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• Action Potential / Nerve Trunks
• Spinal Cord / Spinal Reflexes
• Central Motor Systems
• Eye Movements and Vestibular System
• The Cerebellum and Basal Ganglia

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EXTRACELLULAR RECORDING: Non-invasive recording of action potentials by placing electrodes outside the neuron, on the skin.

• MONOPHASIC RECORDING: Utilizes one electrode plus a ground electrode. The electrical potential outside the neuron is then recorded as action potentials pass through.
• DEPOLARIZATION is represented as an upward peak on the graph, where up is more negative and down is more positive. As the action potential passes the electrode, the outside of the neuron becomes more negative, as Na⁺ flux in.
• BIPHASIC RECORDING: Utilizes two electrodes and measures the potential difference between them.
• Depolarization passes the first electrode: The first electrode becomes negative with respect to the second electrode.
• Negative (upward) deflection on graph.
• Depolarization passes the second electrode: The two electrodes are now both depolarized and therefore have the same volt-potential.
• Graph returns to zero-line.
• Depolarization then reaches second electrode while first depolarizes.
• Positive (downward) deflection on graph.
• THRESHOLD POTENTIAL: With external stimulation, large axons are excited more easily (have a lower threshold potential) than small axons because they have a lower internal resistance.

AXON DIAMETER: Many properties of nerves vary according to axon diameter:

• CONDUCTION VELOCITY: There is a linear relationship between axon diameter and conduction velocity:
• Myelinated Axons: CONDUCTION VELOCITY (m / sec) = 6 x Diameter (micron)
• Unmyelinated Axons: CONDUCTION VELOCITY (m / sec) = 1.7 x Diameter (micron)
• EXTRACELLULAR EFFECTS:
• The amplitude of the extracellular action potential varies directly with cell diameter.
• The threshold for extracellular stimulation varies inversely with axon diameter. The larger the axon, the lower the stimulus threshold.
• LOCAL ANESTHETICS: Small axons are blocked before large axons.
• LARGE AXONS are more sensitive to (blocked first by):
• Temperature change
• Pressure change
• Extracellular positive stimulation
• Asphyxia, anoxia

COMPOUND ACTION POTENTIAL: An extracellularly stimulated action potential that has graded stimulus intensity. It only occurs with artificial stimulation.

• SUMMATION: The potential shows summation of the individual axons contained within the nerve being stimulated.
• At low stimulus intensity, only the largest axons will be stimulated.
• At higher intensity, more axons will be stimulated, and a higher resultant stimulus intensity will be recorded.

CLASSIFICATION OF NERVE TRUNKS:

• ELECTROPHYSIOLOGICAL CLASSIFICATION: Use capital letters. Based on conduction velocities.
• This scheme is used for all nerves but muscle spindle afferents.
• Cutaneous Afferents use this designation.
• CATEGORIES:
• A-alpha = fastest nerves, 120 m / sec: Alpha Motor neurons innervating extrafusal muscles
• A-beta
• A-gamma = Gamma motor neurons innervating intrafusal muscle.
• B
• C
• ANATOMICAL CLASSIFICATION: Use roman numerals. Based on axon diameter.
• Only Muscle Spindle Afferents use this designation.
• CATEGORIES:
• I (largest nerves) = Primary muscle spindle and Golgi Tendon afferents
• II = Secondary muscle afferents; skin, touch, and pressure afferents
• III = Skin, temperature, fast pain; Autonomic
• IV = slow (dull) pain fibers; Autonomic

BELL-MAGENDIE LAW: Afferent nerves enter over the dorsal Root, and efferent nerves leave through the Ventral Root.

• EXCEPTION: Some Pelvic Viscera pain and temperature axons enter the spinal cord through the Ventral Root.
• The Dorsal Root Ganglion is still in dorsal root, but the post-ganglionic axons bends around the Rami Communicans and actually enters the spinal cord through the Ventral Root.
• CLINICAL: Thus, sectioning of dorsal roots will not completely alleviate pelvic pain.

MEASURING CONDUCTION VELOCITY: Conduction velocity of a motor axon cannot be measured directly, because it would include the time for the potential to cross neuromuscular junction and to conduct through the muscle membrane. If you want to just measure conduction through the nerve itself:

• PROCEDURE:
• Place two electrodes on the forearm, on two different parts of the Median Nerve.
• Stimulate the Abductor Pollicis muscle.
• On the graph, record the different in time (latency period) between stimulation and muscle flexion.
• Use equation above to get conduction velocity, m / sec
• PAIN FIBERS: In measuring sensory nerves, sharp pain fibers (pin prick) travel faster than temperature fibers. So, a withdrawal reflex from sharp pain occurs faster than a withdrawal reflex from a hot stove.
• LOCATING AXIAL NEUROPATHIES: We can't directly, non-invasively stimulate nerves that aren't in the extremities, but we can determine conduction problems by using a REFLEX ARC.
• SEGMENTALLY stimulate a sensory nerve going up the arm, and induce a reflex. If a local stimulation shows normal velocity, but the reflex took too long of a time, then you can deduce that their must be a conduction problem in the proximal part of the reflex.
• ELECTROMYOGRAM (EMG): Test to measure muscle contractility and stimulation of motor nerves.
• The amplitude of the muscle response tends to drop off as you go from distal to proximal, by about 15%
• REPEATED STIMULATIONS: The normal response should show the same magnitude for each stimulation with repeated stimulations of low frequency. With higher frequency (i.e. tetanic stimulation), normal response should be a tetanic graph (increasing tension with decreasing magnitude on each successive stimulus).
• MYASTHENIA GRAVIS: On an EMG it will show a Decrescendo (decreasing magnitude) graph with repeated stimulations.
• Low frequency stimulations (non-tetanic) are used to diagnose MG.
• MG is an auto-immune disorder against the post-synaptic neuron (nerve terminal)
• MYASTHENIC (EATON-LAMBERT) SYNDROME: On an EMG it will show a Crescendo (increasing magnitude) graph with repeated stimulations.
• High frequency stimulations (Tetanic Stimulation), which hurts a lot, are used to diagnose Myasthenic Syndrome.
• This syndrome is an auto-immune disorder against the pre-synaptic neuron.

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MOTOR UNIT: An alpha-Motor Neuron, plus all of the muscle cells it innervates.

• alpha-Motor Neurons innervate extrafusal muscles.
• Final Common Pathway
• Any given muscle cell is innervated by only one alpha-Motor Neuron.
• INNERVATION RATIO: The number of alpha-neurons innervating a whole muscle (innervation density) depends on the amount of control over the muscle we need.
• Extraocular Muscles = 9 : 1 (9 muscle cells to 1 neuron) ratio, high innervation density.
• Postural Muscles = 2000 : 1 (2000 muscle cells to 1 neuron) ratio, low innervation density.
• OBLIGATORY, NON-GRADED STIMULATION: Every time an alpha-neuron is fired, it will cause an action potential in every muscle cell it innervates. There are no graded or partial potentials.
• MYASTHENIA GRAVIS and other pathologies may prevent an action potential from happening with every neuron firing -- but this is pathological and not the normal circumstance.
• MOTOR NEURON POOL: All of the motor neurons that innervate a single muscle. They are arranged close to each other in the ventral horn, according to somatotopic organization:
• SPINAL CORD ORIENTATION: The more dorsolateral you go, the more you go distally away from the midline:
• DORSOLATERAL Part of Ventral Horn: Innervates Extremities Muscles
• VENTROMEDIAL Part of Ventral Horn: Innervates Axial Muscles
• FLEXORS: Nerves going to flexors tend to lie dorsally.
• EXTENSORS: Nerves going to extensors tend to lies ventrally.

FORCE TRANSDUCTION: Twitch Tension in a muscle is increased by increasing the frequency with which alpha-motor neurons are fired.

• With high frequency firing, the muscle doesn't get a chance to completely relax before the next action potential.
• Tetanus is maximal twitch tension.
• PRINCIPLE OF ORDERLY RECRUITMENT ACCORDING TO SIZE: INTRACELLULAR, physiological stimulation of nerves, the smallest axons are stimulated first (have the lowest threshold), and largest axons are stimulated last.

• This is another way to increase the force with which a muscle contracts: "Recruit" more alpha-neurons to fire on the muscle. In this case, again, the smallest neurons will fire first (small twitch tension), and larger neurons will fire later (larger twitch tension).
• V = IR: Small neurons have a higher resistance, which means they will show a stronger depolarization (V) for the same current (I).
• That's why they fire first. This is the opposite of external stimulation, where smaller neurons are stimulated last.
• In physiological stimulation, smaller neurons have a smaller threshold potential than larger neurons.

SLOW -vs- FAST TWITCH MUSCLE

	SLOW TWITCH	FAST TWITCH
alpha-Motor Neuron Diameter	Small	Large
Conduction Velocity	Fast	Slow
Muscle Cells innervated (motor unit size)	Fewer cells innervated, and with a smaller diameter	More cells innervated, with a larger diameter
Twitch Tension	Small tension	Large tension
Contraction Speed	Slow speed of contraction	Rapid contraction
Extracellular spike size (magnitude)	Small	Large
Metabolism	Oxidative (lots of mitochondria)	Glycolytic (few mitochondria)
Capillary Supply	High	Low
Resistance to fatigue	High resistance to fatigue	Easily fatigued
Muscle Color	Red (from mitochondria)	White
Functional Adaptation	Generate small forces over a long period of time -- Endurance	Generate large forces for a brief time -- Sprint

MUSCLE SPINDLE: Intrafusal muscle fibers are innervated by afferent nerves that send signals back to the CNS about the muscle's contractility. The muscle spindle is arranged in parallel with extrafusal muscle.

• Two different types of muscle fibers: They run parallel to each other in the muscle spindle. They both have respective equatorial and polar regions.
• BAG FIBERS: The velocity component of the muscle spindle. These fibers convey how quickly the muscle spindle is changing length.
• EFFERENT INNERVATION is by Dynamic Gamma Efferents, which serves to increase the sensitivity of the velocity component.
• AFFERENT INNERVATION is by IA Afferents only, which form Annulospiral Endings
• CHAIN FIBERS: The length component of the muscle spindle. These fibers convey the spindle length at any instant in time.
• EFFERENT INNERVATION is by Static Gamma Efferents, which serves to increase the sensitivity of the length component.
• AFFERENT INNERVATION is by both IA (Annulospiral) and IIA Afferents (Flower Spray)
• Two different regions of the muscle spindle:
• EQUATORIAL REGION: Contains muscle cell nuclei, and no actin or myosin. It behaves like a spring.
• AFFERENT INNERVATION is by Muscle Spindle Ia Afferents. When the spindle is stretched, these afferents fire.
• Stretch Muscle ------> Increase Ia and IIa firing rate
• Contract Muscle ------> Decrease Ia and IIa firing rate
• POLAR REGION: Contains striated muscle, actin, and myosin.
• EFFERENT INNERVATION is by Static Gamma Efferents
• Gamma Firing ------> Contract polar region ------> Stretch whole spindle ------> Increase Ia Afferent firing rate
• IA AFFERENT NERVES: They synapse with alpha-Motor Neurons that go back to the same muscle.
• "Local Sign": The response is confined exclusively to the muscle cell from which the signal originated.
• RAMP AND HOLD EXPT: Stretch a muscle and keep it stretched, and IA afferents will detect both the velocity and length of the muscle.
• They show a marked increase in activity while the muscle is being stretched, then they drop back down once stretching ceases, although they drop down to a higher basal level than before.
• ANNULOSPIRAL ENDINGS: They form annulospiral endings, on both bag and chain fibers, on the equatorial region of the spindle.
• IIA AFFERENT NERVES: Their pathway is more complex. The connection is not monosynaptic but rather involves interneurons.
• RAMP AND HOLD EXPT: Stretch a muscle and keep it stretched, and IIA Afferents will detect only length of muscle spindle.
• They show an increase in firing-rate as muscle is being stretched, and they maintain the new firing frequency once the muscle is being held at the new length.
• FLOWER SPRAY ENDINGS: They form "flower spray" endings on the polar regions of the spindle, which help them detect the current muscle length.
• STATIC GAMMA EFFERENT NERVES: They increase the length sensitivity of the muscle spindle.
• They innervate Chain fibers in the polar regions of muscle spindles.
• They bring about strong contraction in the poles of the spindle.
• FNXNS in the Muscle Spindle:
• Static Gammas increase the sensitivity of IA afferents and IIA afferents to change in spindle length. IA and IIA fibers will fire with higher frequency, in response to less change in length.
• Static Gammas prevent unloading (temporary pause) of spindle afferents, which occurs with spindle shortening.
• DYNAMIC GAMMA EFFERENT NERVES: They increase the velocity sensitivity of the muscle spindle. That is, under the influence of Dynamic Gammas, the spindle will respond more quickly to a faster rate of change of spindle length.
• They innervate Bag fibers.
• They increase muscle tension but there is no contraction -- i.e. spindle length doesn't change.
• FNXN: They produce a large increase in the velocity sensitivity of muscle spindle IA afferents. Dynamic Gammas do not affect IIA afferents.

GOLGI TENDON ORGAN: The muscle receptor responsible for the Inverse Stretch Reflex.

• STRUCTURE: It is a capsule of elastic fibers, in series with (i.e. attached to the end of) 1% of all extrafusal muscle fibers.
• 99% of extrafusal fibers do not connect to the Golgi Tendon Organ.
• FNXN: When Golgi Tendon stretches, it will decrease alpha-Motor Neuron activity back to the same muscle, preventing further contraction and reducing muscle tension.
• Also it will send muscle information back to cerebellum.
• The GTO increases muscle compliance, as in muscles needing to "give" a little (by lengthening to absorb shock) when jumping off a roof and landing on feet.
• Compensation for fatigue.
• 1B AFFERENT NERVES: They innervate the Golgi Tendon Organ. Stretching of the Golgi Tendon fire these nerves.
• They goto spinal cord ------> SYNAPSE with INHIBITORY INTERNEURON ------> Inhibit alpha-Motor Neuron activvity back to same muscle.

STRETCH REFLEX: Contraction of a muscle elicited by stretch of the muscle, such as the patellar tendon reflex.

• AFFERENT LIMB: Muscle spindle IA Afferents.
• EFFERENT LIMB: alpha-Motor Neurons.
• PATHWAY: Monosynaptic. Stretch Muscle ------> Increase firing rate of IA Afferents ------> Fire alpha-Motor Neurons back too same muscle ------> increase muscle tension.
• EXPT: Decerebrated Cat soleus muscle
• Experimenter did a Ramp-and-Hold experiment, stretching the muscle. Muscle tension increased as he stretched the muscle, due to the Stretch Reflex. After a certain point the muscle tension stopped increasing.
• CUT DORSAL ROOTS and the tension was even greater, due to lost inhibition by the Vestibulospinal Tract.

INVERSE STRETCH REFLEX: Once you stretch a muscle past a certain threshold, the rigidity will "melt away" and the muscle will stretch easily. Past the threshold, the muscle is undergoing the inverse stretch reflex.

• AFFERENT LIMB: Golgi Tendon Organ, IB Afferents
• EFFERENT LIMB: alpha-Motor-Neuron disynaptic inhibition
• PATHWAY: The reflex is disynaptic. Stretch Muscle past threshold ------> Golgi Tendon Organ stretches ------> IB Afferents fire ------> SYNAPSE with INHIBITORY interneuron in spinal cord ------> DECREASE alpha-Motor Neuron Activity back to same muscle ------> Decrease muscle tension ------> muscle lengthens easily

WITHDRAWAL (FLEXION) REFLEX: Remove hand from a burning stove, for example.

• Paraplegia / Quadriplegia: It causes an increased Withdrawal Reflex, and it may also result in unintended autonomic responses such as defecation, urination.
• C FIBERS: Pain fibers initiate the reflex.
• PATHWAY: C-Fiber activation ------> Dorsal Root ------>Excitatory synapses to alpha-neuron and gamma-neuron ------> contraction of same muscle.
• Activation of the gamma neuron will cause activation of IA Afferents, which will then initiate the stretch reflex ------> more alpha-activation.
• The net result of this is that you get a large, long lasting reflex. The reflex itself can easily outlast the original pain stimulus.
• There is also a recurring excitatory circuit, some excitatory interneurons will send fibers back to other excitatory interneurons, which potentiates the original signal in the spinal cord.

RECIPROCAL INNERVATION: IA Afferents from an extensor muscle will synapse with an interneuron that inhibits the opposing (i.e. flexor) muscle.

• IA AFFERENTS therefore have two monosynapses in the spinal cord:
• Excitatory (EPSP) to the alpha-Motor Neuron of the same muscle
• Excitatory interneuron ------> Inhibitory (IPSP) to the alpha-Motor Neuron of the opposing muscle.
• The inhibitory arm of the reflex is disynaptic, while the excitatory arm is monosynaptic.

CROSSED EXTENSOR REFLEX: The contralateral reflex for the withdrawal reflex. Step on a tack, and you withdraw one foot while extending the other.

• PATHWAY: Pain fibers synapse with two interneurons in spinal cord -- one to ipsilateral side and one goes across ventral white commissure to contralateral side.
• IPSILATERAL will then make two synapses, to cause FLEXION of the ipsilateral limb.
• EXCITATORY to ipsilateral flexor muscle.
• INHIBITORY to ipsilateral extensor muscle.
• CONTRALATERAL will then make two synapses, to cause EXTENSION of the contralateral limb.
• EXCITATORY to contralateral extensor muscle.
• INHIBITORY to contralateral flexor muscle.

MUSCLE TONE DISORDERS: Hypotonia and Hypertonia arise from disorders in the sensitivity of alpha-Motor Neurons.

• HYPOTONIA: Decreased alpha and gamma neuron excitability. Diminished reflexes and flaccid paralysis.
• Examples: Early phase of spinal cord transection
• HYPERTONIA: Increase tonic stretch reflex, i.e. the response to muscle length when the muscle is not moving. Sustained contraction at rest, increased tonic stretch reflex, increased muscle stiffness
• Examples: Decerebrate Rigidity (UMN Paralysis), Parkinson's Disease
• SPASTICITY: Increased phasic stretch reflex, i.e. the response to muscle velocity when it is stretching. The faster the stretch, the worse is the resistance to the stretch.
• Examples: Late phase of spinal cord transection, Motor Cortex / SMA lesions.
• Factors that contribute to Spasticity:
• Increased synaptic efficacy, i.e. strength of response at a synapse
• Collateral Sprouting of axon terminals, to replace lesioned axons. In the end this can result in higher sensitivity than originally.
• Loss of presynaptic inhibition ------> alpha-Motor Neurons fire more frequently and/or more readily.
• (Minor Contributor): Gamma Efferent hyperactivity.
• CLONUS: Rhythmic series of contractions brought about by quick stretch of a spastic muscle. Clonus can occur with spastic muscles.
• It is a self-sustaining Cycle: Spastic muscle stretch ------> IA fire outburst ------> alpha-Motor strong activation -------> Reflex contraction and muscle shortening ------> ------> Rebound lengthening ------> ------> cycle repeats

SPINAL MUSCULAR ATROPHY (SMA):

• Types of Spinal Muscular Atrophy:
• ACUTE SMA 1: Onset at birth and death before age 2
• SYMPTOMS: Death ultimately from failure of respiratory muscles and respiratory infection.
• INTERMEDIATE (Werdnig-Hoffman) SMA 2: Survival beyond 4 years.
• SYMPTOMS: Diminished reflexes and general muscle weakness. Absent reflexes by age 2.
• Scoliosis.
• Death ultimately by respiratory complications.
• CHRONIC (Kugelberg-Welander) SMA 3
• SYMPTOMS: First presentation is weakness in the proximal lower limbs, then upper extremities later (this pattern holds for all types of SMA).
• GENETIC BASIS:
• SURVIVAL MOTOR NEURON (SMN): The SMN gene is defective (duplication mutation) in virtually all cases of SMA.
• The SMN gene is located on Chromosome 5
• FNXN: The protein product is a membrane receptor. They think that it may be a receptor for a muscle-derived trophic substance. Details are unknown.
• NEURONAL APOPTOSIS INHIBITORY PROTEIN (NAIP): The NAIP gene is defective (duplication mutation) in many SMA cases, however this defect is not required for SMA.
• The NAIP gene is located on Chromosome 5
• The presence and severity of the NAIP defect correlates with how severe the SMA case is.
• FNXN: The NAIP protein product is thought to prevent apoptosis (programmed cell death) during development. Thus in the absence of NAIP, some neurons that were supposed to survive actually die instead.

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Categories of Descending Systems:

• Traditional Categories: Pyramidal and Extrapyramidal. There are problems with this categorization:
• It grossly overemphasizes the importance of the Pyramidal system. You can lesion the pyramidal tract without intractable motor deficits.
• It artificially groups together systems that are functionally unrelated.
• DORSOLATERAL: Tracts located in the dorsolateral fasciculus of the spinal cord. They control distal muscles and are largely crossed. They run close to the distal alpha-motoneuron which also like laterally.
• CORTICOSPINAL TRACT: The traditional pyramidal system. 90% crossed (Lateral CST) and 10% uncrossed (Anterior CST)
• ORIGIN: Motor Cortex
• Somatotopic Organization.
• FNXN: On average, it excites both flexors and extensors, and often shows reciprocal inhibition of the opposing muscle.
• LESIONS:
• CORTICOSPINAL TRACT: Produces loss of independent finger movement and distal weakness. Mild deficits, especially if the red nucleus is intact.
• MOTOR CORTEX LESION: Highly incapacitating. Severe paralysis of contralateral muscles.
• INITIALLY: Flaccid Paralysis
• LATER: Spastic (UMN) Paralysis kicks in as spinal reflexes become hypersensitive.
• PHYLOGENY: New (only mammals)
• RUBROSPINAL TRACT:
• ORIGIN: Red Nucleus.
• Somatotopic Organization.
• LESION of the Rubrospinal System produces little or no deficit if the Corticospinal tract is intact.
• RED NUCLEUS LESION (as opposed to the tract) will cause cerebellar-type disturbances.
• FNXN: Receives influences from both motor cortex and cerebellum, and mediates influence on alpha-motoneurons as a result.
• PHYLOGENY: Relatively new (reptiles)
• VENTROMEDIAL: Tracts located in the ventromedial fasciculus of the spinal cord. The control proximal (axial) muscles and are largely uncrossed. They run close to the proximal alpha-motoneurons which also lie medially.
• LESIONS: Lesions of this system are very incapacitating. Inability to maintain upright posture.
• RETICULOSPINAL TRACT:
• ORIGIN: Reticular Formation
• It is the only descending system that does not show somatotopic organization.
• FNXN: On average, it excites flexors and inhibits extensors.
• These neurons are involved with coordination of limb movement.
• CENTRAL PATTERN GENERATOR (CPG): In the brain stem (Reticular Formation), it mediates the signals that are necessary for locomotion (walking and running). These signals are carried through Reticulospinal Tract.
• PHYLOGENY: Old
• VESTIBULOSPINAL TRACT:
• ORIGIN: Lateral Vestibular Nucleus
• Somatotopic Organization.
• FNXNS: On average, it excites extensors and inhibits flexors.
• These neurons are important for maintaining an upright posture.
• PHYLOGENY: Old
• Interstitial Spinal and Tectospinal Tracts: They are involved in control of head and neck muscles. Other than that don't worry about them.

General Properties of Descending Systems:

• ALPHA-GAMMA CO-ACTIVATION: Descending systems will send excitatory branches to both alpha and gamma neurons at the same time. Since gamma neurons ultimately increase alpha activity, this helps to amplify the excitatory signal.
• AUTOMATIC LOAD COMPENSATION: Muscles will automatically adjust their tension to accommodate the "load" on the muscle.
• INCREASED LOAD will stretch a muscle that is contracting.
• This stretching will trigger Ia Spindle Afferents ------> Increase alpha-activity even further ------> increase muscle tension ------> overcome the increased load.
• Gamma co-activation (which is unaffected by Spindle Afferents) also occurs. This further helps to modulate automatic load compensation.
• HIGHER INFLUENCE on SPINAL REFLEXES:

• INVERSE STRETCH REFLEX: We have higher control over sensitivity of the Inverse Stretch Reflex.
• Under conditions where muscle needs to have higher compliance, the higher systems can fire Inhibitory Ib Interneurons ------> inhibit alpha-neuron activity.
• In effect, this makes the Inverse Stretch Reflex kick in earlier, i.e. at a lower threshold tension.

• "PYRAMIDAL SENSORY" SYSTEM: The Corticospinal system does have "sensory" neurons that serve to screen out routine stimuli, by putting inhibition on sensory nuclei in the brainstem and spinal cord.
• PATHWAY: Descending fibers originate from Primary Somatosensory Cortex ------> Dorsal Column Nuclei and Dorrsal Horn ------> excite or inhibit the dorsal column nuclei.
• These fibers travel in the opposite direction as most neurons in the Somatosensory Cortex.
• These fibers travel through the pyramidal tract.

THE BABINSKI REFLEX: Test for UMN Lesions.

• TEST: Stroke the ventrolateral aspect of the foot (the sole of the foot).
• Normal Response: Toes should point down; Plantarflexion.
• Pathological Response: Toes point upward and fan out; Dorsiflexion. This indicates a problem with the Corticospinal Tract in adults.
• INFANTS normally show a positive Babinski until two years of age.

THE MOTOR (PRE-CENTRAL) CORTEX: BRODMANN'S AREA 4

• SOMATOTOPIC ORGANIZATION:
• MEDIAL: Nearest the top of the cortex. Contains upper neurons for the FOOT
• LATERAL: Nearest the temporal lobe. Contains upper neurons for the HEAD and NECK
• Muscle Groups capable of the most skilled movements (Ocular muscles, facial muscles, and hands) have the largest representation of neurons in the Motor Cortex.
• FORCE TRANSDUCTION: There is a linear relationship between the force of muscle contraction and the firing rate of Upper Motor Neurons
• There is a 70 - 100 msec time difference between the initiation of the UMN signal and contraction of the target muscle.
• LESION: A motor cortex is much more severe than pyramidal tract lesions. In pyramidal tract lesions, the motor cortex is still intact and can still influence the extrapyramidal systems to maintain some motor control.
• INITIALLY: Motor Cortex lesions produce a Flaccid Paralysis, as there is a huge loss of excitatory input on alpha-neurons ------> hyperpolarization.
• LATER (after ~2 months): Spastic Paralysis and Hyperreflexia, as the alpha-neurons compensate for the lost excitatory input by becoming more sensitive and firing spontaneously.

Secondary Cortical Motor Areas:

• SUPPLEMENTARY MOTOR AREA (SMA): BRODMANN'S 6 (Pre-Motor Cortex), most medially.
• FNXN: Involved with executing pre-programmed or planned motor movements (such as playing the piano or typing).
• EXPT: MEASURE CEREBRAL BLOOD FLOW (which indicates neuron activity) in human patients performing motor tasks.
• Simple Finger Flexion Test: Touching index finger to thumb repeatedly.
• MOTOR CORTEX lit up because of movement of fingers
• SOMATOSENSORY CORTEX lit up because of touching the fingers.
• Complex Sequence Test: Touch different fingers to the thumb in a pre-determined, complicated sequence.
• MOTOR and SOMATOSENSORY CORTICES lit up as before.
• SMA also lit up: CONCLUSION = this suggests that the SMA is involved in executing the complex sequences.
• Internal Programming Test: Subject had to rehearse the complex movement of the fingers in his head, without making any actual movements.
• SMA was heavily activated while the MOTOR CORTEX and SOMATOSENSORY CORTEX were not, because the fingers weren't actually moving.
• PREMOTOR CORTEX: BRODMANN'S 6 (Pre-Motor Cortex), most laterally.
• FNXN: Involved with assembly of new motor programs and "learning" of repeated motor sequences.

• PARIETAL AREAS 5 and 7: Selective Attention to areas in EXTRA PERSONAL SPACE. Extra personal space is the space external to our bodies, but within reach.
• PARIETAL AREA 5: It helps control movement of the limbs in response to extra personal space.
• It will send selective attention neurons to influence the Motor Cortex.
• PARIETAL AREA 7: It helps control movement of the eyes in response to extra personal space.
• Three categories of these neurons, each one influencing the respective area of the motor cortex (see Eye-Movement section for details)
• Saccade Related
• Fixation Related
• Smooth Pursuit Related
• NEGLECT SYNDROME: Unilateral lesions of Parietal Cortex, especially to the non-dominant hemisphere.
• SYMPTOMS: Patients ignores the contralateral side of his or her body. Patient will not recognize, dress, take care of, or understand one half of the body.
• There may also be contralateral hemiparalysis.
• Apraxia: Difficulty drawing objects in 3D, such as drawing a clock that is completely round.
• Astereognosis: Failure to recognize objects placed in contralateral hand.
• Anosognosia: Denial of symptoms

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SACCADES: Extremely rapid movement of eyes, creating an instantaneous change in gaze, from one location in space to a different location.

• It is not possible to voluntarily move the eyes in a continuous, smooth path across space, from one side of the room to the other.
• VISUAL FIELD: There is no blur of the visual field with saccades, i.e. you can't see the field move as you move your eyes. This is because:
• The movement is too rapid for the visual apparatus to process.
• COROLLARY DISCHARGE: The same signal that produces the saccade also inhibits the Lateral Geniculate Nucleus from processing visual stimuli during the eye movement.
• VOLUNTARY SACCADE: The signal originates in the Frontal Eye Field (Area 8).
• PATHWAY: Frontal Eye Field (Area 8) ------> Superior Colliculus ------> Reticular Formation ------> Oculomotor Neurons ------> Saccade movement.
• REFLEX SACCADE: Involuntary saccades made to a novel stimulus, such as an unexpected flash of light, that appears in the visual field.
• The reflex involves the SUPERIOR COLLICULUS directly and does not utilize input from the Frontal Eye Field.
• PATHWAY: Novel Stimulus ------> Retinal Ganglion Cells ------> Superior Colliculus ------> Reticular Formation ------> Oculomotor Neurons ------> Saccade response to stimulus
• SOMATOTOPIC ORGANIZATION: Superior Colliculus has somatotopic organization across two layers:
• Superficial Layers of Superior Colliculus contain specific sensory neurons from the visual field.
• Deep Layers of Superior Colliculus contain neurons that effect eye-movements. These neurons have a 1:1 correspondence with the sensory neurons, i.e. the eye movements will move to the same spot from which the sensory neuron originated.

SMOOTH PURSUIT: Eye movements involved in maintaining fixation on a moving target while the head is stationery.

• VELOCITY of movement is less than that for saccades: 30 / sec maximum. You can't keep up with a really fast moving object and hence it will appear as a blur.
• INVOLUNTARY: These actions are an involuntary reflex. You cannot prevent smooth pursuit movements (such as following your finger with your eyes) without shifting your gaze elsewhere.
• PATHWAY: Retinal stimulus (indicating slip of focus) ------> Retinal Ganglion Cells ------> Lateral Geniculate Nucleeus ------> Visual Cortex ------> Reticular Formation ------> Oculomotor Neurons ------> Smooth Pursuit movement.

VESTIBULO-OCULAR REFLEX (VOR): Maintaining gaze on a fixed object while moving your head. The direction of eye movement will be equal and opposite to that of the head, i.e. the eyes will turn medially.

• PATHWAY: DISYNAPTIC. Vestibular Hair Cell Deflection ------> VIIIth nerve ------> Ipsilateral Medial Vestibular Nucleus increases firing rate ------> it SYNAPSES with two different nerves
• EXCITATORY SYNAPSE to ipsilateral Oculomotor Nucleus ------> ipsilateral eye turns medially, in opposite direction as original head movement.
• INHIBITORY SYNAPSE to ipsilateral Abducens Nucleus ------> prevent eyes turning laterally
• CONTRALATERAL SIDE: The exact converse will be going on: Contralateral Medial Vestibular Nucleus is INHIBITED ------> decrease Oculomotor firing and increase Abducens firing ------> contralateral eye turns laterally, in the opposite direction as original head movement.
• MEDIAL LONGITUDINAL FASCICULUS (MLF) also helps to coordinate the gaze between the two eyes. It works in synergy with the VOR reflex.

SEMICIRCULAR CANALS: Detect head turns and keep them in balance; detect angular acceleration.

• FUNCTIONAL PAIRS: Semicircular Canals are divided in PAIRS of canals that counter each other in terms of their response to head turns (one will be stimulated while the other will be inhibited to the same degree).
• Left Horizontal Canal <====> Right Horizontal Canal
• The horizontal canals are actually at an angle 30 above the horizontal. Tilt the head forward to make these canals truly horizontal.
• Left Anterior Canal <====> Right Posterior Canal
• Left Posterior Canal <====> Right Anterior Canal
• ANATOMY:
• The Semicircular Canals are attached to the Utricle.
• They contain Endolymph to make the hair cells move. Endolymph is continuous throughout the Utricle and Semicircular Canals.
• AMPULLA: The enlargement at one end of each canal, where the hair cell receptors are located.
• CUPULA: In the Ampulla, the gelatinous mass into which the hair cells insert.
• HAIR CELLS: Scarpa's Ganglion contains the cell bodies of the hair cells, which form the VIIIth (Vestibular) nerve.
• STEREOCILIA insert into the Cupula and move in response to head movements.
• KINOCILIUM is the end cilium, larger than the other cilia.
• VIIIth NERVE STIMULATION:
• When the stereocilia bend toward the Kinocilium ------> depolarization of VIIIth fibers occurs.
• When the stereocilia bend away from the Kinocilium ------> hyperpolarization of VIIIth fibers occurs.
• ORIENTATION OF KINOCILIUM:
• HORIZONTAL CANALS: The Kinocilium is located closest to the Utricle (i.e. most medially)
• ANTERIOR, POSTERIOR CANALS: The Kinocilium is located furthest from the Utricle, i.e. most laterally.
• EXAMPLE: TURN HEAD RIGHT, The endolymph fluid will move left initially (due to inertia). Hair cells in the Horizontal Canals will deflect to the left.
• RIGHT HORIZONTAL CANAL: Stereocilia move toward Kinocilium ------> activate VIIIth nerve afferents.
• LEFT HORIZONTAL CANAL: Stereocilia move away from Kinocilium ------> inhibit VIIIth nerve afferents.

OTOLITH ORGANS:

• UTRICLE
• SACCULE

VESTIBULO-POSTURAL REFLEX: Compensation for turning the body to the right or the left. Example: TURN BODY RIGHT, and two responses happen

• RIGHT SEMICIRCULAR CANALS ACTIVATE ------> Activate Right VIIIth nerve afferents ------> activate right Vestibulospinal Tract ------> excite extensors on the right ------> net extension on right side.
• LEFT SEMICIRCULAR CANALS DEACTIVATE ------> Inhibit Left VIIIth nerve afferents ------> inhibit left Vestibulospinal Tract ------> inhibit extensors on the left ------> net flexion on left side.
• RESULT: Turn the body right, and the body attempts to fall (flex) toward the left for compensation.

NYSTAGMUS REFLEX: The reflexive response of eye movements to continual rotation in one direction. SPIN BODY TO THE RIGHT, and the eyes will do the following:

• Vestibulo-Ocular Reflex (VOR): Initially there will be slow rotation to the left. However, as rotation continues, the eyes will no longer be able to turn left, so there must be a resetting of gaze.
• Involuntary Saccade: The eyes will instantaneously reset the gaze toward the right, i.e. in the same direction as rotation. This reflex is not VOR but rather is an involuntary saccade.
• NYSTAGMUS is the combination of the two reflexes above, in alternating order with each other (A, then B, then A, then B). This is the eye's response to continual rotational movement.
• The direction of nystagmus, by convention, is the direction of the reflexive saccade. Thus: Spinning the head right results in a "rightward" nystagmus reflex.

BARANY CHAIR TEST: Rotate a person in a chair really fast to the right for about 30 sec; stop the chair, and then test for leftward acceleration reflexes of the eyes.

• Post-rotational Component: After stopping the chair, you will be testing for deceleration to the right, which is the same as testing reflexes for leftward acceleration.
• What the semicircular canals detect is the rate of change of velocity of the fluid (angular acceleration), not the movement of the fluid itself (angular velocity). Net angular acceleration will be to the left in this case.
• EXPECTED RESULTS: You would thus expect a leftward Nystagmus once the chair is stopped.
• So, you look for the patient rotating his eyes toward the right (VOR reflex), and then instantaneously shifting them left (reflex saccade), then rotating eyes rightward again, etc.

INNER NUCLEAR OPHTHALMOPLEGIA: Lesion in the MLF, as often occurs with Multiple Sclerosis.

• SYMPTOM: You lose coordinated gaze of the medial rectus (CN III).
• RIGHTWARD ROTATION VOR: Your right eye would be able to move laterally just fine, but your left eye would not move medially.
• So with this condition, lateral movements are fine but medial movements in the VOR reflex are impaired.

UNILATERAL LABYRINTHECTOMY: Unilateral lesion of VIIIth Nerve.

• VIIIth nerve on both sides has a high basal level of activity.
• LESION the RIGHT VIIIth NERVE: It will produce an effect similar to LEFTWARD ROTATION, i.e. net stimulus of the Left VIIIth nerve:
• SYMPTOM: Leftward Nystagmus

CALORIC STIMULATION: Clinical test for functionality of semicircular canals.

• Tilt head back 60 so that the horizontal canals are oriented vertically.
• Irrigate inner ear with water of different temperature, then, NORMAL RESPONSES:
• Warm Water: Nystagmus toward the ear being irrigated.
• Cold Water: Nystagmus toward the opposite ear (cold water will inhibit the vestibular receptors)

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CEREBELLAR FIBERS AND CELL TYPES:

• AFFERENT FIBERS:
• MOSSY FIBERS: They make excitatory synapses with Granule Cells. They will ultimately influence a large number of Purkinje Cells via the Granule Cell output.
• They receive input from all incoming sources except the Inferior Olive:
• Spinocerebellar Tract (motor info about the extremities)
• Pontine Nuclei (motor info about the head and neck)
• They will send collaterals to the Deep Cerebellar Nuclei, as well as to the Granule Cells
• CLIMBING FIBERS: They make powerful, obligatory excitatory synapses on a very SMALL NUMBER of Purkinje Cells
• They all originate from the Inferior Olivary Nucleus
• They all will send collaterals to the Deep Cerebellar Nuclei directly, as well as to the Purkinje Cells.
• GRANULE CELLS, also called PARALLEL FIBERS, are strictly within the cerebellum, in the folia. They are interneurons in the cerebellar circuit.
• They make excitatory synapses with a LARGE NUMBER of Purkinje Cells
• They are called parallel fibers because their fibers run parallel to the folia (folds) of the cerebellar hemispheres.
• Granule cells will also send excitatory signals to the following inhibitory interneurons:
• Basket Cells: They will in turn inhibit Purkinje Cells
• Stellate Cells: They will in turn inhibit Purkinje Cells
• Golgi Cells: They will provide negative feedback and inhibit the Granule Cells
• PURKINJE CELLS: EFFERENT FIBERS
• They are the only "efferent" fibers in the cerebellar cortex. They will make synapses on the Deep Cerebellar Nuclei ------> transmit info to the rest of the CNS.
• Purkinje cell input onto the Deep Cerebellar Nuclei is always inhibitory, using neurotransmitter GABA.
• DEEP CEREBELLAR NUCLEI: They will project to Thalamus ------> excitatory connection to Motor Cortex ------> excitatory influence on descending systems.
• FNXNS:
• Receives excitatory collateral branches from Mossy fibers and Climbing Fibers.
• Receives inhibitory tonal input from Purkinje Cells.
• Deep Cerebellar Nuclei have a high background firing rate, thus Purkinje Cell inhibitory input is modulated.
• NUCLEI:
• FASTIGIAL NUCLEUS: Medial-most
• INTERPOSITUS NUCLEUS: Middle o' the road
• DENTATE NUCLEUS: Lateral-most

VESTIBULOCEREBELLUM: Archicerebellum.

• STRUCTURE: FLOCCULONODULAR LOBE is the small lobe on the posterior inferior aspect of cerebellum. It modulates VOR and Postural Reflexes.
• FNXNS:
• MODULATE VESTIBULO-POSTURAL REFLEX: Cerebellum does fine tuning of postural reflexes, adjusting the magnitude, strength, and range of movement.
• PATHWAY: VIII Nerve Afferents--> Mossy Fibers to the Cerebellum ------> Fastigial Deep Nucleus ++ Vestibular Nucleus ------> Reticulospinal + Vestibulospinal Tracts ------> influence alpha-motor neurons.
• Excitatory signals to Vestibulospinal will excite (modulate) the extensors.
• Excitatory signals to Reticulospinal will excite (modulate) the flexors.
• Fastigial Nucleus does the calculations for these adjustments, although some fibers also go directly to the descending tracts without going through fastigial nucleus.
• SUPPRESS VOR REFLEX: If you want to follow a moving an object while moving your head too, then you don't want the VOR reflex to move your eyes. Under these circumstances the vestibulocerebellum will supress that reflex.
• PATHWAY: VIIIth Nerve collateral afferents enter cerebellum as Mossy Fibers ------> Excite Granule Cells in cerebellum ------> Excite Purkinje Cells ------> Inhibition of Vestibular Nucleus ------> Cancel or modulate excitatory input from VIIIth afferents.
• Note that the VIIIth nerve is still firing to activate the VOR reflex. The only difference is that now the end-signal is being canceled (or lessened) by the cerebellar input.
• ADJUST REFLEX GAIN: If you put on reversing prisms (which reverse the movement of the visual field), your VOR reflex will compensate for the new visual input within a few days. This change in the VOR reflex is dependent on the Cerebellum and Inferior Olive.
• LESIONS: Can be caused by a medulloblastoma in children, or by chronic alcoholism. It will produce two defects:
• Nystagmus is produced from unmodulated VOR reflex.
• Disequilibrium, an inability to maintain posture, from unmodulated postural reflexes.
• REPAIR SHOP THEORY: Based on reversing prisms experiments and others, this theory says that the cerebellum is responsible for continually responding to the changing behavior of neurons with regard to voluntary movements and reflexes.

SPINOCEREBELLUM: Paleocerebellum

• STRUCTURES
• VERMIS: Midline structure, receives input from Vestibular Nuclei and Spinocerebellar Tract.
• PARAVERMIS: On either side, receives input only from Spinocerebellar Tract.
• FNXN: Continual correction of movements, comparing actual motor movement with motor cortex "intentions" of movement.
• INPUT: Spinocerebellum receives input from motor cortex and spinocerebellar tract.
• It then reconciles those signals with each other (actual action reconciled with intended action), and issues a correction factor.
• OUTPUT:
• Vermis ------> Fastigial Nucleus + Vestibular Nucleus ------> Descending Extrapyramidal Tracts
• Paravermis ------> Fastigial Nucleus + Interpositus Nucleus ------> Descending Extrapyramidal Tracts
• SOMATOTOPIC ORGANIZATION: The spinocerebellum has somatotopic organization with regard to the regions of the body it is "comparing." Head and neck is generally nearest the center, with extremities in the periphery.

CEREBROCEREBELLUM: Neocerebellum

• STRUCTURE: The large lateral hemispheres that make up most of the cerebellum.
• FNXN: Programming of repeated movements. Calculating the "metrics" of movements, such as reaching for an object in space. We don't consciously think about these details of conscious movement.
• INPUT: Pontine Nuclei from Cerebral Cortex.
• OUTPUT: Dentate Nucleus ------> Thalamus ------> Motor Cortex
• PATHWAY of MODULATION: Limbic System initiates the drive or desire to move
• Limbic System ------> Frontal Cortex (conscious or subconscious judgment and intention) ------> Pontine Nuclei ------> Cerebellum ------> Dentate Nucleus ------> Thalamus ------> Motor Cortexx ------> movement is executed
• LESION: CEREBELLAR SYNDROME. This is a lesion of both Spinocerebellum and Cerebrocerebellum, as there is rarely (i.e. never) a lesion of only one or the other.
• Hypotonia: From reduced gamma neuron activity, due to loss of extrapyramidal excitatory input.
• Ataxia, Asynergia: Lack of coordinated movement. Most important, errors in METRICS of movement (reaching arm too far or too close to target)
• INTENTION TREMOR, Dysmetria: A problem terminating movements, or a tremor that only present when moving. This is different than Resting Tremor which occurs with Parkinson's.
• Adiadochokinesis: Inability to make rapid alternating movements, such as pronation and supination of hand.
• LESION: IPSILATERAL DEFICIT. All lesions of the cerebellum produce ipsilateral deficit because the system is double-crossed.
• Deep Nuclei cross the midline to opposite motor cortex.
• Upper motor neurons cross again through pyramidal decussation.

BASAL GANGLIA: Components

• STRIATUM: Uses GABA as inhibitory transmitter; it projects to ------> Globus Pallidus to have inhibitory influence.
• PUTAMEN
• CAUDATE NUCLEUS
• GLOBUS PALLIDUS:
• It receives inhibitory input from the Corpus Striatum.
• Some of these inhibitory fibers carry GABA and Substance P as transmitters. These act on the GPi and are inhibitory.
• Other inhibitory fibers carry GABA and Enkephalins as transmitters. The pathway of these signals:
• Corpus Striatum ------> GPe ------> Subthalamic Nucleus ------> GPi
• FNXN: It projects inhibitory neurons to the thalamus to modulate motor function.
• Loss of this inhibition will result in Hemiballismus.
• INTERNAL SEGMENT (GPi): It is functionally continuous with the Substantia Nigra, Pars Reticularis (SNr)
• FNXN: Along with the SNr, it is the OUTPUT NUCLEUS of the Basal Ganglia. The GPi normally inhibits the Thalamus (via GABA).
• In Parkinson's Disease, it is overactive.
• SOMATOTOPIC ORGANIZATION: Continuous with the SNr, its output goes to the limbs.
• EXTERNAL SEGMENT (GPe)
• SUBTHALAMIC NUCLEUS: The subthalamic nucleus normally stimulates the GPi.
• In Parkinson's Disease, it is overactive.
• In Huntington's and Hemiballismus, it is underactive.
• SUBSTANTIA NIGRA
• PARS RETICULARE (SNr): Ventral part of the Substantia Nigra. It is functionally continuous with the Internal Globus Pallidus (GPi)
• FNXN: Along with the SNr, it is the OUTPUT NUCLEUS of the Basal Ganglia.
• SOMATOTOPIC ORGANIZATION: Continuous with the GPi, its output goes to the head and neck.
• PARS COMPACTA (SNc): Dopamine-containing neurons.
• NIGROSTRIATAL TRACT: Substantia Nigra, Pars Compacta releases Dopamine. Dopamine acts on the Corpus Striatum and has both inhibitory and excitatory effects, depending on the connection.
• CIRCUIT: SNc ------> excitatory on Striatum ------> (Substance P) Inhibitory on GPi ------> result is inhibition of Thalamic projections ------> Cerebral cortex doesn't receive the Thalamic projections.
• CIRCUIT: SNc ------> inhibitory on Striatum ------> (Enkephalins) inhibitory on GPe ------> inhibitory to Subthalamic Nucleus ------> GPi ------> result is inhibition of Thalamic projections ------> Cerebral Cortex doesn't receive the Thalamic projections.
• BASAL GANGLIA Basic Circuitry: Cerebral Cortex ------> Striatum ------> GPi + SNr ------> Thalamus ------> Motor cortical output

PARKINSON'S DISEASE: A lesion of the Dopamine-containing Nigrostriatal Tract, producing a dopamine deficit.

• SYMPTOMS: Parkinson's Disease is a hypokinetic disorder.
• Lead Pipe Rigidity: Resistance to movement.
• RESTING TREMOR: To be distinguished from an intention tremor (as in Cerebellar Syndrome). This is a tremor when there is no movement.
• This tremor is of a lower frequency than corresponding Intention tremor.
• The tremor is better when in motion, so it is less debilitating than a moving tremor.
• Akinesia / Bradykinesia: Inability to initiate movement, or slow initiation of movement.
• This symptom responds well to treatment.
• Postural Instability
• Cognitive Problems
• ETIOLOGY: Deficiency of dopamine exerts its effects through two pathways. Both pathways ultimately result in over activity of the Globus Pallidus Interna ------> Over suppression of Thalamus ------> fewer thalamic projections to the Motor Cortex.
• In Parkinson's Disease, the subthalamic nucleus is overactive.
• Dopamine can get to 20% below normal before Parkinsonian symptoms will occur.
• PROGRESSION OF DISEASE: Cognitive loss and eventual death from respiratory failure.
• TREATMENT:
• L-DOPA is drug of choice.
• CONVERSION: L-DOPA is a Dopamine precursor that can get through the blood-brain barrier. It is converted to Dopamine by DOPA-Decarboxylase once in the brain.
• CARBIDOPA: This is always given with L-DOPA. It is a DOPA-Decarboxylase Inhibitor which blocks conversion of L-DOPA ------> Dopamine in the periphery.
• SIDE-EFFECTS:
• ON-OFF Phenomenon: Suddenly therapy is ineffective, periodically.
• Freezing Phenomenon: All of the sudden become rigid and stop, unable to initiate movement.
• The drug becomes less effective with long-term use.
• Dyskinesias: Involuntary movements (another form of tremors, hyperkinetic) result from the excessive dopamine.
• THALAMOTOMY: Surgical lesion of Ventral Lateral Thalamus, for the treatment of tremors. this surgery does not alleviate the original problem, so it is only symptomatic treatment.
• CANDIDATES: People who don't respond well to L-DOPA (~10%), have terrible side-effects with L-DOPA, or who have debilitating tremors.
• Must have no cognitive deficiencies and be able to respond well to surgery.
• ELECTRO-STIMULATION OF THALAMUS: Surgically implant an electrode on the Thalamus and another in the chest. Then use a magnet to stimulate thalamus periodically and INHIBIT it.
• This is a surgical alternative to outright Thalamotomy, leaving the VL Thalamus intact and only inhibiting it as necessary.
• PALLIDOTOMY: Surgical lesion of Globus Pallidus Interna. This surgery has been shown to be the most effective.
• CANDIDATES: Pretty much the same as for thalamotomy.
• RISKS: Loss of visual field, because the GPi is very close to Optic Tract.
• ELECTROSTIMULATION is on the horizon, and currently experimental at KUMC.
• HISTORICAL STUFF:
• Stereotactic Surgery: Early attempts to place a brain lesion in specific place, using a pineal calcification (on a skull film) as a reference point.

HUNTINGTON'S CHOREA: Lesion of the Corpus Striatum, involving GABA and Enkephalin neurons

• ETIOLOGY: Loss of Corpus Striatum GABA/Enk neurons ------> Disinhibition of the Globus Pallidus Externa ------> Excessive inhibition of the Subthalamic Nucleus.
• The subthalamic nucleus is deficient
• SYMPTOMS: Huntington's is a hyperkinetic disorder.
• The result is a lesion similar to the effects of a Subthalamic Nucleus lesion (i.e. Hemi-ballismus).

HEMIBALLISMUS: Lesion of Subthalamic Nucleus, ruins the GPi inhibitory neurons that project to the thalamus ------> over excitation.

• SYMPTOM: Violent, involuntary movement of contralateral limb.
• ETIOLOGY: Usually created be a vascular lesion (stroke) specific to the Subthalamic Nucleus.
• The subthalamic nucleus is deficient

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