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Neuro D&D > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Symptoms appropriate for PTs to treat

A
  • symptoms change with position or postural changes
  • active or passive ROM
  • resistive or special tests
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2
Q

Red Flag Symptoms

A
  • DO NOT TREAT!! REFER TO PERSONS
  • visceral pain patterns
  • consistent pattern symptoms
  • existing symptoms that do not vary with active or passive ROM, resistance testing, or postural changes
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3
Q

Initial Screen using WHO levels

A
  • body structures and functions impairments
  • activity limitations
  • participation restrictions
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4
Q

Initial Eval using systems review

A
  • neuromuscular
  • musculoskeletal
  • cardiopulmonary
  • integumentary
  • also gastrointestinal, urogenital, reproductive, endocrine, psychological (not really for PTs)
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5
Q

Purposes of Examination and Evaluation in the clinic

A
  • Examine and evaluate to determine impairments, activity limitations, and participation restrictions
  • Establish a clinical diagnosis and prognosis
  • Select and apply best available evidence-based interventions
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6
Q

Examination tests and measures Priority items

A
  • height and weight
  • BMI
  • Blood pressure (BP)
  • Heart rate (HR)
  • Respiratory rate
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7
Q

Two classes of cells in the Nervous System

A
  • neurons (nerve cells)

- glia (supporting cells)

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8
Q

Parts of a neuron

A
  • dendrites
  • cell body
  • axon hillock
  • axons
  • presynaptic terminal
  • presynaptic neuron
  • post-synaptic neuron
  • node of ranvier
  • presynaptic terminal
  • synaptic cleft
  • postsynaptic membrane
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9
Q

Axon Hillock

A
  • where axon meets cell body before it synapses

- the closer the first order neurons are to this, the more likely they are to get the neuron to fire

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10
Q

Glial Cells

A
  • Schwann cells (PNS)

- Oligodendrocyte cells (CNS)

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11
Q

Node of Ranvier

A
  • areas where there is no myelin
  • sodium goes in, potassium goes out
  • area that causes depolarization
  • helps speed up the contraction
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12
Q

Saltatory Conduction

A
  • with unmyelinated neuron

- sodium and potassium exchange must occur entire length of axon vs. when myelinated

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13
Q

Dendritic Aborization

A
  • takes in all of the signals
  • many dendrites to one axon
  • moreso with sensory info where need to collect detailed info from everywhere (sensory integration)
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14
Q

Motor Nerve

A
  • less dendrites than with sensory
  • synapse on muscle fibers
  • multipolar neuron
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15
Q

Structural Classes of Neurons

A
  • Bipolar (interneuron)
  • Unipolar (sensory neuron)
  • Multipolar (Motorneuron)
  • Pyrimidal Cell
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16
Q

Sensory neurons

A
  • considered unipolar
  • one cell body with two axons going both ways from cell body whereas bipolar has one half dendrite and one half axon
  • still has small area of dendrites
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17
Q

4 Main Functions of Glial Cells

A
  • provides structure for the neurons, surrounds neurons and holds them in place
  • forms the (lipid) myelin sheath, speeds NCV (voltage gated ion channels are concentrated in nodes of ranvier), insulates one neuron from another
  • supplies nutrients and oxygen to neurons
  • destroys pathogens and removes dead neurons
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18
Q

Glial Cells of PNS

A
  • Schwann Cells
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19
Q

Glial Cells of CNS

A
  • Oligodendrocytes
  • Astrocytes
  • Microglia
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20
Q

Schwann Cells

A
  • PNS
  • usually only myelinates one neuron
  • myelin spirals around axon to form myelin sheath
  • nodes of ranvier
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21
Q

Nerve Conduction Velocity (NCV) of myelinated vs unmyelinated axons

A
  • unmyelinated axon (C-sensory nerve): axon diameter 1 um & NCV = 0.5-2 m/s
  • myelinated (alpha MN): axon diameter 12-20 um & NCV 72-120 m/s
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22
Q

Astrocytes

A
  • CNS
  • most common glia
  • fill most of brain space not occupied by neurons
  • astrocytes are supporting cells within CNS
  • provide structural support and insulate neurons from each other
  • maintenance of blood-brain barrier
  • during inflammation and injury, they divide and wall off damaged areas
  • act as scavengers: remove neurotransmitters from synaptic cleft, clean up debris during early development and during recovery after injury
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23
Q

Microglia

A
  • CNS
  • contain branched cytoplasmic processes and play an important phagocytic role
  • protective and destructive roles (delicate balance between the two)
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24
Q

Microglia protective jobs

A
  • activated and mobilized after injury, infection, disease
  • important during brain development
  • function as phagocytes (ingest and destroy bacteria, cells and other materials)
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25
Q

Microglia destructive jobs

A
  • in diseases such as Alzheimer’s and aging
  • release of toxic compounds into neural environment
  • HIV/AIDS can activate microglia and stimulate a cascade of cellular breakdown
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26
Q

CNS Demyelination

A
  • damage to myelin sheaths in brain and SC
  • multiple sclerosis (MS): autoimmune disease in which the oligodendrocytes are attacked by the person’s own antibodies, produce patches of demyelination = plagues in the white matter
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27
Q

CNS vs PNS

A
  • CNS: brain and spinal cord

- PNS: everything that is not brain or spinal cord

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28
Q

Within one musculocutaneous nerve, what could all be in it

A
  • Ia phasics
  • Ia tonics
  • Ibs
  • III and IVs
  • Alpha MNs
  • Gamma MNs
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29
Q

LMN lesion S&S

A
  • atrophy
  • weakness
  • hypotonic DTRs
  • decreased muscle tone
  • fasciculations
  • in peripheral nerve (or cranial nerve) distribution
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30
Q

UMN lesion S&S

A
  • spasticity
  • hypertonic and hypotonic DTRs
  • clonus
    • Babinski or Hoffman’s reflexes
  • Weakness
  • Synergistic movement patterns
  • usually effects one or both sides of body
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31
Q

Fasciculations

A
  • rapid, fine, can be painless but usually painful contraction of groups of muscle fibers
  • visible by not strong enough to move limbs
  • commonly seen in anterior horn disorders (ALS)
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32
Q

Patterns of Motor and Sensory Loss for UMN Brain

A
  • motor loss of a body part
  • sensory loss of body part
  • glove-like or sock-like (both sides of arm or leg)
  • reflexes: hypo or hypertonic
  • sensory loss: post-central gyrus (3, 1, 2)
  • motor loss: pre-central gyrus (4)
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33
Q

Patterns of Motor and Sensory Loss for UMN SC

A
  • motor loss: myotome or loss below level of injury
  • Sensory loss: Dermatome or loss below level of injury
  • reflexes: hypo or hypertonic
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34
Q

Patterns of Motor and Sensory Loss LMN Nerve Root

A
  • Motor loss: myotome
  • Sensory loss: dermatome
  • Reflexes hypotonic
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35
Q

Patterns of Motor and Sensory Loss Peripheral Nerve

A
  • Motor loss: nerve distribution
  • Sensory loss: nerve distribution
  • Reflexes hypotonic
  • Peripheral nerve compression somewhere after the plexi (after the peripheral nerves have been formed)
    Perform sensory & motor examination to determine which nerve has an compression site (and where)
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36
Q

UE PND (peripheral nerve distribution) for Radial Nerve

A
  • motor: elbow extension, wrist and finger extension, supination
  • sensory: back of arm, web space between thumb and pointer finger, triceps area, lateral upper arm sliver, sliver down to dorsal forearm
  • radial (C6-8, T1)
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37
Q

UE PND (peripheral nerve distribution) for Median Nerve

A
  • Motor: Pronation, Wrist flexion, Long finger flexors
  • Sensory: palmar side of digits 1-3 and 1/2 of 4. tips of both sides of 1 and 2,
  • C6-8, T1
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38
Q

UE PND Ulnar Nerve

A
  • Motor: Little finger abduction, interossei
  • Sensory: palmar side of 1/2 ring finger and pinky…dorsal of 3-5, middle of upper arm on biceps and down medial lower arm down to pinky
  • C8, T1
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39
Q

LE PND for Deep peroneal nerve

A
  • Motor: Dorsiflexion, Toe extension

- Sensory: medial top of foot

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40
Q

LE PND for Superficial peroneal nerve

A
  • Motor: Eversion

- Sensory: lateral 1/2 of front of leg 1/2 way down below knee and wrap to little bit on back

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41
Q

LE PND for Common peroneal nerve

A
  • Motor: all
  • Sensory: all
  • L4-5, S1-2
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42
Q

LE PND for Tibial nerve

A
  • Motor: Ankle plantarflexion, Inversion, Toe flexion
  • Sensory: medial and lateral calcaneal
  • L4-5, S1-3
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43
Q

Botulism Etiology

A
  • neurotoxin produced by Clostridium Botulinum
  • anaerobic, gram-positive rods
  • found in improperly preserved or canned foods and contaminated wounds
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44
Q

Botulism Classification (mode of acquisition)

A
  • food-bourne (ingested) i.e. honey
  • wound
  • unclassified
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45
Q

Botulism Mechanism

A
  • toxin enters PREsynaptic terminals
  • blocks fusion of ACh vesicles with presynaptic membrane (myoneural junction)
  • inhibit ACh release into neuromuscular junction
  • nerve impulse fails to transmit across the neuromuscular junction
  • muscle paralysis
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46
Q

Incidence of Botulism

A
  • 10 adults and 100 infants (under 9wks) in US per years
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47
Q

Signs and Symptoms of Botulism

A
  • develop within 12-36 hrs following ingestion of contaminated food (acts quickly since enters the blood upon digestion)
  • Gradual recovery over weeks – months (typically get full recovery in both adult & infant)
  • Flaccid symmetrical paralysis
  • Blurred & double vision, photophobia, ptosis (dropping of eyelids)
  • Dry mouth, nausea, & vomiting
  • Lethargy
  • Difficulty in swallowing (dysphagia) & speech (dysarthria)
  • Can progress to involve respiratory
  • muscles: respiratory failure can occur in 6-8 hours
  • No sensory involvement
  • Autonomic involvement
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48
Q

Botulism deaths

A
  • more in A&E and none in type B

- respiratory failure is main problem

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49
Q

Prevention Botulism

A
  • boiling food X 10 minutes will destroy toxin
  • avoid honey for children under one year of age
  • appropriate wound care and sterile technique
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50
Q

Intervention of Botulism

A
  • 8-20% overall mortality rate (fatal within 24 hrs secondary to resp failure)
  • ABE serum antitoxin (antibodies of type A, B, E toxin)
  • debridement and antibiotics for wound
  • removal of toxin from GL gastric lavage (pumping stomach)
  • supportive measures, e.g. IV mechanical vent
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51
Q

Recovery of Botulism

A
  • sprouting of new terminal nerve filaments and formation of new synapses
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52
Q

Botox

A
  • botulinum toxin (BT)
  • BT type A is a prescription medicine, pharmacological management of spasticity
  • physician should have considerable experience in use, knowledge of its indications, effects and safety in clinical practice
  • Dysport and Botox type A toxins are both licensed medications for the treatment of focal spasticity.
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53
Q

Botox is used to treat Spasticity in indiviuduals with

A
  • SCI
  • MS
  • Dystonia
  • CVA
  • TBI
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54
Q

How does BT Work?

A
  • prevent release of acetylcholine from the PRESYNAPTIC nerve terminal, thus blocking peripheral cholinergic transmission at neuromuscular junction (NMJ)
  • Dose-dependent, reversible reduction in muscle power.
  • the clinical effects are temporary, the toxin degrades and becomes inactive within the nerve terminal
  • NMJ atrophies and then regenerates with re-sprouting.
  • muscle weakness resolves over three to four months.
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55
Q

Myasthenia Gravis Breakdown

A
  • my = muscle
  • asythenia = weakness
  • gravis = large
  • post-synaptic membrane disease at neuromuscular junction
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56
Q

Myasthenia Gravis Pathology

A
  • widened synaptic cleft
  • loss of folds (muscle endplate membrane)
  • reduction in number and density of ACh receptors
  • results in weakness or paresis
  • ACH neurotransmitter is less likely to find a receptor before it is hydrolyzed by ACHesterase
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57
Q

What is Myasthenia Gravis

A
  • acquired autoimmune disease
  • past or present viral infection
  • 70% - hyperplasia of the thymus
  • 10- 15% - tumors of the thymus
  • The thymus is a specialized organ of the immune system. Thymus influences the T-lymphocytes (T cells), which are critical cells of adaptive immune system.
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58
Q

Myasthenia Gravis Breakdown

A
  • my = muscle
  • asythenia = weakness
  • gravis = large
  • POST-SYNAPTIC membrane disease at neuromuscular junction
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59
Q

Myasthenia Gravis Pathology

A
  • widened synaptic cleft
  • loss of folds (muscle endplate membrane)
  • reduction in number and density of ACh receptors
  • results in weakness or paresis
  • ACH neurotransmitter is less likely to find a receptor before it is hydrolyzed by ACHesterase
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60
Q

What is Myasthenia Gravis

A
  • acquired autoimmune disease
  • past or present viral infection
  • 70% - hyperplasia of the thymus
  • 10- 15% - tumors of the thymus
  • The thymus is a specialized organ of the immune system. Thymus influences the T-lymphocytes (T cells), which are critical cells of adaptive immune system.
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61
Q

Myasthenia Gravis Prevalence

A
  • 1 in 10 – 20,000 (US)
  • onset: 15 – 30 years and 60 – 75 years of age
  • females > males (3:2)
  • disease of younger females (peak incidence age 30 YO) and older men (peak incidence age 60 YO) (Bimodal)
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62
Q

Myasthenia Gravis Pathology

A
  • widened synaptic cleft
  • loss of folds (muscle endplate membrane)
  • reduction in number and density of ACh receptors
  • results in weakness or paresis
  • ACH neurotransmitter is less likely to find a receptor before it is hydrolyzed by ACHesterase
  • ACh is released but less receptors and broken down quickly, no clefts to capture it
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63
Q

Myasthenia Gravis Disease Progression

A
  • slow, progressive weakness (maximal weakness occurs in first year in 2/3 of all cases)
  • after 15-20 years, weakness becomes fixed
  • remissions occur in about 25% of cases
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64
Q

Myasthenia Gravis Classifications

A
  • ocular myasthenia (~10-15%): symptoms confined to extra-ocular muscles; mostly see diplopia (double-vision) and ptosis (drooping eyelids)
  • generalized weakness (~85%): Myasthenic crisis: respiratory failure
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65
Q

Myasthenia Gravis S&S

A
  • ptosis (bilateral weakness of eyelid muscles) (CN III)
  • dipolpia (double vision)
  • facial weakness (CN VII)
  • oropharyngeal weakness
  • chewing, swallowing and speaking difficulties
  • may have weakness: BUE or BLE (proximal > distal), respiratory muscles
  • weakness fluctuates (over hours, days, weeks)
  • better in A. M., declines as the day progresses (or declines during exercise)
  • remissions and exacerbations
  • normal reflexes, sensory function and coordination
  • crisis – respiratory distress or swallowing crisis
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66
Q

MG Diagnosis

A
  • presence of circulating antibodies to ACH receptors have been identified in the blood of 90% of myasthenia gravis patients: antibodies cause Ach receptor changes and block Ach binding to receptors
  • increased incidence of diabetes, lupus, RA, thyrotoxicosis and cancer in the myasthenia gravis population
  • EMG: normal at rest, decremental response to repeated stimulation (mirrors fatigue with exercise)
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67
Q

Myasthenia Gravis S&S

A
  • ptosis (weakness of eyelid muscles…droopy) (CN III)
  • dipolpia (double vision)
  • facial weakness (CN VII)
  • oropharyngeal weakness
  • chewing, swallowing and speaking difficulties
  • may have weakness: BUE or BLE (proximal > distal)
  • RESPIRATORY MUSCLES
  • weakness fluctuates (over hours, days, weeks)
  • BETTER IN A. M., DECLINES AS DAY PROGRESSES (or declines during exercise)
  • remissions and exacerbations
  • normal reflexes, sensory function and coordination
  • crisis – respiratory distress or swallowing crisis
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68
Q

MG Diagnosis

A
  • presence of circulating antibodies to ACH receptors have been identified in the blood of 90% of myasthenia gravis patients: antibodies cause Ach receptor changes and block Ach binding to receptors
  • increased incidence of diabetes, lupus, RA, thyrotoxicosis and cancer in the myasthenia gravis population
  • EMG: normal at rest, DECREMENTAL response to repeated stimulation (mirrors fatigue with exercise)…stronger response and then fades out
  • Tensilon Test
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69
Q

MG Interventions

A
  • Anticholinesterase drugs
  • Immunosuppressive drugs
  • Intravenous immunoglobulin (IVIG)
  • Plasmaphoresis
  • Thymectomy
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70
Q

Anticholinesterase drugs for MG treatment

A
  • slows down the breakdown of ACh –> acetate + choline in cleft
  • ACh is around longer, thus has an increased chance of binding to the receptor
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71
Q

Immunosuppressive drugs for MG treatment

A
  • Prednisone
  • Cyclosporine
  • Myophenolate mofetil
  • Azathioprine
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72
Q

Plasmaphoresis for MG treatment

A
  • blood is routed to a machine that separates the plasma and cells
  • Plasma filtration: Two venous lines are used
  • plasma is filtered using standard hemodialysis equipment.
  • continuous process requires less than 100 ml of blood to be outside the body at one time.
  • temporarily (4-6 weeks) reducing anti-ACh receptors antibodies
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73
Q

Thymectomy for MG treatment

A
  • mainly carried out in an adults
  • role of the thymus: cause T-cell specific response
  • 70% of individuals with MG have hyperplasia of the thymus
  • 10- 15% - tumors of the thymus
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74
Q

PT MG Care

A
  • have patients swallow with chin tucked to avoid aspiration
  • don’t speak with food in mouth
  • monitor tidal volume, vital capacity, and inspiratory force during PT
  • plan PT for time periods when have the most energy
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75
Q

PT MG Precautions

A
  • PT focus is usually supportive, obtain equipment, maintain health & function, exercise as tolerated
  • avoid strenuous exercise
  • excessive exposure to heat or cold can exacerbate symptoms
  • allow for regular rest periods for muscle recovery
  • osteoporosis may be a secondary complication from prolonged steroid use
76
Q

Signs of Impending MG Crisis: (Call EMS!)

A
  • increased muscle weakness
  • respiratory distress
  • difficulty talking, chewing, or swallowing
77
Q

BT Administration

A
  • BT is injected intramuscularly into specifically selected muscles
  • although BT can diffuse through muscle fascia barriers, its effect is concentrated in the injected muscles so that it is possible to generate highly focal weakness
78
Q

Botox Dosage

A
  • currently available in vials of 50U and 100U and Dysport in vials of 500U
  • max recommended dose in limb spasticity is 1,000U Dysport or 360 Botox in a single adult injection session
  • larger doses carry increasing risk of systemic adverse effects
  • dose should also be reduced if the target muscles are already weak, or if there is an increased risk of side effects in an individual patient. pre-existing local tissue disruption or conditions causing systemic weakness such as in myopathy, myasthenia gravis, motor neuron disease, or neuropathy should provoke extreme caution but not absolute contraindictions
79
Q

Planning and siting of Botox injections

A
  • larger superficial muscles may be identified with knowledge of surface anatomy
  • EMG, nerve, or muscle stimulation or ultrasound imaging may be needed for smaller, less accessible mm and may require additional techniques to ensure correct placement of injection, especially in presence of adipose tissue, or where normal anatomy is contorted by deformity in target muscles
  • best sites for injection are theoretically the nerve end-plate zones deep in muscle bulk, but BT can diffuse to appropriate NMJ site
  • small and moderate-sized muscles will usually respond to BT injected simply into belly of muscle
  • some authorities recommend multiple scattered smaller injections to spread the toxin even in medium-sized muscles. the justification for multiple injections within a single muscle partly depends on the theoretical concept of BT saturation of a volume of muscle
80
Q

Duration of Effects of Botox

A
  • BT is taken up by the NMJ within 12 hours
  • clinical effect occurs gradually over 4-7 days, occasionally longer
  • BT interferes with neuromuscular synaptic transmission for about 12-16 weeks, and causes clinically detectable weakness for 3-4 months in most situations, sometimes rather longer
81
Q

Post Injection Management for Botox

A
  • PT is mandatory
  • assess the need for orthotics/splinting or review existing orthoses and assess patient compliance
  • provide patient education on stretching
  • take care not to over-stretch weakened mm (intensity of stretches could prevent intramuscular hematomas due to tearing)
  • increase muscle strength of the opposing muscle groups, facilitate activity in opposing mm groups
  • consider other treatments that may enhance the effects of BT such as constraint therapy or electrical stimulation as appropriate
82
Q

Side Effects of Botox

A
  • can be life threatening and extremely serious!!!
  • problems swallowing, speaking, or breathing due to weakened associated muscles, can be severe and result in loss of life
  • when given inapropriate dose may cause loss of strength and all-over muscle weakness, double vision, blurred vision, drooping eyelids, hoarseness or change or loss of voice (dysphonia), trouble saying words clearly (dysarthria), loss of bladder control, trouble breathing and swallowing
83
Q

Cerebellum Overview

A
  • contains more neurons than any other brain region
  • integration of vast amounts of information
  • performs complex movement computations
  • damage = poor coordination without overt muscle weakness
84
Q

How can the cerebellum be damaged?

A
  • blow to the back of the head (TBI)
  • stroke
  • tumor
  • degenerative disease
  • congenital malformation
85
Q

What do the cerebellar peduncles contain?

A
  • all the axons that transmit information to and from the cerebellum
  • inferior olive is caudal/inferior to the cerebellum
86
Q

The neuronal circuits of cerebellum

A
  • are constructed in a very uniform manner throughout the entire cerebellum
  • neuronal circuits are in the gyri (ridges)
  • 8 cell types: purkinje cell, granule cell, golgi cell, parallel fibers, stellate cell, basket cell, mossy fibers, climbing fibers
  • the two major afferent inputs into the cerebellum: mossy fibers and climbing fibers
87
Q

Anatomical Divisions of Cerebellum

A
  • anterior lobe: anterior to primary fissure
  • posterior lobe: posterior to anterior lobe
  • flocculonodular lobe: most inferior
88
Q

Tensilon test

A
  • repetitive movements or holding a position
  • compare performance following giving Tensilon (anticholinesterase) vs. Placebo (saline)
  • Tensilon inhibits acetylcholinesterase (hydrolyzes ACh so it stays in synapse longer)
  • if strength/endurance is improves, then has myosthnia gravis
  • muscle biopsies can be done: count ACh receptors at motor encounters
89
Q

Basal Ganglia

A
  • composed of caudate nucleus, putamen and globus pallidus with related structures of STN (sub-thalamic nucleus) and substantia nigra
  • caudate putamen and GP surrounds thalamus, sending its info to thalamus
90
Q

Basal ganglia simple system

A
  • basal ganglia to thalamus to cortex to either back to basal ganglia or to descending motor tracts (hyperkinetic)
  • always through the thalamus and then the cortex
  • basal ganglia is not on its own
91
Q

more complex basal ganglia system

A
  • VL of the thalamus
  • goes to the cortex
  • goes to the caudate and putamen = striatum
  • goes to the subthalamic nucleus
  • substantia nigra has 2 parts…SNc and SNr
  • globus pallidus has 2 parts…LGP or MGP
  • then from the subthal nucleus and all the parts goes to the
  • VL of the thalamus
92
Q

SNc

A
  • substantia nigra pars compacta

- the nucleus that degenerates overtime with parkinson’s disease

93
Q

SNr

A
  • substantia nigra pars reticulata
94
Q

LGP or EGP

A
  • lateral or external globus pallidus
95
Q

MGP or IGP

A
  • medial or internal globus pallidus
96
Q

Classes of Basal Ganglia movement disorders

A
  • Hyperkinetic movement disorders (facilitated cortex or over-excited)
  • Hypokinetic disorders (under-facilitated cortex or under-excited)
97
Q

Huntington’s Chorea

A
  • hyperkinetic disorder (thalamus is overdriving the cortex)
  • neurons from the striatum to the substantia nigra pars reticulata are damaged or not functioning as well and don’t inhibit thalamus as much, so thalamus OVERDRIVES cortex producing too much movement
  • involuntary small amplitude, rapid movements
  • results from degeneration of the striatal neurons to the SNr and LGP
  • The thalamus inhibition is much less
  • end result: cerebral cortex is on over-drive (facilitated much more)
  • symptoms: chorea, akinesia and bradykinesia, hypotonia, wide and staggering gait, cognitive problems
  • End results are that the cerebral cortex is on over-drive (facilitated)
98
Q

Tourette’s Syndrome

A
  • impulsions and compulsions to perform fragments of motor programs (examples: touching, vocalizations, jumping, skipping)
  • tics
  • results from discturbance in the limbic circuits of the basal ganglia
  • the limbic system inhibits the substantia nigra pars compacta so less excitation of direct pathways of BG system > end results is that the cortex is on overdrive
99
Q

Dystonia

A
  • A movement disorder characterized by sustained muscle contraction in an extreme end range of motion, frequently with a rotational component
  • General dystonias involve the entire body
  • Focal dystonias involve one joint or a few related joints
100
Q

General Dystonia

A
  • whole body semi-twists up on itself
  • genetic, involving DYT gene
  • individual will begin a movement then usually a torsional rotation of the trunk, then proceed into UEs and LEs
  • assume a fixed posture for several seconds or minutes, often cannot move
  • can be painful
101
Q

Focal Dystonia

A
  • usually localized, one or two joints
  • results from damage to GP and/or putamen resulting in release of the usual inhibition of the thalmaus by the direct and indirect pathways leading to excessive cortical facilitation
  • most common - spasmodic torticollis: involuntary contraction of the neck muscles resulting in head turning with rotation over a few minutes to hours
  • other focal dystonias: vocal cords, tongue and swallowing mm, facial mm, eyes, hands, toes, writers cramp
102
Q

Idiopathic Parkinson’s disease or MPTP (impurities in synthetic heroine)

A
  • Hypokinetic: inhibit BG output, inihibits thalamus more, gets less facilitation. substantia nigra pars compacta degenerates, giving less dopamine to striatum
  • Signs & symptoms: loss of ability to initiate movement (akinesia), bradykinesia, rigidity, resting tremor, impaired
    posture, gait and balance due to akinesia, bradykinesia, etc.
103
Q

Parkinson’s classic signs

A
  • 2 of 4 signs to be diagnosed
  • resting tremor: resting tremor rate 4-6 Hz often in hand or foot, clasically stops when individual starts to move body part. pill rolling. happens only when body part is resting
  • bradykinesia: slow movements, slow force production, loss of spontaneous movements
  • rigidity: cogwheel, lead-pipe (when rigidity becomes severe)
  • postural instability: hypometric anticipatory postural adjustments
104
Q

Cogwheel Rigidity vs. lead pipe

A
  • cogwheel: rigid in a body part/joint and they are rigid and then let go a little and then are rigid again quickly after
  • lead pipe: rigid in a body part…had to move the body part/joint. constant rigidity
105
Q

Parkinson’s Symptoms

A
  • difficulty with swallowing and chewing
  • speech impairments: speak too softly, monotone, hesitant, slurred, repeating words
  • masked face (flat affect)
  • fatigue
  • sleep problems
  • decreased strength in muscles of respiration
  • dementia or other cognitive problems
106
Q

Postural changes with parkinson’s

A
  • kyphotic posture with forward-flexed trunk
  • forward head
  • crouched/flexed legs
107
Q

Gait with Parkinson’s

A
  • difficulty INITIATING gait
  • freezing gait (more obvious when change in floor pattern): patient will report that it feels like feet are stuck on the ground/heavy and they cannot move
  • festinating gait: steps too small, causes COM to get in front of BOS (upper body going faster than lower body), can’t always catch themselves so typically fall forward, decreased foot clearance
  • decreased or no trunk rotation
  • decreased or no arm swing
108
Q

Micrographia

A
  • in parkinson’s disease

- handwriting is slow and looks cramped or small

109
Q

Parkinson’s Disease Progression

A
  • PD is not by itself a fatal disease, but it does get worse over time
  • in later stages of disease, PD-related complications can lead to death, such as choking, pneumonia, and falls
  • progression of symptoms may take 20 years or more (in sone, PD progresses more quickly)
110
Q

Stage one of Parkinson’s

A
  • unilateral, one side of body
  • symptoms mild, inconvenient but not disabling
  • usually presents with tremor of one limb
  • friends noticing change in posture, gait, facial expression
111
Q

Stage two of Parkinson’s

A
  • bilateral, both sides of body
  • minimal disability
  • posture and gait affected
112
Q

Stage three of Parkinson’s

A
  • Significant slowing of movement
  • Early impairment of equilibrium on gait or standing
  • Generalized dysfunction that is moderately severe
  • By the time people reach Stage 3, quality of life is usually significantly affected
113
Q

Stage four of Parkinson’s

A
  • Severe symptoms
  • Can still walk to a limited extent
  • Rigidity and bradykinesia
  • No longer able to live alone
  • Tremor may be less than earlier stages
114
Q

Stage Five of Parkinson’s

A
  • Cachectic stage: loss of weight and muscle wasting secondary to serious disease or disorder:
  • Invalidism complete
  • Cannot stand or walk
  • Requires constant nursing care
115
Q

Parkinson’s Disease Diagnosis

A
  • Medical history & neurological exam
  • Difficult to diagnose accurately
  • Early signs and symptoms may be dismissed as the effects of normal aging
  • Clinical signs and symptoms
  • Must have two or more classical signs (*slide 3)
  • Positive response to dopamine-like medications
  • CT or MRI in PD usually appear normal, but may be needed to rule out other diseases
116
Q

Parkinson’s Neurologic Basis

A
  • Normal: a balance between DA & Ach in BG

- Abnormal (PD): ↓ DA results in ↑ AC

117
Q

PD Mediciations

A
  • Dopamine: DOES NOT CROSS THE BLOOD-BRAIN BARRIER

- Levodopa (L-dopa): A dopamine precursor that crosses the blood-brain barrier and then converts to dopamine

118
Q

Dopamine Replacement:Rationale for Levodopa therapy for Parkinson’s

A
  • Attempt to increase dopamine in BG
  • Direct administration of DA is ineffective because of BBB
  • Must provide precursor to dopamine
  • Levodopa (L-DOPA)
119
Q

Levodopa (L-dopa) for PD

A
  • Side effects increase with continued usage, including: Nausea, Hypertension, Dyskinesias
  • “Tolerance” develops with continued usage
  • Period of effectiveness after each dose begins to shorten
  • Larger doses may be needed to be effective
  • “On-Off” effects of medication
  • “delicately balanced”
120
Q

Levodopa with Carbidopa (Sinemet)

A
  • Action: converts to dopamine after crossing blood brain barrier –> resolution of dopamine deficiency
  • Therapeutic Effect: decreases symptoms of Parkinson’s less muscle rigidity, less bradykinesia
121
Q

Dopamine and Levodopa and Carbidopa with Parkinsons

A
  • Dopamine does not cross the blood brain barrier
  • Levodopa is converted to dopamine in the periphery so only 1% of the drug actually reaches the brain
  • Carbidopa: inhibits Dopa decarboxylase, prevents premature conversion in the bloodstream
  • Carbidopa and levodopa often given in same pill (Sinemet): addition of carbidopa decreases the amount of levodopa needed to achieve a therapeutic effect
  • Often 4:1 ratio of carbidopa to levodopa (sometimes 10:1 ratio)
  • Carbidopa does not cross the BBB which is good since do not want levadopa to not convert to dopamine once it is in the brain
122
Q

Side Effects of Levodopa with Carbidopa (Sinemet)

A
  • GI irritation: severe nausea and vomiting with initial administration
  • Postural hypotension/orthostatic hypotension
  • Cardiac arrhythmias
  • Large incidence of dyskinesias (chorea-athetoid movements)
  • Psychosis, depression, anxiety
123
Q

Medication Treatment issues with Parkinson’s

A
  • On-Off phenomenon: Fluctuations in response to levodopa
    peak: too much movement; end of dose akinesia
  • Diminished response to levodopa over time
  • Tolerance: Benefits may be lost after 4-5 years of L-DOPA therapy
  • Wait to use in later stages? Save it until you need it
  • Other view: Substantia nigra deteriorates and not enough cells left to manufacture dopamine so OK to use in earlier stages
  • Drug “holidays”
124
Q

Dopamine Agonists (may be combined with L-DOPA for optimal effects) for Parkinson’s

A
  • Pramipexole (Mirapex)
  • Ropinirole (Requip); Rotigotine (Neupro patch)
  • Action: Cross BBB; directly stimulate dopamine receptors (similar function to dopamine). Neuro-protective effects
  • Therapeutic Effect: Treatment of Parkinson’s disease
  • Side Effects: Less adverse effects –> dyskinesias and motor response issues are rare, nausea, vomiting, postural hypotension
125
Q

Magic number of dopamine producers that show Parkinson’s

A
  • 80% of dopamine production is dysfunctional or atrophied before start seeing signs and symptoms
  • coincides with functioning neurons in the bodies that produce dopamine (?)
126
Q

Parkinson’s Disease Ablation (stereotaxic surgery)

A
  • Selectively destroying specific cells that contribute to the symptoms
  • Pallidotomy (reduce tremor, rigidity, and bradykinesia)
  • Thalamotomy (reduce tremor)
127
Q

Parkinson’s Disease Deep brain stimulation (DBS)

A
  • Electrodes implanted in thalamus, subthalamic nucleus, and globus pallidus
  • Electrodes connected to a pulse generator
  • The pulse generator and electrodes painlessly stimulate the brain
  • Blocks electrical signals from targeted areas
  • Reduces the need for medications
128
Q

External Sensory cues with Parkinson’s

A
  • A deficit to execute movements can be overcome in the presence of external sensory cues (e.g. visual, auditory, proprioception)
  • Rationale: Distinct contribution of the cortico-striatal (implicit) and cortico-cerebellar (explicit) systems to motor learning and control
129
Q

Intervention for Freezing Gait in Parkinson’s

A
  • Visual cue on floor within one step length will stimulate a step
  • Can add hand triggered laser light to a walker
  • LaserCane projects a bright red line across your path
130
Q

Music Therapy and Parkinson’s

A
  • Embed auditory pulse or beat within music
  • Ed Roth, Professor, Music Therapy, Western Michigan University
  • beats help create movement with patients and helps keep them walking on the beat
131
Q

Functions of the vestibulocerebellum

A
  • coordination of eye-head movements
  • equilibrium and balance
  • movements of the axial body (head/neck and trunk), pelvis/hips and scapula/shoulders for posture, equilibrium and balance
  • equilibrium particularly during rapid changes in body position or in the direction of movement
132
Q

Spinocerebellum divisions

A
  • vermis

- intermediate zone

133
Q

Spinocerebellum Vermis inputs

A
  • dorsal spinocerebellar, cuneocerebellar, and trigeminocerebellar tracts from the trunk and head (somatosensory info head/trunk)
  • vestibular nuclei (linear and angular head/body position info)
  • tectospinocerebellar tract (visual and auditory info)
134
Q

Spinocerebellum Vermis Output

A
  • ventromedial descending system (spinal tracts) Group A
  • fastigial nucleus > reticular nuclei > reticulospinal tracts (CMRST)
  • vestibular nuclei > lateral and medial vestibulospinal tracts
  • thalamus > cortex (MI or Broadman area 4 ) > anterior CST
135
Q

Spinocerebellum Vermis Functions

A
  • Gross motor movements
  • coordination of axial and girdle (scapula/shoulder and pelvis/hip) musculature
  • regulates rhythmic walking movements (regulate CPGs of gait)
  • adjusts the timing of locomotor movements
  • modulation of interlimb coordination durding locomotion
136
Q

Spinocerebellum Intermediate Zone Inputs

A
  • dorsal spinocerebellar and cuneocerebellar from the extremities (somatosensory info extremities)
137
Q

Spinocerebellum Intermediate Zone Outputs

A
  • dorsolateral descending system (spinal tracts) Group B
  • interposed nuclei > red nucleus > rubrospinal tract
  • thalamus > cortex (MI or Broadman area 4 and SMA) > lateral CST
  • reticular nuclei > reticulospinal tracts (CPRST)
138
Q

Spinocerebellum Intermediate Zone Functions

A
  • Fine Motor Movements
  • coordination of distal musculature of the extremities (hands and feet)
  • rubrospinal tract only innervates UPPER extremities
139
Q

Neocerebellum (lateral zones) pontocerebellum or cerebrocerebellum Inputs

A
  • cerebral cortex (motor, sensory, PMA…ipsilateral frontal and parietal lobes > pontine nuclei > neocerebellum
140
Q

Neocerebellum Outputs

A
  • dentate nucleus > ventral lateral nucleus of the thalamus > premotor (PMA) and motor (MI) area of the cerebral cortex
141
Q

Neocerebellum Functions - THERES A LOT!!

A
  • planning and timing of voluntary movements (ipsilateral movements) particularly learned, skillful movements that become more rapid/precise and automatic with practice
  • motor planning of sequential motor movements or the ability to progress smoothly from one successive movement to next
  • onset, duration, amplitude and rate/slope of muscle contraction or the timing, duration, amplitude and rate of rise of agonist and antagonist muscle bursts (rate, range, force, and direction of movement)
142
Q

Comparator function of both the spinocerebellum and neocerebellum

A
  • compares the actual outcomes of a motor program with the intended motor program
  • receives continuous info about the desired program from the MI, PMA, and SMA cerebral cortex
  • receives continuous information from the peripheral muscle spindles, GTOs, proprioceptors and tactile receptors in muscle, joint, and skin about instantaneous status of the body and its parts about position, rate of movement, forces acting on the body, etc
  • compares actual with intended
  • instantaneously corrects or attempts to correct the movement if the velocity of movement allows this correction (100-200 ms needed to make corrections)
143
Q

Muscle tone function of both the vestibulocerebellum and spinocerebellum

A
  • vestibulocerebellum and spinocerebellum have general excitatory influence on the gamma motor neurons
  • damage results in decreased excitation of gamma MNs > reduced sensitivity of the muscle spindles > decreased muscle tone
  • hypotonicity
  • this is usually with acute cerebellar damage; hypotonia decreases over time
144
Q

Medications for Dystonia

A
  • botox (effective 3-4 months for focal)
  • common medications for general: baclofen, artane, sinemet, klonopin
  • surgeries: deep brain stimulation (DBS) of globus pallidus
  • rhizotomy: resection of anterior (motor) cervical spinal nerve roots
145
Q

Hyperkinetic disorders due to basal ganglia system pathology

A
  • huntington’s chorea
  • tourette’s syndrome
  • dystonia (general and focal)
146
Q

Hypokinetic disorders due to basal ganglia system pathology

A
  • parkinson’s disease
147
Q

Normal physiological tremor

A
  • 8-12 cycles/Hz per second
148
Q

cerebellar intention tremor

A
  • when you have a lower-amplitude tremor
  • about 3-5Hz
  • starts out low amplitude and then gets worse as gets towards the target
149
Q

Antiparkinsonian Agents Treatment Issues

A
  • Treatment Issues
  • On-Off phenomenon: Fluctuations in response to levodopa
  • peak: too much movement; end of dose akinesia
    Diminished response to levodopa over time
  • Tolerance: Benefits may be lost after 4-5 years of L-DOPA therapy
  • Wait to use in later stages? Save it until you need it
  • Other view: Substantia nigra deteriorates and not enough cells left to manufacture dopamine so OK to use in earlier stages
  • Drug “holidays”
150
Q

Huntington’s Chorea prominence

A
  • 6.5 per 100,000 people (varies by location-see next slide)
  • Autosomal dominant genetic disease = short arm of chromosome 4
  • FYI: More repeats in the cytosine-adenine-guanine (CAG) DNA sequence
  • Onset is usually after 30 years old
  • Death: about 15-20 years after onset
151
Q

Huntington’s Chorea symptoms

A
  • Chorea: involuntary small amplitude, rapid movements (ataxic, dance-like movements)
  • Akinesia and bradykinesia
  • Hypotonia
  • Wide, staggering gait
  • Speech lacks normal timing and rhythm
  • Difficulty swallowing
  • Vision: poor control of saccadic eye movements
  • Cognitive problems
  • Dementia
  • Poor judgment
  • Loss of long term memory
  • Depression
  • IQ decreases
  • Irritability
152
Q

Unified Huntington’s D Rating scale (UHDRS) 6 Components

A
  1. Motor Assessment
  2. Cognitive Assessment
  3. Behavioral Assessment
  4. Independence Scale
  5. Functional Assessment
  6. Total Functional Capacity (TFC)
153
Q

Early Stage of HD

A
  • Symptoms become noticeable enough to warrant a diagnosis.
  • Can generally continue to work, drive, and live independently.
  • Motor symptoms: Usually begin in the extremities of the body, Involuntary twitches in their fingers, toes, and face. Subtle loss of coordination
  • Cognitive Symptoms: More difficult for people to think through complicated tasks, May be harder to work and perform at their usual level
  • Behavioral Symptoms: Depression, irritability and disinhibition (saying whatever is on your mind, appropriate or not)
154
Q

Middle Stage of HD

A
  • Often lose their ability to work and drive and might be unable to perform household chores
  • motor symptoms: eating can become challenging, pts have trouble performing series of mvmts to swallow leading to weight loss, speech slurrs, walking staggered, falls likely, invol dance-like movements (chorea)
  • cognitive symptoms: have trouble organizing information and thinking clearly, can’t solve problems they were normally capable of working through
  • behavioral symptoms: continued worsening of behavioral signs seen earlier, becoming apathetic, losing interest in activities they used to enjoy
155
Q

Late Stage of HD

A
  • Totally dependent for all care, confined to bed, often SNF
  • unable to speak
  • choking is a major concern, tube feeding
  • motor symptoms: severe rigidity, dystonia, bradykinesia, chorea usually stopped although minority of pts continue severe chorea, cannot initiate movement
  • cognitive symptoms: debilitating, though pts can usually still understand speech and recognize loved ones
  • behavioral symptoms: depression, tends to fade in late stages, possibly since pt has come to terms with illness or apathetic, psychosis is rare problem that causes ppl to have visual and auditory hallucinations occur in 3-11% of pts in late stages
156
Q

Medications for HD

A
  • Cholinergic or GABA-containing agonists
  • Perphenazine
  • Haloperidol (Haldol)
  • Reserpine
  • Riluzole
157
Q

Dystonia Etiology

A
  • unknown, idiopathic in most cases
  • defected DYT1 gene in early onset dystonia
  • secondary to some other neurologic disorders such as PD, stroke, TBI, CP, etc
158
Q

Dystonia Pathogensis

A
  • lesions at caudate, putamen, globus pallidus
  • overactive direct pathway within the basal ganglia circuitry increases motor activity
  • hyperkinetic disorder
159
Q

Characteristics of Dystonia Movements

A
  • definition: abnormal muscle tone with simultaneous contraction of agonist and antagonist
  • invol muscle co-contraction force affected parts of the body into contorted or twisted postures
  • rapid or slow, rhythmic or un-patterned
  • duration varies: a few seconds of minutes, hours or longer
  • may be increased with stress, during purposeful movements, task-specific (Sx only present during specific tasks, i.e. writing, playing instruments)
  • decreases upon relaxation and disappear during sleep
  • often painful condition
160
Q

Focal Dystonia

A
  • affect one body part
  • pharyngeal (neck and vocal cords)
  • cervical (NOT TORTICOLLIS)
  • Writer’s cramp
  • Musician’s cramp
161
Q

Pharyngeal Focal Dystonia

A
  • spasmatic dysphonia
  • distorted speech, affects vocal cords
  • treated with botox injections
162
Q

Cervical Focal Dystonia

A
  • most common
  • hypertrophy of SCM muscle
  • lateral flexion toward, rotation away
  • typically painful
  • NOT torticollis (musculoseletal disorder with mm fibrosis)
163
Q

Writer’s cramp focal dystonia

A
  • task-specific focal dystonia

- spasm affecting certain muscles of the hand and/or fingers

164
Q

Muscician’s Cramp focal Dystonia

A
  • task specific
165
Q

Dystonia Disease Onset

A
  • onset: generalized ~8y.o, focal 30-50 y.o
166
Q

Dystonia Disease Progression

A
  • dystonia is NOT FATAL
  • it IS CHRONIC and often painful and debilitating
  • generalized begins in legs and progresses to rest of body
  • focal progresses for about 5years then plateaus.
  • spontaneous recovery in 30%
167
Q

Cerebellar dysfunctions

A
  • abnormal movements are ipsilateral to the lesion
  • have hypotonicity, asthenia, intention tremors, disturbances of posture and balance, dysmetria, dysdiadochokinesea, ataxic gait, movement decomposition, poor coordination in speech, eye movements, Time-asymmetric velocity profiles, delays in force production and errors in force maintenance
168
Q

Hypotonicity in Cerebellar Dysfunctions

A
  • ipsilateral to lesion
  • reduced firmness to palpation
  • reduced tone during PROM
  • reduced DTRs secondary to momentum
  • reduced extensor tone: trouble remaining upright against gravity,
169
Q

Asthenia in Cerebellar Dysfunctions

A
  • generalized weakness or decreased activity and easily fatigued
170
Q

Intention tremors in Cerebellar Dysfunctions

A
  • 3-5 Hz

- tremor amplitude increases as effector approaches the target

171
Q

Disturbances of posture and balance in Cerebellar Dysfunctions

A
  • flexed posture, wide base of support
  • poor equilibrium and balance especially movements of the axial body (head/neck and trunk), pelvis/hips and scapula/shoulders
  • poor balance and equilibrium particularly during rapid changes in body position or in the direction of movement
172
Q

Dysmetria in Cerebellar Dysfunctions

A
  • over-or-under shooting the range of motion
  • impaired ability to properly scale movement distance
  • think in a 3-D way (over-under shoot, off to R or L, off up or down, triphasic AG, ANTAG, and AG2 mm/EMGs are not programmed correctly)
173
Q

Dysdiadochokinesea in Cerebellar Dysfunctions

A
  • deficit in coordination between agonist-antagonist muscles during rapid alternating movements
  • resulting in errors in range/amplitude and rate/timing
  • poor timing between cessation of agonist muscle activity and initiation of antagonist muscle activity
174
Q

Ataxic Gait in Cerebellar Dysfunctions

A
  • disruption in rhythm of gait, wide based gait, unsteady

- fall backwards, and towards side of lesion

175
Q

Movement decomposition in Cerebellar Dysfunctions

A
  • disrupted sequences in a multi-step task

- breaking a multi-joint movement down into a series of separate movements

176
Q

Poor coordination of muscles associated with speech in Cerebellar Dysfunctions

A
  • dysarthria (slurred speech)

- explosive speech, staccato speech

177
Q

Eye Movements in Cerebellar Dysfunctions

A
  • gaze-evoked nystagmus
  • ocular dysmetria when performing saccades
  • disrupted smooth pursuit
  • poor coordination of eye-head movements
178
Q

Time-asymmetric velocity profiles in cerebellar dysfunctions

A
  • spend more time accelerating or decelerating
179
Q

Delays in force production and errors in force maintenance in cerebellar dysfunctions

A
  • the cerebellum appears to play role in maintaining constant force
  • have trouble generating enough force (i.e. cannot pick something up)
  • and if can pick it up, can’t continuously produce force (i.e. holding box but pretty quickly starts to lower because arms are losing strength force)
180
Q

Neuropathologies of the Cerebellum

A
  • Friedreich’s ataxia
  • Vascular Disorders (stroke)
  • Tumors
181
Q

Cerebellar stroke

A
  • less than 5% of all strokes involve cerebellar arteries
  • posterior inferior cerebellar artery, anterior inferior cerebellar artery, superior cerebellar artery
  • best predictor of recovery: post-CVA
  • if deep nuclei are involved (b/c a lot of output goes to deep nuclei) have a worse prognosis
182
Q

Tumors in the Cerebellum

A
  • more common in children than adults
  • worse prognosis for adults
  • children have a good prognosis for recovery since most tumors are benign and can be removed surgically
  • tumors in adults tend to be more aggressive canvers and have poorer prognosis
183
Q

Friedreich’s Ataxia

A
  • hereditary (autosomal recessive)
  • lesion: cerebellum, dorsal root ganglia (sensory inputs), dorsal columns (conscious proprioception, vibration, fine touch), spinocerebellar tracts (unconscious proprioception), Time-asymmetric velocity profiles
184
Q

Friedreich’s Ataxia onset

A
  • Between 5 - 15 y. o. (some later)

- 25% of offspring have FA

185
Q

Friedreich’s Ataxia course

A
  • Generally lose ability to walk and confined to WC within 10-20 years after onset
186
Q

Friedreich’s Ataxia Prognosis

A
  • Some survive into their 60’s & 70’s IF NO HEART ATTACK

- seems to be higher percentage of heart problems in this population

187
Q

Friedreich’s Ataxia signs and symptoms

A
  • Ataxia
  • Most common Sx
  • Gait ataxia is usually the first symptom
  • Ataxia gradually worsens and spreads to the arms and the trunk
  • Clumsiness and intention tremor
  • Muscle weakness and wasting
  • Loss of sensation in extremities
    • Babinski (esp. if corticospinal tract involved)
  • Decreased DTRs
  • Tone is normal at rest
  • May get flexor spasticty
  • nystagmus (20% cases)
  • impaired smooth pursuit
  • heart disease: various forms (e.g. cardiomyopathy, dysrhythmia) ….60% of population
  • Easily fatigued
  • Scoliosis
  • Dysarthria/tongue and oral motor issues

Neuro D&D (3 decks)

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