Ferezy's MSR's

Presented By: Joseph S. Ferezy, D.C.

Examination Components I. History and mental status II. Cranial nerve (special senses) III.Somatic motor IV.Somatic sensory V. Reflex VI.Tone, posture, station and movement 2

Ferezy’s MSR’S Motor Reflex  STV  Deep  Strength  Superficial  Tone  Visceral  Volume  Pathologic Sensory Serebellar  Deep  Station   Superficial Movement 3

1 Basic Exam Organization Sitting (Chair)  History of Present Illness  Observe Mental Status ‐ Include  Cleanliness  Stream of Talk  Mood  Content of Thought  Intelligence  Sensorium (Cognitive) 4

Basic Exam Organization Standing Free, Heel/toe, Tandem Walking/Hopping/Knee Bend Romberg Posture (observe –tremor, asymmetry, atrophy, Etc.) T & L ROM’s

Basic Exam Organization • Sitting (Exam Table) ▫ Cranial Nerve Examination. ▫ Motor Tests ‐ Strength, Tone, and Volume (most other then spinal extensors). ▫ Coordination Tests (Drift, Finger To Finger/Nose, Heel to Shin, Rapid Alternating Movements, Etc.). ▫ Intrathecal Tests. ▫ Orthopedic Tests (Most). ▫ Muscle stretch reflexes.

2 The Examination of Station, Movement and Gait  Station ‐ The place at which someone is positioned or is assigned to remain, the act or manner of standing.  Gait ‐ a manner of walking or moving on foot.  Station and gait disorders are among the most common reasons patients seek outpatient neurologic consultation.  A careful assessment of station and gait provides a quick, reliable snapshot of the integrated function of the patient's motor and sensory systems of both the central and peripheral nervous systems.  Often involved in both somatoform (psychogenic) disorders as well as mistaken as psychogenic in etiology.

The Examination of Station, Movement and Gait  A normal examination requires nervous system function at the highest level, integration and performance.  Disorders of motor or sensory systems of the peripheral or central nervous system may affect movement.  Each system will affect movement in a characteristic way.  Because it is a sensitive (but not specific) test, the good clinician will test movement in even a cursory neurologic examination.  Abnormal responses to the integrated testing of station and movement require additional testing to challenge each system independently in order to determine which system is failing and at what level.

The Examination of Station, Movement and Gait  Patient standing  Eyes open  Eyes closed  Broad base  Narrow base Patient sitting (or standing)  Arms outstretched and supinated

3 The Examination of Station, Movement and Gait  Ask patient to walk  Free walk  Tandem (heel to toe) walk  Heel walk  Toe walk  Ask patient to do a shallow to deep knee bend  Ask patient to hop on one foot in place (then the other)  Sit down  Get up from a seated position 10

Movement  Requires extensive pre‐requisite knowledge about multiple motor and sensory systems and how the nervous system integrates function.  Brain is the “Puppet Master”.  Coordinated movement requires sensory input and integration of four so‐called “motor systems”.  Superimposed on tone and posture  Tone and posture change instantly with superimposed movement.  Creates a sensory‐motor‐sensory‐motor continuous loop 11

Motor Systems ‐ Clinical Classifications  Pyramidal (AKA: cotricospinal, UMN, Betz cell, long tracts) –direct influence on lower motor neurons involved in willfully directed muscular contractions.  Extrapyramidal – tone, posture, gait and other “pre‐ programmed” movements. Modulates pyramidal system, does not travel in the pyramids.  Cerebellar – Balance, tone and fine coordination of willfully directed muscular contractions.  Reflex arc – (AKA: LMN, final common pathway) to target muscle.  ALL motor systems are useless unless they can affect the muscle. 12

4 Basic clinical concepts of pyramidal system innervation  Covered in “Examination of the Somatic Motor System”.  Voluntary movements are mediated through the motor cortex (UMN).  Each area of this cortex controls an area of the face and body  Extrapyramidal and cerebellar systems are also involved. 13

Motor cortex neurons

 Control cranial nerves via corticobulbar tract to lower motor neurons in brainstem nuclei.  Descend along cortico‐ spinal path, through brainstem down spinal cord to synapse on LMN’s in anterior horn.

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Extrapyramidal System  A neural network located in the brain.  Called "extrapyramidal" to distinguish it from the pyramidal pathways (corticospinal and corticobulbar tracts) as it does not pass through the medullary pyramids.  Centers around the modulation and regulation (indirect control) of anterior (ventral) horn cells.

6 Extrapyramidal System  Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control.  Deeply interconnected to and modulated by the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex.  All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity but we tend to discuss sensory and cerebellar areas separately.

EXTRAPYRAMIDAL SYSTEM Basal Nuclei (Ganglia) ‐ Caudate, Putamen and Globus Pallidus Subthalamic Red Nucleus Substantia Nigra Parts of Reticular Formation Inferior Olivary Other 20

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Basilar Nuclei  Nuclei that make up the basal ganglia, along with their major subdivisions, are:  the striatum (Huntington’s Disease)  putamen  caudate nucleus  nucleus accumbens (ventral striatum)  external segment of the globus pallidus (GPe)  internal segment of the globus pallidus (GPi)  subthalamic nucleus (STN)  substantia nigra (SN)  pars compacta (SNc) (Parkinson’s Disease)  pars reticulata (SNr)  pars lateralis (SNl)

Basal Nuclei

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Basal Nuclei Neurotransmitters  Classic Connectivity Diagram showing glutamatergic pathways as red, dopaminergic as magenta and GABA pathways as blue

9 Extrapyramidal Pathways

EXTRAPYRAMIDAL FUNCTION Regulation of Tone, Movement and Posture Sets Background for Complex Motor Activity by Setting Balance Gamma and Alpha (Lower) Motor Neurons (Final Common Pathway)

THE EXTRAPYRAMIDAL SYSTEM The extrapyramidal system can be divided into three controlling systems: the cortically originating indirect pathways, the feedback loops, and the auditory‐visual‐vestibular descending pathways.

10 THE EXTRAPYRAMIDAL SYSTEM The extrapyramidal system can be divided into three controlling systems: the cortically originating indirect pathways, the feedback loops, and the auditory‐visual‐vestibular descending pathways.

Cortically Originating Indirect Descending Pathways  Signals transmitted over the pyramidal system to produce voluntary movement are preceded by activity in neurons of the extrapyramidal system and relayed to the basal nuclei, red nucleus, and brainstem reticular formation (probably mechanism for reinforcement of MSR’s).  Basal nuclei contribute to background muscle tone and probably aid in fine tuning motor skills of the distal upper extremity.  The impulses projecting to the red nuclei influence spinal cord alpha and gamma motor neurons via

rubrospinal and other descending tracts. 32

Feedback Loops  Neural circuits in which a signal sample is fed back to a "comparator," which can compare the signal with some pre‐programed desired condition and subsequently take steps to "adjust" or "modify" it.  The extrapyramidal system includes two such feedback systems connecting from above and below:  cortically originating extrapyramidal system feedback loops (COEPS feedback loops) modifying feedback signals are returned to the cortex via the thalamocortical fibers.  proprioceptor originating extrapyramidal system feedback loops (POEPS feedback loops) modifying feedback signals through cerebellum to the spinal cord motor neurons.

11 Auditory Visual Vestibular Descending Pathways Postural adjustments in response to auditory (startle reflex), visual (hands protect face), and vestibular signals (veering) is an additional way to regulate the activity of spinal motor neurons.

EXTRAPYRAMIDAL FUNCTION  The basal ganglia have a “limbic” sector whose components are the nucleus accumbens (NA), ventral pallidum, and ventral tegmental area (VTA).  VTA efferents provide dopamine to the nucleus accumbens (ventral striatum) same as substantia nigra cells provive dopamine to the striatum.  Evidence suggests a central role in reward learning.  A number of highly addictive drugs, including cocaine, amphetamines, and nicotine, are thought to work by increasing the efficacy of the VTA→NA dopamine signal.  There is also evidence implicating over activity of the VTA dopaminergic projection in schizophrenia. 36

12 Clinical Signs of Basal Nuclei and Related Brainstem Dysfunction  Chorea may be associated with dysfunction of the corpus striatum.  Sydenham's chorea, may be seen as a complication of rheumatic fever in children. Recovery from this form of the disease is usually complete.  Huntington's chorea, is a hereditary disease which becomes progressively worse and often leads to severe mental debilitation loss of motor control and early death.  Athetosis is also associated with damage to the striatum and lateral parts of the globus pallidus.

Clinical Signs of Basal Nuclei and Related Brainstem Dysfunction  Ballismus, monoballismus and hemiballismus is generally associated with damage to the subthalamus and can occur spontaneously or be brought on by the initiation of a voluntary movement involving the affected limb.  Parkinson's disease (paralysis agitans) causes hypokinesia, tremor during rest and characteristic “pill‐rolling” principally involves the dopamine‐ releasing fibers of the substantia nigra (nigro‐striatal pathway).

EXTRAPYRAMIDAL DISEASE Diffuse and Chronic Acute, Well Circumscribed or Completely Destructive Lesions Rarely Cause Classic Picture

13 EXTRAPYRAMIDAL DISEASE Gradual Onset Hyperkinesia Hypertonia Emotional (Rigidity) Lability Bradykinesia Dementia Hypokinesia

EXTRAPYRAMIDAL DISEASE  Parkinson’s Disease  Obsessive‐compulsive  Parkinsonian disorder Syndromes  Attention‐deficit  Wilson’s Disease hyperactivity disorder  Congenital Athetosis (ADHD)  Sydenham’s Chorea  Cerebral palsy: basal ganglia  Huntington’s Chorea damage during second and  Hemiballismus third trimester of pregnancy  Tourette’s Syndrome  Tardive dyskinesia, caused by chronic antipsychotic treatment 41

Muscular Anatomy and the Motor Unit  The nerve cell body (LMN), the axon, plus its terminal branches and all the muscle fibers supplied by these branches, together constitute a motor unit.  Terminates in an end plate inside a skeletal muscle.  The structural unit of contraction is the muscle cell or fiber.  This muscle fiber has a length ranging from a few millimeters to 30 centimeters and a diameter of 10 to 100 um.  On contracting it will shorten to about 57% of its resting length.

14 Anterior Horn Cells ‐ The Motor Unit UMN – descending inhibition

Functional Roles of Muscles  Most muscles are capable of functioning in several different ways depending on  starting position  motion being performed  relation to gravity  direction of the motion  how much resistance it must overcome  As the variables change, so do the roles the muscle play.  All of these factors are “automatically” accounted for with every voluntary movement by reflex connections in the nervous system.

Functional Roles of Muscles Five primary roles  Agonist or prime mover  UMN –for “voluntary” movement selects lmn’s to activate specific muscles.  Synergist  Antagonist  Stabilizer or fixator  Neutralizer

15 Functional Roles of Muscles Agonist –a muscle or group of muscles that causes the motion The muscle contracts isotonically to produce a motion or isometrically to maintain a position.

Functional Roles of Muscles Synergistic – aids in the movement of a prime mover  Assistive – assists in prime mover muscle action  Neutralizers ‐ prevents unwanted movements inherent in the action of the agonist (e.g. pronator teres contraction to stop bicep induced supination during elbow flexion).

Functional Roles of Muscles Antagonist ‐ performs the opposite motion of the prime mover  It contracts eccentrically or "relaxes" and lengthens to prevent, slow or control a motion.  Reciprocal Inhibition  When an agonist contracts, it usually causes the antagonists to relax.

16 Reciprocal Inhibition Red = Motor Blue = Sensory Green = Inhibitory

Attempt to flex the elbow (Biceps contracts)

Requires Triceps to relax

Sensory neurons in biceps

Functional Roles of Muscles  Stabilizer – (AKA: fixators) the muscle may contract to hold a body part immobile while another body part is moving.  The sustained stabilizing contraction is frequently isometric. In most normal activities, proximal joints are stabilized by muscle contractions during movement of more distal joints.

Functional Roles of Muscles Stabilizers and Neutralizers both use co‐contraction to prevent motion. Stabilizers are associated with joints; Neutralizers are associated with muscle.

17 Testing Movement Crude. Sensitive. Specific? More Definitive Tests Isolate System Involved.

Gait Observation  Phases of gait.  Foot Placement Specific.  Heel Striking First  Controlled Placement of Foot and Big Toe.  Smooth and Rhythmic.  Arm Swing Symmetrical and Natural.  Base Should Be Narrow

Narrow Base Broad Base 54

18 The Gait Cycle Definition ‐ The rhythmic alternating movements of the biped lower extremities. The manner in which we walk. The activity that occurs between heel strike of one limb (reference limb) and the subsequent heel strike of that same limb. 55

The Gait Cycle Two Phases  STANCE ( support) PHASE – Reference lower extremity is touching the ground  During gait only one foot is touching the ground for most of the cycle.  Each foot should touch the ground with a tripod of support due to the arches of the forefoot.  SWING PHASE ‐ Reference lower extremity is not touching the ground

There are 3 types of arches in the foot.  Medial Longitudinal arch: This longer inner arch is central to flexibility, shock absorption, and when functioning well gives us the spring in our step. Unfortunately, this is also the arch that is most likely to cause the most concern with our foot.  Lateral Longitudinal arch: The shorter arch on the outer side of the foot.  Transverse arch: this series of smaller arches run crossways along the sole of the foot from the inner to the outer side. 57

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The Gait Cycle  Stance (supported) Phase ‐ Begins when the heel of the reference limb makes contact with the ground and ends when the toe of the same limb leaves the ground.  Three Sub‐Phases  Heel Strike ‐ heel of forward/reference foot touches the ground. Absent in foot drop.  Mid Stance ‐ foot is flat on the ground and the weight of the body is directly over the supporting limb.  Toe Off – (Propulsion) Only the big toe of the reference limb (now behind you) is in contact with the ground. 59

The Gait Cycle  SWING ( unsupported ) PHASE ‐ Begins when the foot is no longer in contact with the ground.  Two Sub‐Phases  Acceleration ‐ the swinging limb catches up to and passes the torso  Deceleration ‐ forward movement of the limb is slowed down to position the foot for heel strike.  Tread mills injure in this stage hips due to decelerating limb striking target moving at a greater speed.  DOUBLE SUPPORT ‐ both limbs are in contact with the ground simultaneously .

20 Analysis of the Gait Cycle ‐ Joint Position  Heel Strike (Contact)  Ankle joint = is in a neutral position, neither dorsiflexed nor plantar flexed  Knee joint = flexed  Weight of body behind knee  Slight flexion helps absorb impact of the foot contacting the ground.  Hip joint flexed  lengthens limb in preparation for contact between heel and ground. Helps provide for proper placement of foot so that the heel make contract with the ground.  Foot = supinated

Analysis of the Gait Cycle ‐ Joint Position Midstance  Ankle joint = dorsiflexed  Knee joint = extended  lengthens limb to help support weight of torso which is now directly over limb  Hip joint = Neutral  Foot = metatarsal strike  5‐4 (foot inverted/supinated)  Foot = metatarsal strike

 3‐2‐1 yeilds slight (foot everted/pronated). 62

Analysis of the Gait Cycle ‐ Joint Position

 Toe Off (propulsion)  Ankle joint = plantar flexed  triceps surae (gastroc/soleus complex) begin to contract strongly bringing the ankle joint into a plantar flexed position  Knee joint = flexed  contraction of the gastrocnemius muscle causes active flexion of the knee joint  shorten limb to allow clearance from ground  Hip joint = Extended  Torso on the opposite side has moved forward of reference limb  Foot = supinated 63

21 Analysis of the Gait Cycle ‐ Joint Position  Acceleration  Ankle joint = neutral  Knee joint = flexed  shorten limb to maintain foot off of the ground  Hip joint = flexed  Limb catches up to and then passes the torso  Foot = slight pronation

22 Heel Strike (Right)

Mid‐Stance (Right)

Toe Off (Propulsion) ‐ (Right)

23 Swing Phase Acceleration (Left)

Swing Phase Deceleration (Left)

Gait Observation  Observe  doctor/patient interaction.  Patient exam performance.

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Slow Motion Follow along with the patients gait. Identify: Stance phase  Heel strike  Mid‐stance  Toe off (propulsion) Swing phase  Acceleration

 Deceleration 74

25 INTERVAL JOINT POSITION MUSCLE ACTIVITY

Acceleration to Heel Strike Hip Flexed Gluteus Maximus Hamstrings Gluteus medius & minimus

Knee Flexed Quadriceps femoris Ankle Neutral Anterior crural muscles

Heel Strike to Midstance Hip Neutral Gluteus medius & minimus

Knee Extended Quadriceps femoris Ankle Dorsiflexed Gastrocnemius; soleus Tarsal Inverted Tibialis anterior Tibialis posterior Midstance to Toe Off Hip Extended - Knee Flexed Gastrocnemius Ankle Plantar flexed Gastrocnemius; soleus Tarsal Everted Fibularis longus Fibularis brevis

Toe Off to Acceleration Hip Flexed Iliopsoas Adductors longus, brevis, magnus Knee Flexed Gastrocnemius Ankle Neutral Anterior crural muscles Tarsal Neutral - 76

Changes in gait  Orthopedic  Myopathic problems  Neurological gait  May be due to weakness of any muscle involved in gait due to central or peripheral neuropathic disease.  Foot drop  May be due to failure of central “motor” systems  UMN (Pyramidal)  Hemiparetic gait  Sizzors  Extrapyramidal  Propulsion or festinating gait  Cerebellar  Broad based, unsteady gait 77

Named Gaits  Propulsive gait – (AKA: festinating) a stooped, rigid posture, with the head and neck bent forward, typically associated with Parkinson’s Disease.  Scissors gait ‐‐ legs flexed slightly at the hips and knees, giving the appearance of crouching, with the knees and thighs hitting or crossing in a scissors‐like movement  Steppage gait –patient elevates lower extremity with foot drop, where the foot hangs with the toes pointing down to avoid dragging the toes on the ground.  Waddling gait ‐‐ a distinctive duck‐like walk that is associated with proximal muscular weakness, usually attributed to myopathy. 78

26 Astasia‐abasia  Inability to either stand or walk in a normal manner.  Patients exhibit an unusual and dramatic gait disturbance, lurching in various directions and falling only conveniently so they will not harm themselves.  Astasia ‐ refers to the inability to maintain station (stand upright) unassisted.  Abasia ‐ The term literally means that the base of gait (the lateral distance between the two feet) is inconstant or unmeasurable. The gait is bizarre and is not suggestive of a specific organic lesion.

Hemiparetic Gait  (AKA: Spastic ) ‐ a stiff, foot‐dragging walk caused by a cortical hemisphere lesion.  Asymmetrical.  Stikes with toe, no heel strike phase due to central foot drop.  Circumduction of LE during swing phase of gait.  UE flexion posture and loss of arm swing on the affected side.

27 The Cerebellar System  “Little brain”  Clinical  Coordinates willfully directed muscular contractions.

The cerebellum  Outgrowth of the vestibular system, sits atop the brainstem.  accounts for approximately 15‐25% of the brain.  communicates with almost all regions of the neuroaxis, with the single exception of the striatum, and has been implicated in cognitive, emotional, sensory, motor and speech processing.  has been shown to display neuroplasticity and learning and memory and may serve as an integrative interface for cognition, emotion, motor functioning and memory. 83

The cerebellum  Typically thought of as a motor center to coordinate fine motor control including speech and visual processing, including the visual guidance of movement.  Electrical‐electrode stimulation or damage to this structure can trigger rage reactions and hyperactivity including “mania”.  Abnormalities in the cerebellum have also been implicated in the pathogenesis of schizophrenia and autism.  Monkeys reared under deprived conditions displayed abnormal activity in the cerebellum and autistic behavior.

28 The cerebellum  Exerts a tonic and stabilizing influence on motor function and can coordinate, smooth, fine tune, and exert a timing influence on motor movements.  Some cerebellar neurons become activated just thinking about making a movement.  Not just associated with motor functioning, but classical conditioning and the learning of new complex motor programs.  The cerebellum may slowly assume control over learned movements, which become "automatic" and can be performed with little or no help from the cerebrum which is then free to do other things. 85

The cerebellum  Conversely, cerebellar lesions slow or abolish the acquisition and retention of conditioned responses and compound movements more severely then simple movements.  These and other findings suggests that the cerebellum may act to integrate and combine different movements, and movement sequences.

The cerebellum

29 The cerebellum

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Cerebellar Anatomy  Posterior fossa of skull  Straddles pons and medulla.  Outgrowth of the vestibular nuclei.  Surface composed of sulci and gyri.  Two lateral masses or hemispheres  Flocculonodular  median vermis. 93

31 Cerebellar Lobe Functions  Flocculonodular lobe; archicerebellum; vestibulo-cerebellum.  Reptile-like  Associated with coordination of the head and trunk.  Outgrowth of the vestibular nuclei system.  Insufficient social-emotional or physical stimulation would also result in insufficient vestibular activation.  Consider the electrophysiological changes in the dentate gyrus of the cerebellum in monkeys reared under deprived conditions and demonstrated autistic behavior. 94

The vestibulo‐cerebellum  Regulates balance and eye movements.  Receives vestibular input from both the semicircular canals and from the vestibular nuclei, and sends fibers back to the medial and lateral vestibular nuclei.  It also receives visual input from the superior colliculi and from the visual cortex for visual balance and eye‐ body coordination.  Lesions of the vestibulocerebellum cause nystagmus and disturbances of balance and gait.

Cerebellar Lobe Functions Anterior lobe spinocerebellum; somatocerebellum; paleocerebellum. Concerned with lower limb coordination. Receives input from ascending spino-cerebellar tracts.

32 The Spino‐cerebellum

 Regulates body and limb movements.  It receives proprioception input from the dorsal columns of the spinal cord (including the spinocerebellar tract) and the trigeminal nerve, as well as from visual and auditory systems.  It sends fibers to deep cerebellar nuclei which in turn project to both the cerebral cortex and the brain stem, thus providing modulation of descending motor systems.  The spinocerebellum contains sensory maps as it receives data on the position of various body parts in space: in particular, the vermis receives fibres from the trunk and proximal portions of limbs, while the intermediate parts of the hemispheres receive fibers from the distal portions of limbs.  The spinocerebellum is able to elaborate proprioceptive input in order to anticipate the future position of a body part during the course of a movement, in a "feed forward" manner.

Cerebellar Lobe Functions  The posterior lobe; hemispheres; cerebro-cerebellum; pontocerebellum; neocerebellum)  Coordinates voluntary movement of the ipsilateral body side.  Input from and output to (feedback loop) to the contralateral cerebral motor areas from the Dentate nucleus.  The neocerebellum is involved in planning movement that is about to occur and has purely cognitive functions as well.

33 The Neocerebellum  Involved in planning movement and evaluating sensory information for action.  Receives input exclusively from the cerebral cortex (parietal‐frontal) via the pontine nuclei (forming cortico‐ponto‐cerebellar pathways).  Sends fibers to the ventrolateral thalamus (connected to motor areas of the premotor and primary motor area of the cortex) and to the red nucleus (connected to inferior olivary nucleus, which links back to the cerebellar hemispheres).

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Cerebellar Connections  Three pair of peduncles.  Superior peduncle (brachium conjunctivum)  Carries information back to the motor cortex.  Some incoming (afferent) fibers from the anterior spinocerebellar tract are conveyed to the anterior cerebellar lobe via this peduncle, most of the fibers are exiting (efferent).  Major output pathway of the cerebellum.  Most of the efferent fibers originate within the dentate nucleus which in turn project to various midbrain structures including the red nucleus, the ventral lateral/ventral anterior nucleus of the thalamus, and the medulla.

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Cerebellar Connections

 Three pair of peduncles.  Middle peduncle (brachium pontis) corticopontine fibers enter the cerebellum.  Composed entirely of incoming (afferent) fibers originating within the pontine nuclei as part of the massive cortico-ponto-cerebellar pathyway.  These fibers descend from the sensory and motor areas of the cerebral neocortex and make the middle cerebellar peduncle the largest of the three cerebellar peduncles.

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34 Cerebellar Connections  Three pair of peduncles.  Inferior peduncle (restiform body) Mostly vestibular and proprioceptive information (from the dorsal spinocerebellar tract).  Carries many types of input and output fibers that are mainly concerned with integrating proprioceptive sensory input with motor vestibular functions such as balance and posture maintenance.  Dorsal spinocerebellar information synapses within the paleocerebellum.  Vestibular information projects onto the archicerebellum.  The climbing fibers of the inferior olive run through the inferior cerebellar peduncle.  This peduncle also carries information directly from the Purkinje cells out to the vestibular nuclei in the dorsal brainstem located at the junction between the pons and medulla.

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Cortico-pontinePonto-cerebellar pathway Pathway Hemispheres – Motor Cortex Dentate Nucleus Cerebro-cerebellum Superior Peduncle Brachium Conjunctivum Major efferent peduncle

Cerebellar Middle Peduncle Brachium Pontis Pons Processing Major afferent peduncle

Inferior Peduncle Spinocerebellum Restiform Body (Anterior Lobe)

Posterior Spino-cerebellar tract

Unconscious proprioception 105

35 Movement Corticospinal (pyramidal) pathway Thought of movement Motor Cortex Cortico-pontine pathway

Red Nucleus Thalamus Pons

Ponto-cerebellar Pathway Superior Peduncle Middle Peduncle Brachium Conjunctivum Cerebellar Brachium Pontis Major efferent peduncle Processing Major afferent peduncle

Rubrospinal pathway to cord assist with background muscles 106

Movement Corticospinal (pyramidal) Motor Cortex pathway

Thalamus

Superior Peduncle Cerebellar Inferior Peduncle Brachium Conjunctivum Processing Restiform Body Major efferent peduncle

Anterior Spino-cerebellar tract Posterior Spino-cerebellar tract

Unconscious proprioception 107

Movement Corticospinal (pyramidal) Motor Cortex pathway

Thalamus

Inferior Peduncle Vestibulo-cerebellar Restiform Body Processing

Vestibular nuclei

Vestibulo-spinal Pathways Inner ear 108

36 General Cerebellar Circuitry  From motor cortex to pontine nuclei (synapse).  The pontocerebellar neurons decussate and arrive via white matter to synapse on purkinje fibers of the cerebellar cortex.  Purkinje fibers travel in white matter to the dentate nucleus of the cerebellum.  Then from cerebellum (decussate) prior to distribution to red nucleus communication).  Then to thalamus.  Then to motor cortex (corticospinal).

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Synapse/Decussate

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The Cerebellar Double Cross

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37 Clinical Signs Of Cerebellar  General weakness and fatigue.  Swaying when standing with a narrow base.  Ataxia/dystaxia  Also common with disturbances of proprioception or other sensory modalities, disturbances of the motor system, or joint disease.

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Clinical Signs Of Cerebellar Dysfunction

 Cerebellar Gait  Broad-based

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Clinical Signs Of Cerebellar Dysfunction  Dysarthria (slurring of speech)  Listen for dysarthria of recent onset.  "Whosoever, whatsoever, or perfect pleasures" or any tongue twister.  Tremor  Nystagmus

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38 Patient Video Vignette  Listen to the slurring of speech and faulty articulation of the following patient who has a pre‐natal variety of cerebral palsy.

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Clinical Signs Of Cerebellar Dysfunction  Hypotonia.  “Rag doll” posture and gait.  Decomposition of movement.  "Movement by the numbers”.  Dysdiadochokinesia  Inability to perform rapidly alternating movements.  Rapidly supinate and pronate the hands.  Thigh slap.  Tap foot rapidly.

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39 Patient Video Vignette  Observe the uncoordinated rapid hand supination and pronatation in this patient.  Observe the asymmetrical and uncoordinated “Thigh Slap”.

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Clinical Signs Of Cerebellar Dysfunction The pendular reflex?

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40 Overshooting And Undershooting  Difficulty in measuring distances will overestimate or underestimate the distance to a particular point.  Eyes open.  Finger-to-nose test.  Observe for intention tremor  More objective method is wrist slap test.  Lower extremity = heel-to-shin test.  The rebound sign test 121

Patient Video Vignettes  In the two following patients we will perform some cerebellar test.  As always, observe the doctors instructions and communication, as well as the technical test performance by the patient.  In the second case you will see how removing visual clues from the patient causes the test to become a proprioceptive test.

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Wrist Counter Pressure

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Wrist Slap

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42 Syndromes Of Cerebellar Disease A cerebellar syndrome is recognized for each of the anatomical areas. Dystaxia and nystagmus are shared by all of the syndromes described.

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Syndromes Of Cerebellar Disease  There are many genetic and idiopathic cerebellar syndromes which also effect other parts of the CNS so combinations of pyramidal, extrapyramidal and cerebellar signs and symptoms are often seen together in the same patient.  Any brain disorder that effects tracts going in or out of the cerebellum may cause cerebellar findings upon examination of that patient.

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Syndromes Of Cerebellar Disease  Rostral vermis or anterior lobe syndrome  Primarily spinocerebellar pathology causes decreased coordination of the lower extremities and trunk.  Most commonly associated with alcoholism and nutritional deficiencies.  Caudal vermis or flocculonodular lobe syndrome  Pathological involvement of the vestibulo-cerebellum produces mostly stance and gait impairments.  Often associated with a neoplasm of the cerebellopontine angle.

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43 Syndromes Of Cerebellar Disease

 Hemisphere or posterior lobe syndrome  Affects the ipsilateral side of the body.  In a child, a neoplasm or brain abscess should be suspected.  Pancerebellar syndrome  Hereditary or toxic-metabolic disease is the usual cause.  All cerebellar components are affected, resulting in movement disturbances involving the whole body.

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Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 131 Pathol Reflexes Present (late stage) N/A N/A

44 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 133 Pathol Reflexes Present (late stage) N/A N/A

45 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 136 Pathol Reflexes Present (late stage) N/A N/A

46 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 139 Pathol Reflexes Present (late stage) N/A N/A

47 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 142 Pathol Reflexes Present (late stage) N/A N/A

48 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 145 Pathol Reflexes Present (late stage) N/A N/A

49 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 148 Pathol Reflexes Present (late stage) N/A N/A

50 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 151 Pathol Reflexes Present (late stage) N/A N/A

51 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 154 Pathol Reflexes Present (late stage) N/A N/A

52 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 157 Pathol Reflexes Present (late stage) N/A N/A

53 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 160 Pathol Reflexes Present (late stage) N/A N/A

54 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 163 Pathol Reflexes Present (late stage) N/A N/A

55 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 166 Pathol Reflexes Present (late stage) N/A N/A

56 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 169 Pathol Reflexes Present (late stage) N/A N/A

57 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 172 Pathol Reflexes Present (late stage) N/A N/A

58 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 175 Pathol Reflexes Present (late stage) N/A N/A

59 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 178 Pathol Reflexes Present (late stage) N/A N/A

60 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 181 Pathol Reflexes Present (late stage) N/A N/A

61 Pyramidal Extrapyramida Cerebellar Reflex Arc l Strength Decreased Decreased Decreased Decreased (if at level involved) Tone Spastic Rigid Hypotonic Decreased (if at level involved) Volume Mild Atrophy of N/A N/A Decreased (if at Disuse level involved) Posture/ Stiff; upper limb Motionless; “Rag Doll”; Fasciculations Observation typical posture Masked Facies Decomp of Early; Edx Movement Tremor N/A Resting, “Pill Intention N/A Rolling” Gait Hemiparetic Festinating Broad Based Weak mm at level involved MSR Hyperactive N/A (Rigid) N/A (Pendular?) Hypoactive (if at level involved) Superf Reflex Hyperactive N/A (Rigid) N/A Hypoactive (if at level involved) Visceral Reflex N/A N/A N/A N/A 184 Pathol Reflexes Present (late stage) N/A N/A

62 Observation of station  It is common practice to integrate many tests together when performing an examination.  This allows a more efficient and practical approach performing an examination.  One such integration is asking the patient to hold a sustained posture.

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Observation of station Here strength (pyramidal), balance, posture and tone reflexes (extrapyramidal), sensory (vestibular/proprioceptive) input and cerebellar fine tuning can all be observed working together. While simple observation of characteristic signs may be sufficient to identify which system appears to be responsible for abnormal performance, confirmatory testing of each system on examination in a more independent fashion is necessary for a more definitive diagnosis.

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Observation of station Ask the seated (or standing) patient to hold both arms out in front of them with their palms turned upward toward the ceiling. After they comply, ask them to hold that pose and close their eyes for about 20‐30 seconds.

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63 Observation of station Observe  Flexion of the elbow and pronation of the hand.  Pronator drift ‐ Early weakness in hemiparesis may be revealed as it requires energy to hold this posture and hemiparetic muscles fatigue quickly.  This test is very practical as it not only is a quick screening process for a number of systems, but it may be even more sensitive to hemiparesis then standard manual muscle testing because of the fatigue.

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Observation of station  Observe  Veering and drift.  Patients with vestibular disease often have a sensation of movement which they begin to compensate for by leaning and “drifting” to one side. Always the same direction. Like they are being pulled.  May be confirmed by asking the patient to walk around the table or a chair. In one direction they may continue to bump into the chair as they walk around it. They do not have the same difficulty if you change the direction and they walk around the other way.  Proprioceptive disease may also cause some drifting of the outstretched extremity.  Drift is usually corrected quickly when the patient opens their eyes and sees the drift as the eyes now settle the issue of where the patients body is in space.

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Observation of station  Observe  Veering and drift  In proprioceptive disease the extremity may drift but it is not quite the same as the veering which involves both extremities as well as the trunk.  You may differentiate by testing proprioceptive function in the extremity separately. A simple method of doing this is to grab one of the patients upper extremities and with the patients eyes closed elevate the extremity and bend it into a certain position. Ask the patient to move the other extremity into the same position. This rapidly checks both sides proprioceptive function.

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64 Observation of station  Observe  Drift or veering.  If one extremity drifts up and laterally, it may be a problem with one of the cerebellar hemispheres. Observe for intention tremor and perform other cerebellar tests such as finger to nose for confirmation.  Placing the head and neck in various positions, particularly rotation or extension rotation, while doing this test, may cause drift in vertebral artery disease; particularly in cases of where it is cervical spondylosis compressing the vertebral arteries.  Asking the patient to shake their head in a “no” fashion may cause some drift in cervicogenic disequilibrium due to confusion from cervical proprioceptors.

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Patient Video Vignettes Cases with various normal and abnormal gait examples. Observe doctor/patient interaction. Patient exam performance.

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65 Discussion  Was the gait normal? No.  What did you notice? Foot drop.

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Write it down!

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66 199

Discussion

 Was the gait normal? No.  What did you notice?

Scissor Gait; Bilateral foot drop;. Hyperlordosis; favors right LE.

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67 202

Discussion  Was the gait normal? No.  What did you notice? Broad based gait; stutter step; stumbling.

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Slightly Broad Based

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68 The Cerebellar Two-Step (AKA: The Stutter Step)

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Tandem Gait

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See how you do.

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69 208

Discussion  Was the gait normal? No.  What did you notice? Disorganized rate, direction and rhythm of gait; Falls toward convenient support.  Likely Diagnostic consideration?

Somatoform Disorder.

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70 211

Discussion  Was the performance within normal limits? No.  What did you notice? Dragging toes without lifting leg is not consistent with know reaction to  Likely Diagnostic consideration?Severe foot drop. We would expect a “stepage” gait. Somatoform disorder.

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Ridiculous Gait

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71 Heel‐Toe and Tandem Gait  Heel to toe  Walk on toes  Walk on heels

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Discussion  Was the performance within normal limits?  What did you notice? YES!

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72 217

Discussion  Was the performance within normal limits?  What did you notice? No!

Unable to stand with a narrow base.

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Coordination Tests – UE & LE  Was the performance within normal limits?  What did you notice?

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73 220

Discussion Yes!  Was the performance within normal limits?  What did you notice?

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74 Discussion  Was the performance within normal limits?  What did you notice? YES!

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Discussion NO!  Was the performance within normal limits?  What did you notice?

Classic cerebellar dysmetria characterized by rhythmic overshooting and undershooting.  Likely Diagnostic consideration?

Cerebellar disease.

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75 226

Discussion  Was the performance within normal limits?  What did you notice? No

Uneven performance – especially last test on left UE.

 Likely Diagnostic consideration?

Cerebellar disease.

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76 Discussion  Was the performance within normal limits?  What did you notice? No

Uneven performance especially on the left side.

 Likely Diagnostic consideration?

Cerebellar disease.

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Discussion  Was the performance within normal limits?  What did you notice? YES!

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77 232

Discussion  Was the performance within normal limits?  What did you notice? Equivocal Slight broad based.

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78 Discussion No.  Was the performance within normal limits?

 What did you notice? Broad base? Poor stability on tandem walking with the “cerebellar two step”.

 Likely Diagnostic consideration?

Cerebellar disease.

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Presented By: Joseph S. Ferezy, D.C.

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79 Examination of station and gait  Routine part of examination.  Disorders affecting balance and movement can be challenging due to complex sensory and motor systems interactions.  When any of these systems fail the nervous system displays predictable deficits.  Recognizing and testing the nervous system reveals these deficits and is a pre‐requisite to arriving at a diagnosis which is a pre‐requisite for proper management.

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