MD Lecture

8/7/2019 MD Lecture

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MOVEMENT DISORDERSLife Neurology Club - 09.09.10

by Matthew Antonucci, DC

8/7/2019 MD Lecture


FREEZING IN PARKINSON’SHave You Seen An Older Lady Like This Before?

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Thank You Dr. Fredrick R Carrick

Dr. Joseph Jenchovic

Dr. Stanley Fahn

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Movement Disorders (MD)Estimated 4o million Americans have a movement disorder

1 in every 7

2x the amount of diabetes

4x the number of people that survived cancer

21% of children have a tic

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Easy To Define“A disorder of movement”

Either too much or not enough You can also have poor quality

Subluxation is a movement disorder of the spine.

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Hard To Identify The average MD patient will see 15 doctors over a 5 year period before receiving a diagnosis.

If a doctor can not identify the etiology of a MD (AKA a “functional” lesion), the patient gets labeled as having a “psychogenic” MD

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So Many of Them...■ Akathisia (feeling of inner restlessness)■ Akinesia (lack of movement )■ Associated Movements (Mirror Movements or Homolateral

Synkinesis )■ Athetosis (contorted torsion or twisting )■ Ataxia■ Ballismus ( violent involuntary rapid and irregular movements )■ Hemiballismus (affecting only one side of the body )■ Bradykinesia (slow movement )■ Cerebral palsy (hypoxic injur y)■ Chorea (rapid, involuntary mo vement )■ Coprolalia (freezing and sometimes cursing vocal tic)■ Corticobasal D egenera tion (degeneration of frontal lobe and BG)■ Sydenham's chorea (autoimmune post-strep)■ Huntington's d isease (genetic chore a)■ Hyperekplexia (excessive startle)■ Dystonia (sustained torsion )■ Dystonia muscularum (gross sustatined torsion)■ Blepharospas m (exce ssive or sustained blinking)■ Writer's cramp (focal hand dy stonia while writing)■ Spasmodic tor ticollis (twisti ng of head and neck )■ Dopamine-res ponsive dyston ia (hereditary progressive dystonia

with diurnal uctuation or Segawa's disease)■ Lesch-Nyhan Syndro me (self mutilating disorder)■ Latah (excess ive startle with vocal and sometimes violent bursts)

■ Geniospasm (episodic involuntary up and down movements of the chin and lower lip )

■ Myoclonus (brief, involuntary twitching of a muscle or a group of muscles )

■ Multiple System Atrophy (Similar to PD with Autonomic damage)■ Parkinson's di sease (bradykine tic disorder associated with SNc)■ PKAN (Iron deposition disease)■ PSP (degener ation beginning in the mes and descending)

■ Restless Legs Syndrome RLS (Witt Maack-Ekboms disease)■ SCA (genetic atrophy of the sp inocerebellar sys tem)■ Spasms (contractions )■ Stereotypy (repetitive, purposeless movements )■ Tardive dyskinesia (movement dis order secondary to drugs)■ Tic disorders (involunt a ry, compul sive, repetitive, stereotyped )■ Tourette's syn drome (classied by vocal and motor tics)■ Tremor (oscilla tions ) (rhyth mic alternating contractions of agonist)■ Rest tremor ( 4 -8 Hz ) (only at rest )

■ Postural tremo r (only in c ertain postures)■ Kinetic tremor (only wh en moving)■ Essential tremor (6-8 Hz variable amplitude )■ Cerebellar tre mor ( 6-8 Hz variable ampl itude )■ Parkinsonian tremors (4-8 Hz variable amplitude )■ Physiological tremor ( 10-12 Hz low amplitude )■ Wilson's disea se (copper storage d isease ■ ......

http://en.wikipedia.org/wiki/Wilson%27s_disease

http://en.wikipedia.org/wiki/Dopamine-responsive_dystonia


http://en.wikipedia.org/wiki/Spasmodic_torticollis


http://en.wikipedia.org/wiki/Writer%27s_cramp


http://en.wikipedia.org/wiki/Blepharospasm

http://en.wikipedia.org/wiki/Dystonia

http://en.wikipedia.org/wiki/Huntington%27s_disease



http://en.wikipedia.org/wiki/Sydenham%27s_chorea


http://en.wikipedia.org/wiki/Chorea_(disease)



http://en.wikipedia.org/wiki/Cerebral_palsy

http://en.wikipedia.org/wiki/Bradykinesia



http://en.wikipedia.org/wiki/Hemiballismus

http://en.wikipedia.org/wiki/Ataxia

http://en.wikipedia.org/wiki/Athetosis




http://en.wikipedia.org/wiki/Parkinsonian_tremors

http://en.wikipedia.org/wiki/Essential_tremor

http://en.wikipedia.org/wiki/Amplitude

http://en.wikipedia.org/wiki/Hertz

http://en.wikipedia.org/wiki/Tremor

http://en.wikipedia.org/wiki/Oscillation

http://en.wikipedia.org/wiki/Tourette_syndrome



http://en.wikipedia.org/wiki/Tic_disorder



http://en.wikipedia.org/wiki/Tardive_dyskinesia




http://en.wikipedia.org/wiki/Stereotypy


http://en.wikipedia.org/wiki/Spasm

http://en.wikipedia.org/wiki/Restless_Legs_Syndrome


http://en.wikipedia.org/wiki/Parkinson%27s_disease






























http://en.wikipedia.org/wiki/Myoclonus

http://en.wikipedia.org/wiki/Myoclonus

http://en.wikipedia.org/wiki/Geniospasm

http://en.wikipedia.org/wiki/Geniospasm



























http://en.wikipedia.org/wiki/Associated_Movements

http://en.wikipedia.org/wiki/Associated_Movements

http://en.wikipedia.org/wiki/Akinesia

http://en.wikipedia.org/wiki/Akinesia

http://en.wikipedia.org/wiki/Akathisia

http://en.wikipedia.org/wiki/Akathisia

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MD and Chiropractic?Define Chiropractic for me...

Functional Neurology DOES help

Chiropractic is a tool of the Functional Neurologist

Most cases you won’t adjust these patients because it furthers theMD

NOBODY can help these patients except for YOU!

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PHENOMENON BLUE Justification of Functional Neurology?

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Movement DisordersClinical diagnosis remains the basis for diagnosis and treatment.

Crucial to be able to identify phenomenology It’s the difference between helping a patient and making them worse

No shotgun approaches!

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Terminology Phenomenology: the phenotypic expression of the disorder.

Your empirical observations of the presentation.

Diagnosis: the name of the syndrome created by identifying all phenotypic movements

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Prefixesa- “without”

brady- “slow”

dys- “abnormal”

hyper- “increased”

hypo- “decreased”

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Suffixes-kinesia: “movement”

-tonia: “tone”

-phrenia: “thought”

-phagia: “swallowing”

-arthria: “speaking”

-phonia: “projecting”

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5-Step Diagnostic ProcessStep 1: Is it a movement disorder?

Step 2: Akinetic/Rigid or Hyperkinetic?

Step 3: Jerky or Non-Jerky?

Step 4: Random or Patterned?

Step 5: Voluntary or Involuntary?

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Step 3: Jerky or Non-Jerky



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Identifying The DisorderIdentification is based upon taking all of your observations andcomparing them with the criteria for MDs.

When describing a MD, you always start with the most prevalent movement.

ie: Parkinson’s= Bradykinesia (prevalent in all movements)

with tremor (only present in corticospinal distribution)The more specific, the better.

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FACIAL TICSIdentify The Phenomenology

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HUNTINGTON’S CHOREA Identify The Phenomenology...

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REEMERGENT TREMOR Identify The Phenomenology...

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CERVICAL DYSTONIA Describe the Phenomenology

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DRPLA Identify The Phenomenology...

Text

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TRUNCAL DYSTONIA Scoliosis??

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LATE STAGE PDIdentify The Phenomenology...

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STOP!

There are only a few bradykinetic disorders. They are:

Parkinson’s

PSP

CBD

MSA

Alzheimer’s

Dementia

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New Tests!Shoulder Shrug

Finger Tap

Foot Tap

Pull Test Posture

Timed Get-Up-And-Go

Sit in Chair -> Walk 10 feet -> Return -> Sit

7-10 sec is normal

Look for Lack of Arm Swing

Check for Arm Swing With Cortical Engagement

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Pull Test The pull test evaluates the patient’s center of pressure (COP)

As frontal lobe fxn declines, people develop a posterior COPMakes them think that they are falling backwards

Increases their flexor tone

The pull makes them feel even more posterior so they stumble

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NORMAL PULL TEST Observe The Number of Steps Until Recovery

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POSITIVE PULL TESTSObserve...

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PRACTICE THE PULL TEST

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COP and Eye MovementsIf you have a posterior COP, which eye muscles become more plastic?

Which eye muscles become less plastic?

Which eye movements will be limited?

What would you see in a vertical OKN?If you have an anterior COP, how will this differ?

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PATHOPHYISIOLGY HOW DOES THIS HAPPEN?

These are watered-down explanations for conceptual learning.Movement disorders have many different mechanisms.

For a more detailed explaination, take the advanced test and come to adv club!

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THE BASAL GANGLIA THE MOVEMENT REGULATOR OF MOVEMENT

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PARKINSON’S

Caudate

SN(c)

BGThalamus

Frontal Lobe

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Disinhibition of Thalamus When this happens, you get tremor and posturing (PD+ dystonia)

Posturing in PD is increased flexor tone

camptocormia

shoulders forward

arms rigid

knees bent

hips flexed

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Cerebellar Stim May Worsen It

Posturing and spasticity does what to the feedback into thecerebellum? Increase or Decrease?

It will do this to all of the postsynaptic areas including the frontallobe.

By adjusting joints and increasing feedback to these areas, wouldthat be good or bad?

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But How Does The SN Die?This has not been discovered yet. But there is a really strong theory.

A protein called alpha-synuclein becomes deposited in different

areas of the brain in different areas at different times- starting inthe olfactory bulb. This is described in Braak Staging.

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Early Signs? Alpha-Synuclein first deposits in a specific pattern.

1) Olfactory bulb (about 20 year prior to PD diagnosis)

2) DMN of X (15 years prior to dx) and Frontal Decline

3) SN(c) and Amygdala (12 years prior to dx)

4) Neocortex and Meysner’s Plexus (10 years prior)

5) Myocardium (5 years prior)

By the time a tremor is present, 90% of the SN(c) is dead.

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Clinical GemsHorizontal OPK are pontine, parietal and feed forward frontal andcerebellar

Not really a good representation of frontal lobe integrity Good for a baseline physiology assessment

Vertical OPK are much more frontally based

With frontal lobe demise, upward refixation saccades go first!

Downward OPK will be worse than upwards

Compare horizontal to vertical OPK ALWAYS!

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Where Does It Come From?It makes up 1% of our neural tissue cytosol.

Something (we don’t know what) causes it to be deposited (or not removed)

Current thoughts:

Oxidative stress

Genes

Gluten Sensitivity Segers-Nolten IM, Wilhelmus MM, Veldhuis G, van Rooijen BD, Drukarch B, Subramaniam V. Tissue transglutaminase modulates alpha-synucleinoligomerization. Protein Sci 2008;17: 1395-1402

Ricotta M, Iannuzzi M, De Vivo G, Gentile V. Physio-pathological roles of transglutaminase-catalyzed reactions. World J Biol Chem 2010 May 26; 1(5): 181-187.

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Where Do You Apply YourTreatment?

The SN(c) has stopped producing dopamine, but not completely otherwise they’d be dead.

Goal is to increase the dopamine production without exceeding themetabolic capacity of the fragile SN(c). Monitor movement parameters and autonomics.

Cerebellar Stim (Starting Distally)

Vertical Eye Movements

Visual Stim from Periphery (Patterned Check)

Head Movement Perameters

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Nutrition?Glucose and Insulin

Adrenals (HPA/Hippocampal Health)

Gut

Blood Brain Barrier

Sex Hormones

Neurotransmitter Support

Promote Autophagy (Dark Berries and Fasting)

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CHOREA/ BALLISM

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How Does The STN Stop Working?

Damage to the Subthalamic Nucleus of Louis (STN)

Usually a stroke of the MCA or the lenticulostriate branchesPost-strep infections can cause this (Sydenham’s Chorea)

Heavy-metal accumulation

Liver/Kidney Failure

MANY other

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How Do You Treat It?

The SN(r) inhibits the thalamus, just like the GPi- which is the target of theSTN. It also decreases dopamine release from the SN(c).

Increasing the function of the SN(r) may decrease spontaneous movements.

Targeted saccadic eye movements elicit excitation of the SN(r) via it’sinhibitory effect on the superior colliculus.

Nigral neurons also appear to be sensitive to color frequencies of activation.Combining the above with cognitive (frontal) activities can prove to be very effective.

Forced respiratory exercises also help.

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Nutrition?

These patients have a very high metabolic baseline, to the point

where they exceed their own metabolic capacity.High protein, low carbohydrate diets make calories less readily available. This slows down their system and allows it to “cooloff”.

As with any individual it is important to monitor all of their bloodlevels (glucose, liver, RBC, iron, etc)

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DYSTONIA The 3rd Most Prevalent Movement Disorder

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Solving The Mystery...

Prof. Carrick has a lab at Harvard University studying dystonia

using fMRI and SPECT scans

He has great success with dystonic patients

He has discovered that dystonia is a problem with the collicularrelationship to the parietal lobe...

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Unraveling Dystonia

There is a change in thesomatotopic map seen on fMRI

We need a good map in order toknow what to move and how

Bad map = Bad movement

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Somatosensory MapLower forms of life don’t have higher brain function such asfrontal lobes.

They’re all mesencephalic (fish)

The mesencephalon and the hippocampus are made of 3 layers

The “primitive parietal lobe” where we have our map, is on layer3 of the cortex

The mesencephalon expanded from the superior colliculus intothe parietal lobe for spatial and somatotopic mapping.

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What Does This Mean?

Your perception in space is determined by your superiorcolliculus, hippocampus and parietal lobe.

When you have aberrant saccades, you have aberrant spatial perception.

Aberrant spatial preception creates aberrant motor patterns andCOP

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The Treatment... Address targeting of the saccades

Look at the muscles that would be activated as a consequenceof an aberrant COP and activate the paretic muscles

Start with very small saccades in the direction that’sappropriate rehab the colliculus.

You can use a labyrinthine VOR to assist

Once the integrity of eye muscles are being re-estabilished you can integrate cerebellar mechanisms.

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Eye Muscle Integrity...

Posture

What is the COP? What are the plastic eye muscles?

What are the paretic eye muscles?

What is the eye movement that you want to promote?

What if it is an ipsilateral brain lesion?

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