MOTOR SYSTEMS Muscles and Joints Muscles Moving The Spinal Cord Spinal Reflexes Reciprocal Control of Opposing Muscles Polysynaptic Adaptations and Reflexes The Motor Cortex The Basal Ganglia Limbic System The Cerebellum Cranial Nerves

Muscle groups are complex; attach bone to bone via tendons and ligaments

A muscle group has many fibers

The Neuromuscular junction (NMJ): The receptive portion of muscle-the motor end-plate

The NMJ ( sometimes called the motor end-plate)

nACHr

End-plate potential Larger Longer Leads to Ca+ influx in sarcolema of muscle – Ca+ causes muscle contraction

Disease of the NMJ? MG

MG

muscle fibers encase myofibrils. The casing is called the sarcolema Muscle group Muscle fiber myofibril

End-plate potential causes ca+ influx into sarcolemma

Myofibrils in turn contain “Actin and Myosin” filaments

When the NMJ is activated Actin-myosin interact to shorten the length of a muscle fiber

Sliding filament model of muscular contraction

Muscle shortens=work

Cortical vs Spinal control of behavior Goal-directed Complex Higher levels of control Plastic Numerous reflexive behaviors are involved Reflexive Simple Automatic inplastic

Spinal reflex ARCs Monosynaptic – stretch Polysynaptic – Withdrawal – Antagonist muscle groups – Synergistic muscle groups – Polysegmental relexes – Cross-spinal reflexes

A “monosynaptic” spinal reflex arc- the Stretch reflex

The stretch reflex involves neuromuscular “spindles”

Stretch reflex regulates muscle tension in every muscle group

The polysynaptic part of stretch reflexes: inhibition of Antagonist muscles

Spinal inhibition of antagonist muscles require inhibitory interneurons

The “withdrawal reflex arc” a polysynaptic spinal reflex

Also involves interneurons

And may involve more than one spinal cord segment

And/or Cross spinal reflex arcs

The Goli tendon organ (GTO) reflex

Neural activity of spinal neurons related to whole muscle group activity

Lower motor neurons “the final common pathway”

Goal-Directed Behavior and Reflexive Behavior Goal-DirectedReflex Relatively ComplexRelatively Simple Consciousness? IntentionAutomatic PlasticRelatively Inplastic Requires CortexCortex not required Learning /experiences are major influence Genetics are major influence

Goal-Directed Behaviors Require: Goal selection and prioritization Resistance to distracters -Cross-modal Sensory integration – Perception of target – Awareness of location of movable body part – Ability to aim movement of body part – Ability to detect errors and re-adjust, (use feedback) – Ability to use feedback to control movement of body part

Sensory-Motor Integration in the frontal lobes

THE DLPFC: “The conductor” Integrates cross modal input- may initiate goal-directed behaviors Lesions of the dorsolateral frontal areas results in a number of “executive” motor impairments. These include perseveration, incoordination, motor impersistence, apraxias and hypokinesia.

The premotor and supplementary motor ctx: “The sections” Stimulation= complex sequences of behavior (aimless behavior)

Damage to the secondary Motor Cortex? Ideomotor Apraxia This apraxia is associated with great difficulty in the sequencing and execution of movements. A common test of apraxia is to request the patient to demonstrate the use of a tool or household implement (e.g., "Show me how to cut with scissors"). Difficulties are apparent when the patient moves the hand randomly in space or uses the hand as the object itself, such as using the forefinger and middle finger as blades of the scissors. They have additional trouble sequencing the correct series of movements and make errors in orienting their limbs in space consistent with the desired action. Imitation of the movements of others will usually improve performance but it is still usually defective. Memories for skilled acts are probably stored in the angular gyrus of the parietal lobe in the left hemisphere.

The primary motor cortex; “the instrument” Stimulation = relatively simple fragments of behavior

TWO MAJOR DESCENDING PATHWAYS FROM THE PRIMARY MOTOR CORTEX: The Dorsolateral pathway

And the VM Path. The VM pathway does not discretely decussate, but does branch and innervate contra lateral segments in the spinal cord.

DL vs VM descending motor paths Dorsolateral Decussates at medullary pyramids Distal muscle groups More direct More volitional control Higher resolution of control Ventromedial Does not cross Medial muscle groups Gives off spinal collaterals Yoking Lower resolution of control

Other Motor Pathways In addition there are other motor paths that have relays in the brainstem These other paths innervate nuclei of the RAS, cranial nerve nuclei, etc…

Descending paths get additional inputs

Both pathways terminate in spinal cord segments

According to part of the body they control

On lower motor neurons (alpha motor neurons)

Amyotropic lateral sclerosis (ALS) disease of the alpha motor neurons

ALS

Alpha motor neurons project to form part of spinal nerve pairs

Terminate on muscle fibers

At each spinal segment

BASAL GANGLIA Nigro-striatal Pathway Striato-Pallidal pathway

Basal Ganglia Neostriatum – Caudate (kaw-date) nucleus and putamen (pew-TAY-men) Globus Pallidus ( GLOB-us PAL-i-dos) Substantia nigra (included by functional not anatomical relationship) Subthalamus others

Basal ganglia- Complex ccts The basal ganglia are involved in motor regulation, but are only one component of the control of behavior. The way in which the basal ganglia controls movement is complicated and not completely understood, but at his time may be fairly described as the gate-keeper of movement. Disorders of the basal ganglia can either lead to too much behavior or too little behavior.

Basal Ganglia-Neostriatum ( composed of the caudate nucleus and the Putamen)

The Nigro-striatal pathway- the behavioral “grease” system

The Globus Pallidus ( the striato-pallidal circuit= the behavioral “brakes” system)

Basal Ganglia Syndromes too much or too little behavior Damage to the Nigro-striatal pathway – Parkinsons (not enough behavior) – 01,GGIC:en&um=1&q=parkinsons&ndsp=20&ie=UTF-8&sa=N&tab=iv# 01,GGIC:en&um=1&q=parkinsons&ndsp=20&ie=UTF-8&sa=N&tab=iv# – 01,GGIC:en&um=1&q=parkinsons&ndsp=20&ie=UTF-8&sa=N&tab=iv# 01,GGIC:en&um=1&q=parkinsons&ndsp=20&ie=UTF-8&sa=N&tab=iv#

Basal Ganglia syndromes Strato-Pallidal Pathway- too much behavior – Huntingtons – Tourettes’ – Balisms – Others

Huntington's Chorea is principally characterized by hyperkinesias - abnormal, purposeless, involuntary motor movements that can occur spontaneously or only when the patient is trying to do something. These movements may be repetitive or non- repetitive.

Tourettes Syndrome TS usually becomes apparent in children between ages 2 to 15, with approximately 50% of patients affected by age 7. The age of symptom onset is typically before the age of 18. TS is more frequent in males than females by a ratio of about 3 or 4 to 1. The disorder is thought to affect 0.1% to 1.0% of individuals in the general population.

Tourettes Motor tics Initially, patients develop sudden, rapid, recurrent, involuntary movements (motor tics), particularly of the head and facial area. At symptom onset, motor tics usually consist of abrupt, brief, isolated movements known as simple motor tics, such as repeated eye blinking or facial twitching. Simple motor tics may also include repeated neck stretching, head jerking, or shoulder shrugging. Less commonly, motor tics are more "coordinated," with distinct movements involving several muscle groups, such as repetitive squatting, skipping, or hopping. These tics, referred to as complex motor tics, may also include repetitive touching of others, deep knee bending, jumping, smelling of objects, hand gesturing, head shaking, leg kicking, or turning in a circle. In addition to affecting the head and facial area, motor tics also affect other parts of the body, such as the shoulders, torso, arms, and legs. The anatomical locations of motor tics may change over time. Rarely, motor tics evolve to include behaviors that may result in self-injury, such as excessive scratching and lip biting.

Vocal tics Vocal tics are sudden, involuntary, recurrent, often relatively loud vocalizations. Vocal tics usually begin as single, simple sounds that may eventually progress to involve more complex phrases and vocalizations. For example, patients may initially develop simple vocal tics, including grunting, throat clearing, sighing, barking, hissing, sniffing, tongue clicking, or snorting. Complex vocal tics may involve repeating certain phrases or words out of context, one's own words or sounds (palilalia), or the last words or phrases spoken by others (echolalia). Rarely, there may be involuntary, explosive cursing or compulsive utterance of obscene words or phrases (coprolalia).

LIMBIC STRUCTURES AMYGDALA HIPPOCAMPUS SEPTUM

AFFECTIVE IMPUSLES The 4-F’s, but different