigra o COGNITIVE CONTROL OF SEQUENCES OF MOTOR PATTERNS – THE CAUDATE CIRCUIT  Cognition: thinking processes of the brain, using both sensory input to the brain plus information already stored in memory  Cognitive Control of Motor Activity – actions occur as a consequence of thoughts generated in the mind  The caudate nucleus extends into all lobes of the cerebrum beginning anteriorly in the frontal lobes, then passing posteriorly through the parietal and occipital lobes, and finally curving forward into the temporal lobes  It receives large amounts of inputs from association areas of the cerebral cortex overlying the caudate nucleus  Pathway: From the cerebral cortex  caudate nucleus  internal globus pallidus relay nuclei of the ventroanterior and ventrolateral thalamus  Back to the prefrontal, premotor, and supplementary areas of the cerebral cortex  Almost none of the returning signals pass through the primary motor cortex, going instead to the accessory motor regions in the premotor and supplementary motor areas concerned with putting together sequential patterns of movement lasting 5 or more seconds instead of exciting individual muscles Cognitive control of motor activity determines subconsciously, and within seconds, which patterns of movement will be used together to achieve a complex goal that might itself last for many seconds.

CHANGING THE TIMING AND SCALING THE INTENSITY OF MOVEMENTS  Two important capabilities of the brain in controlling movement: o To determine how rapidly the movement is to be performed o To control how large a movement will be e.g. writing the letter “a” quickly or slowly, or large or small  In patients with severe lesions of the basal ganglia, these timing and scaling functions are poor, sometimes nonexistent  Posterior parietal cortex – locus of spatial coordinates for motor control of all parts of the body as well as for the relation of the body to its parts to all its surroundings  Because the caudate circuit of the basal ganglia system functions mainly with association areas such as the posterior parietal cortex, presumably the timing and scaling of movements are functions of this caudate cognitive motor control circuit Neurotransmitters in the Basal Ganglial System Dopamine pathway: from substantia nigra to caudate nucleus and putamen  GABA pathway: from caudate nucleus and putamen to globus pallidus  ACh pathway: from cortex to caudate nucleus and putamen  Multiple general pathways from the brain stem that secrete NE, serotonin, enkephalin, and other 

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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neurotransmitters in the basal ganglia as well as in other parts of the cerebrum Multiple glutamate pathways that provide most of the excitatory signals that balance out the large numbers of inhibitory signals transmitted by the dopamine, GABA, and serotonin inhibitory transmitters GABA neurons in the feedback loops from the cortex through the basal ganglia and then back to the cortex make virtually all these loops negative feedback loops, thus lending stability to the motor control systems Dopamine also functions as an inhibitory transmitter in most parts of the brain thus functioning in stability

CLINICAL SYNDROMES OF BASAL GANGLIA DAMAGE Parkinson’s Disease  AKA paralysis agitans  Results from widespread destruction of the pars compacta of the substantia nigra which sends dopamine-secreting fibers to the caudate nucleus and the putamen  Characterized by (1) rigidity of much of the musculature of the body, (2) involuntary tremor of the involved areas even when the person is resting at a fixed rate of 3 to 6 cycles per second, and (3) serious difficulty in initiating movement called akinesia  Destruction of dopaminergic neurons allow the caudate nucleus and putamen to become overly active and possibly cause continuous output of excitatory signals to the corticospinal motor control

system leading to excitation of many or all muscles, resulting to rigidity  Oscillation of feedback circuits because of high feedback gains after loss of their inhibition leads to tremor  Dopamine secretion in the limbic system, especially in the nucleus accumbens is often decreased along with its decrease in the basal ganglia, suggesting that this might reduce psychic drive for motor activity so greatly that akinesia results Huntington’s Disease (Huntington’s Chorea)  Hereditary disorder with symptoms showing at age 30-40 years  Characterized by flicking movements in individual muscles and then progressive severe distortional movements of the entire body plus dementia  Probable cause: Loss of most of the cell bodies of GABA-secreting neurons in the caudate nucleus and putamen and of ACh-secreting neuron in many parts of the brain  Loss of GABA neuron inhibition of globus pallidus and substantia nigra allows spontaneous outbursts activity that cause distortional movements  Loss of ACh-secreting hormones especially in the thinking areas of the cerebral cortex results to dementia  The abnormal gene has a many-times-repeating codon (CAG) that codes for multiple extra glutamine amino acids in the molecular structure of an abnormal neuronal cell protein called huntingtin causes the symptoms In summary, the basal ganglia are essential to motor control by performing the following important functions: (1) to help the cortex execute subconscious but learned patterns of movement and (2) to help plan multiple parallel and sequential patterns of movement that the mind must put together to accomplish a purposeful task.

TRANSCRIBERS: Maja, Von, Catie, Kenan, Eli, Rissa, Trisha, Eunika

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