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Neuro D&D > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

what are the 2 distinct classes of cells?

A
  • Neurons (nerve cells)

* Glia (supporting cells)

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2
Q

What are the parts of the neuron?

A
  • Dendrites
  • Cell body
  • Axon hillock
  • Axons
  • Presynaptic terminal
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3
Q

What is the axon hillock?

A

Where the axon meets the cell body before it synapses

*The closer they are to this then the more likely they are to get the neuron to fire

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4
Q

What is the Node of Ranvier?

A

*The gap between the myelin sheath and its important bc Na+ will go in and K+ will go out and cause depolarization. It’s quicker bc of saltatory conduction. With an unmyelinated neuron you have to do the Na+/K+ exchange all the way down the neuron instead of just in the places you’d like.

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5
Q

What types of neurons are there?

A
  • Bipolar (interneuron)
  • Unipolar (sensory)
  • Multipolar (motorneuron)
  • Pyrimidal cell
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6
Q

What are the glial cells?

A
  • Schwan cells (PNS)
  • Oligodendrocytes (CNS)
  • Astrocytes (CNS)
  • Microglia (CNS)
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7
Q

What is the function of a purkinje cell?

A
  • Takes sensory info from all over the body (through dendritic arborization) to help the body with coordination. It does sensory integration
  • There are many dendrites to one axon
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8
Q

What are the 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
    - Insulates one neuron from another
  • Supplies nutrients and oxygen to neurons
  • Destroys pathogens and removes dead neurons
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9
Q

What are the characteristics of a Schwann cell?

A
  • Usually only myelinates one neuron
  • Myelin spirals around axon to form the myelin sheath
  • at Nodes of Ranvier
  • NCV= 100 m/s for myelinated neuron, and 1 m/s for unmyelinated
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10
Q

What are the characteristics of oligodendrocytes?

A
  • One cell myelinates many CNS neurons
  • Insulates and protects nerves
  • Increase NCV
  • Involved in pathologies such as alzheimers disease and multiple sclerosis
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11
Q

What are the characteristics of Astrocytes?

A
  • Supporting cells in the CNS
  • Most common glia
  • Fill most of brain space not occupied by neurons
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12
Q

What are the functions of astrocytes?

A
  • Provide structural support and insulating neurons from each other
  • Maintenance of the blood brain barrier
  • During inflammation and injury, they divide and wall off damaged areas
  • Acts as scavengers by removing neurotransmitters from synaptic cleft
  • Clean up other debris during both early development and during recovery after injury
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13
Q

What do Microglia do?

A

*They contain branched cytoplasmic processes and play an important phagocytic role?

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14
Q

What are the protective roles of Microglia?

A
  • Activated and mobilized after injury, infection or disease
  • Important during brain development
  • Function as phagocytes (Ingest and destroy bacteria, cells and other materials)
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15
Q

What are the destructive roles of microglia?

A
  • In diseases such as Alzheimer’s and aging
    • release of toxic compounds into the neural environment
  • HIV/AIDS can activate microglia and stimulate a cascade of cellular breakdown
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16
Q

What is Multiple Sclerosis (MS)?

A
  • 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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17
Q

What are the signs of LMN injury?

A
  • Atrophy
  • Weakness or paralysis
  • Hypotonic DTRs
  • Decreased muscle tone
  • Fasiculations
  • In a peripheral nerve distribution
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18
Q

What are the signs of UMN injury?

A
  • Spasticity
  • Hypertonic or hypotonic DTRs
  • Clonus
    • Babinski or Hoffman’s reflexes
  • Weakness
  • Synergistic movement patterns
  • Effects one or both sides of body
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19
Q

What is a fasciculation?

A
  • Rapid, fine, painless or painful contraction of groups of muscle fibers
    • Visible but not strong enough to move limbs
    • Commonly seen in anterior horn cell disorders (ex. ALS)
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20
Q

If a stroke occurs in the pre-central gyrus what would the symptoms be?

A

*you would have motor loss

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21
Q

If a stroke occured in the post-central gyrus what would the symptoms be?

A
  • Glove/sock like sensory loss

* Sensory loss in general

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22
Q

If you have an UMN injury in the brain what can be the signs and symptoms?

A
  • Motor/sensory loss of body part
  • Glove/sock like sensory loss
  • Hypo/hypertonic reflexes
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23
Q

If you have an UMN injury in the spinal cord what can be the signs?

A
  • Motor loss: mytotome or loss below level of injury
  • Sensory loss: dermatome or loss below level of injury
  • Hypo/hypertonic reflexes
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24
Q

If you have a LMN injury at the nerve root what can be the signs?

A
  • Motor loss: myotome
  • Sensory loss: dermatome
  • Reflexes: Hypotonic
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25
Q

If you have a LMN injury at the peripheral nerve what can be the signs?

A
  • Motor Loss: Nerve distribution
  • Sensory loss: nerve distribution
  • Reflexes hypotonic
  • Peripheral nerve compression somewhere after the plexi (after the nerves have been formed)
  • Perform sensory and motor exam to determine which nerve has a compression site and where
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26
Q

If you have an injury to the radial nerve what would be the signs?

A
  • Motor loss: elbow extension, wrist and finger extension, supination
  • Sensory loss
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27
Q

If you have an injury to the median nerve what would be the signs?

A

Motor loss: Pronation, wrist flexion, long finger flexors

Sensory loss

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28
Q

If you have an injury to the ulnar nerve what would be the signs?

A

Motor loss: little finger abduction, interossei

Sensory loss

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29
Q

If you have an injury to the deep peroneal nerve what would be the signs?

A

Motor loss: dorsiflexion, toe extension

Sensory loss

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30
Q

If you have an injury to the superficial peroneal nerve what would be the signs?

A

Motor loss: Eversion

Sensory loss

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31
Q

If you have an injury to the tibial nerve what would be the signs?

A

Motor loss: Ankle plantarflexion, inversion, toe flexion

Sensory loss

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32
Q

What are two neuromuscular junction diseases?

A
  • Botulism

* Myasthenia Gravis

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33
Q

What is the etiology of botulism?

A
  • Neurotoxin produced by Clostridium Botulinum
  • Anaerobic, gram-positive rods
  • Found in improperly preserved or canned foods and contaminated wounds
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34
Q

What is the classification (mode of acquisition) of botulism?

A
  • Food borne (ingested ex. Honey)
  • Wound
  • Unclassified
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35
Q

What is the mechanism of botulism?

A
  1. Botulinum toxin enters presynaptic terminals
  2. Blocks the fusion of ACh vesicles with presynaptic membrane (myoneural junction)
  3. Inhibits ACh release into neuromuscular junction
  4. Nerve impulse fails to transmit across the neuromuscular junction
  5. Muscle paralysis
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36
Q

What is the Incidence of Botulism?

A
  • 10 adult and 100 infant cases in US each year (infant is 3 wk to 9 mo)
  • Signs and symptoms- develop within 12-36 hours following ingestion
  • Mortality rate- respiratory failure can occur in 6-8 hours so immediate treatment is crucial
  • Gradual recovery over weeks/months- typically full recovery occurs
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37
Q

What are the Signs and symptoms of botulism?

A
  • *Develop within 12-36 hours of ingestion
  • Flaccid symmetrical paralysis of face
  • Blurred and double vision, photophobia, ptosis (drooping of eyelids)
  • Dry mouth, nausea, vomiting
  • Lethargy
  • Difficulty swallowing (dysphagia) and speech (dysarthria)
  • can progress to respiratory failure in 6-8 hrs
  • -No sensory involvement
  • -Autonomic involvement
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38
Q

How do you prevent botulism?

A
  • Boil food x 10 min will destroy the toxin
  • Avoid honey for children under one year of age
  • Appropriate wound care and sterile technique
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39
Q

What is the intervention for botulism?

A
  • 8-20% overall mortality rate (fatal within 24 hours secondary to respiratory failure)
  • ABE serum antitoxin
  • Debridement and antibiotics for wound
  • Removal of toxin from GI/pumping of stomach
  • Supportive measures (ex. IV, mechanical Vent)
  • Recovery: sprouting of new terminal nerve filaments and formation of new synapses
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40
Q

What is BoTox used for and who should prescribe it?

A
  • It’s used for the management of spasticity after botulism or other injuries
  • Physician should have experience in use, knowledge of indications, effects and safety in clinical practice
  • Dysport and Botox type A toxins are both license medications for the treatment of focal spasticity
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41
Q

BoTox is used to treat spasticity in individuals with what injuries?

A

*Spinal cord injury
*Multiple sclerosis
*Dystonia
*Cerebral vascular accident
Traumatic Brain Injury

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42
Q

How does BoTox work?

A
  • Prevents the relese of ACh from the presynaptic nerve terminal, thus blocking peripheral cholinergic transmission at the 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
  • The NMJ atrophies and then regenerates with re-sprouting
  • The muscle weakness resolves over 3-4 months
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43
Q

How is BoTox administered?

A

*Injected intramuscularly into specifically selected muscles so it can generate highly focal weakness

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44
Q

What should be considered when determining dosage of BoTox?

A
  • Larger doses carry increasing risk of systemic adverse effects
  • Dose should be reduced if target muscles are already weak or if there is an increased risk of side effects
  • Pre-existing local tissue distruption, or conditions causing systemic weakness such as in myopathy, myasthenia gravis, motor neuron disease, or neuropathy should provoke extreme caution
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45
Q

When administering BoTox how do you plan the site of injections?

A
  • Larger superficial muscles may be identified with knowledge of surface anatomy
  • EMG, nerve or muscle stimulation or ultrasound my be needed for smaller muscles
  • BEST site are the nerve end-plate zones deep in the muscle bulk
  • Small and moderate sized muscles will respond to injection into muscle belly
  • Some authorities recommend multiple scattered smaller injections
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46
Q

What are the duration of effects with BoTox?

A
  • Botox is taken up by the NMJ within 12 hours
  • Clinical effect occurs gradually over 4-7 days, occasionally longer
  • Botox interferes with neuromuscular synaptic transmission for about 12-16 wks and causes clinically detectable weakness for 3-4 months, sometimes longer
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47
Q

What is the post-injection management for Botox?

A
  • PT is Mandatory!
  • Assess need for orthotics/splinting or review existing orthoses and assess pt compliance
  • Provide pt education on stretching
  • Take care not to over-stretch weakened muscles
    - intensity should be graded over time to prevent intramuscular hematomas due to tearing of stiffened muscle fibers
  • Increase muscle strength of the opposing muscle groups; faciliate activity in opposing muscle groups
  • consider other treatments that might enhance effects of botox like constraint therapy or Estim
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48
Q

What are the side effects of botox?

A
  • Problems swallowing, speaking, or breathing due to weakening of associated muscles, can be severe and result in loss of life
  • When given an inappropriate dose the effect of botox may affect areas away from the injection site and cause loss of strength and overall muscle weakness, double vision, blurred vision and ptosis, hoarseness or change/loss of voice (dysphonia), trouble speaking (dysarthria), loss of bladder control, trouble breathing, trouble swallowing
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49
Q

What is Myasthenia Gravis?

A
  • Post-synaptic membrane disease at neuromuscular junction
  • Acquired autoimmune disease
  • 70% hyperplasia (overgrowth) of the thymus
  • 10-15% tumors of the thymus
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50
Q

What is the mechanism of Myasthenia Gravis?

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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51
Q

What is the prevalence of Myasthenia Gravis?

A
  • 1 in 10-20,000
  • Onset: 15-30 (women) years and 60-75 (men)
  • Disease of younger females and older males (bimodal)
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52
Q

What is the disease progression of myasthenia gravis?

A
  • Slow, progressive weakness (max 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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53
Q

What are the classifications of MG?

A
  • Ocular Myasthenia (10-15%)
    - Symptoms confined to extra-ocular muscles, mostly see diplopia and ptosis
  • Generalized weakness (85%)
  • Myasthenic crisis: respiratory failure
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54
Q

What are the signs and symptoms of MG?

A
  • Ptosis (CN 3)
  • Diplopia
  • Facial weakness (CN 7)
  • Oropharyngeal weakness
  • Chewing, swallowing and speaking difficulties
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55
Q

If you have MG where might you have weakness?

A
  • BUE or BLE (proximal before distal)
  • Respiratory muscles
  • Weakness fluctuates (over hours, days, weeks)
  • Better in AM, declines as the day progresses or during exercise
  • Remissions and exacerbations
  • Normal reflexes, sensory function and coordination
  • Crisis- respiratory distress or swallowing crisis
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56
Q

What occurs with a diagnosis of MG?

A
  • Presence of circulating antibodies to ACH receptors have been identified in the blood of 90% of MG pts
    - antibodies cause ACH receptor changes and block ACH binding to receptors
  • Increased incidence of diabetes, lupus, RA, thyrotoxicosis and cancer in the MG population
  • EMG
    • Normal at rest
    • Decremental response to repeated stimulation (mirrors fatigue with exercise)
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57
Q

What is the Tensilon Test with MG?

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 the synapse longer)
  • If strength/endurance is improved, then MG

**Muscle biopsies can be done: count the ACH receptors at motor end plates

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58
Q

What does anti-cholinesterase do?

A

*Slows down the breakdown of ACH which leaves acetate and choline in cleft (ACh is around longer, thus has an increased chance of binding to the receptor)

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59
Q

What are the immunosuppressive drugs used as an intervention in MG?

A
  • Prednisone
  • Cyclosporine
  • Myophenolate Mofetil
  • Azathioprine
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60
Q

What are the interventions used in MG?

A
  • Anticholinesterase drugs
  • Immunosuppressive drugs
  • Intravenous Immunoglobulin (IVIG)
  • Plamaphoresis
  • Thymectomy
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61
Q

What is Plasmaphoresis?

A
  • Blood is routed to a machine that separates the plasma and cells
  • Plasma filtration: two venous lines are used. The plasma is filtered using standard hemodialysis equipment. This continuous process requires less than 100 ml of blood to be outside the body at one time
  • Temporarily (4-6 wks) reducing anti-ACh receptors antibodies
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62
Q

What is a thymectomy?

A
  • Mainly carried out in adults
  • Role of the thymus: cause T-cell specific response
  • 70% of MG pts have hyperplasia of thymus while 10-15% have tumors in the thymus
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63
Q

How should a PT care for a pt with MG?

A
  • Have pts 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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64
Q

What precautions should a PT show when working with a pt with MG?

A
  • PT focus is usually supportive, obtain equipment, maintain health and 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
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65
Q

What are the signs of impending MG crisis?

A
  • *You should call EMS!!
  • Increased muscle weakness
  • Respiratory weakness
  • Difficulty talking, chewing, or swallowing
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66
Q

What are the hyperkinetic disorders due to basal ganglia system pathology?

A
  • Huntington’s Chorea
  • Tourette’s Syndrome
  • Dystonia- generalized and local
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67
Q

What are the hypokinetic disorders due to basal ganglia system pathology?

A

*Parkinson’s Disease

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68
Q

What is the basal ganglia composed of?

A
  • Caudate Nucleus
  • Putamen
  • Globus Pallidus with related structures of Sub-thalamic nucleus and substantia nigra
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69
Q

How does the neural network of the basal ganglia work?

A
  • There is no direct output to motor units (always through cerebral cortex)
  • Mainly indirect effects on movement through cortex

*Basal ganglia output is to the thalamus, and thalamus influences the cortex. Any descending tracts that influence muscles come from the cortex. The BG system doesn’t directly effect the body, it’s through the thalamus/cortex

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70
Q

What are the parts to the substantia nigra and globus pallidus?

A
  • Substantia nigra has two parts
    • Substantia nigra pars compacta (SNc)
      - Substantia nigra pars reticulata (SNr)
  • Globus Pallidus has two parts
    - Lateral or external globus pallidus (LGP or EGP)
    - Medial or internal globus pallidus (MGP or IGP)
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71
Q

What does the substantia nigra pars compacta do?

A

*This is the nucleus that degenerates and produces dopamine that happens over time with PD

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72
Q

What parts of the BG essentially function together?

A

*The caudate and Putamen = Striatum

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73
Q

The output from the thalamus to the cortex is what?

A

*Facilitory

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74
Q

The output from the cortex to the thalamus is what?

A

*Inhibitory

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75
Q

What is GABA?

A

*An inhibitory neurotransmitter

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76
Q

What is Huntington’s Chorea?

A

*Involuntary small amplitude, rapid movements

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77
Q

What occurs in Huntington’s Chorea?

A
  • Results from degeneration of the striatal neurons to the SNr and LGP
  • The thalamus inhibition is much less so it’s hyperkinetic and is overdriving the cortex
  • The end result is the cerebral cortex is on over-drive (facilitated much more)
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78
Q

What are the symptoms of Huntington’s Chorea?

A
  • Chroea
  • Akinesia and bradykinesia
  • Hypotonia
  • Wide, staggering gait
  • Cognitive Problems
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79
Q

What is Tourette’s Syndrome?

A
  • Impulsions and compulsions to perform fragments of motor programs (Ex. touching, vocalizations, jumping, skipping)
  • “Tics”
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80
Q

What does Tourette’s Syndome result from?

A
  • Results from disturbance in the limbic circuits of the basal ganglia
  • The limbic system inhibits the sunstantia nigra pars compacta so less excitation of direct pathways of BG system > End results is that the cortex is on overdrive
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81
Q

What is Dystonia?

A

*A movement disorder characterized by sustained muscle contraction in an extreme end range of motion, frequently with a rotational component

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82
Q

What is the main difference between general and focal dystonias?

A
  • General dystonias involve the entire body

* Focal dystonias involve one joint or a few related joints

83
Q

What is General dystonia?

A
  • Genetic, involving DYT gene
  • Individual will begin a movement then usually a torsional rotation of the trunk then proceed into UE’s and LE’s
  • Assume a fixed posture for several minutes and often cannot move
  • May be painful
  • May start more proximally then this position will work its way to their arms and legs
84
Q

What is Focal Dystonia?

A
  • Results from damage to the GP and/or putamen resulting in release of the usualy inhibition of the thalamus 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 (Usually bc of SCM)
85
Q

What are some other focal dystonia’s?

A
  • Vocal cords
  • Tongue and Swallowing muscles
  • Facial muscles including eye
  • Hand
  • Toes
  • Writer’s camp/musicians- task specific dystonia
86
Q

What is Idiopathic Parkinson’s Disease?

A

*MPTP which is caused by impurities in synthetic heroine

87
Q

What are the signs and symptoms of idiopathic parkinson’s disease?

A
  • Loss of ability to initiate movement (Akinesia)
  • Bradykinesia
  • Rigidity
  • Resting tremor
  • Impaired posture, gait and balance due to akinesia, bradykinesia, etc.
88
Q

What occurs in Parkinson’s disease?

A
  • degeneration of SNc with loss of dopamine
  • End result is loss of drive to the cerebral cortex
  • Inhibit the thalamus so you get less facilitation
89
Q

What are the classic signs of Parkinson’s Disease?

A
  • Resting Tremor (tremor when the body part is supported)
    • Resting tremor rate is 4-6 Hz (often in hand or foot) and classically stops when individual starts to move body part
      - Pill Rolling
  • Bradykinesia
    - Slow movements: slow force production
    - Loss of spontaneous movements
  • Rigidity
    - Cogwheel-you apply some pressure and they release and then hold continuously
    - Lead pipe (when rigidity becomes severe) feels like lead when elongating passively
  • Postural instability
    - Hypometric anticipatory postural adjustments

**These are all without medication

90
Q

What are the symptoms of Parkinson’s disease?

A
  • Difficulty swallowing and chewing
  • Speech impairments: speak too softly, monotone, hesitant, slurred, repeating words
  • “masked” face (flat affect/no expression)
  • Fatigue
  • Sleep problems
  • Decreased strength in muscles of respiration
  • Dementia or other cognitive problems
91
Q

What are the postural changes seen in Parkinson’s disease?

A
  • Kyphotic posture with forward-flexed trunk
  • Forward Head
  • Crouched legs
92
Q

What are the problems with Gait with a PD patient?

A
  • Difficulty initiating gait
  • Freezing gait (more obvious with a change in floor pattern)
    • Pt reports that it feels like their feet are stuck on the ground/heavy and they cannot move
  • Festinating gait
    - Steps too small
    - Causes COM to get in front of BOS and they can’t catch themselves so they typically fall forward
    - Decreased Foot clearance
  • Decreased or no trunk rotation
  • Decreased or no arm swing
93
Q

What does a festinating gait look like?

A

*It’s due to bradykinesia. A person is crouched and doesn’t swing their arms. It looks like they’re falling forward and are trying to catch up. Some people will even run into an object and continue trying to walk

94
Q

What is Micrographia?

A

*Often seen in parkinson’s. The handwriting is slow and looks cramped or small

95
Q

What is parkinson’s Disease Progression?

A
  • PD is not by itself fatal, but it gets worse over time
  • In the later stages of the disease, PD-related complications can lead to death, such as choking, pneumonia, and falls
  • Progression of symptoms may take 20 years or more
96
Q

What is stage one PD progression?

A
  • Unilateral, one side of the body
  • Symptoms mild, inconvenient but not disabling
  • Usually presents with tremor of one limb
  • Friends noticing change in posture, gait, facial expression
97
Q

What is stage two of PD progression?

A
  • Bilateral, both sides of the body
  • Minimal disability
  • Posture and gait affected (festinating gait)
98
Q

What is stage three of PD progression?

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
99
Q

What is stage four of PD progression?

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
100
Q

What is stage five of PD progression?

A
  • Cachectic stage: loss of weight and muscle wasting secondary to serious disease or disorder
  • Invalidism compete
  • Cannot stand or walk
  • Requires constant nursing care
101
Q

How do you diagnose PD?

A
  • Medical history and neurological exam
  • Difficult to diagnose accurately
    • Early signs and symptoms may be dismissed as the effects of early aging
  • Must have 2 of the 4 classical signs
  • Positive response to dopamine-like medications
  • CT or MRI in PD usually appear normal, but may be needed to rule out other diseases
102
Q

What needs to happen before you start to see signs and symptoms of PD?

A

*A reduction of about 80% of Dopamine

103
Q

What are the PD medications?

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

104
Q

What are the side effects of Levodopa (L-dopa)?

A
  • Side effects increase with continued usage
  • 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”
105
Q

What are some antiparkinsonian agents?

A
  • Levodopa

* Levodopa with carbidopa =Sinemet

106
Q

What is the action of antiparkinsonian agents?

A

*Converts to dopamine after crossing the BBB which helps with the resolution of dopamine deficiency

107
Q

Where is levadopa converted to dopamine?

A

*In the circulatory periphery so only 1% of the drug actually reaches the brain

108
Q

What does carbidopa do?

A
  • Inhibits Dopa Decarboxylase, prevents premature conversion in the bloodstream
  • It doesn’t cross the BBB which is good since we don’t want levadopa to not convert to dopamine once it’s in the brain
109
Q

What does the portion of Carbidopa in Sinemet do?

A
  • It decreases the amount of levadopa needed to acheive therapeutic effect
  • Often 4:1 ratio of carbidopa to levodopa (sometimes 10:1)
110
Q

What is the therapeutic effect of Sinemet?

A

*Decreases symptoms of Parkinson’s causing less muscle rigidity, less bradykinesia

111
Q

What are the side effects of Sinemet?

A
  • GI irritation: severe nausea and vomiting with initial administration. Should be taken with food to decrease effects
  • Postural hypotension/orthostatic hypotension
  • Cardiac arrhythmias
  • Large incidence of dyskinesias (chorea-athetoid movements)
  • Psychosis, depression, anxiety
  • If dopamine reaches limbic system then less psychotic effects
112
Q

What are the treatment issues with Antiparkinsonian agents?

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
    • Save it until you need it or use it in earlier stages
  • Drug Holidays- when ppl stop taking their meds or really reduce the dosage to reboot their system
113
Q

What are the Dopamine Agonists?

A
  • Pramipexole (Mirapex)

* Ropinirole (Requip); Rotigotine (Neuro patch)

114
Q

What is the action of Dopamine agonists?

A

*Action: Cross BBB; directly stimulate dopamine receptors (similar function to dopamine). Neuro protective effects

115
Q

What are the side effects of Dopamine Agonists?

A
  • Less adverse effects for dyskinesias and motor response issues are rare
  • Nausea, vomiting, postural hypotension
116
Q

What is Ablation in PD?

A
  • Stereotaxic surgery
  • Selectively destroying specific cells that contribute to the symptoms
  • Pallidotomy (reduce tremor, rigidity, and bradykinesia)
  • Thalamotomy (reduce tremor)
117
Q

What is Deep Brain Stimulation?

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
118
Q

How are external sensory cues an implication for intervention in PD?

A
  • A deficit to execute movements can be overcome in the presence of external sensory cues (ex. Visual, auditory, proprioception)
  • Rationale: distinct contribution of the cortico-striatal (implicit) and cortico-cerebellar (explicit) systems to motor learning and control
119
Q

What is the intervention for freezing gait in PD?

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
120
Q

What is the big picture of the cerebellum?

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
121
Q

How can the cerebellum be damaged?

A

*Can be damaged by a blow to the back of the head (TBI), stroke, tumor, degenerative disease or congenital malformation

122
Q

What are the cerebellar peduncles and why are they important?

A
  • They are the superior, inferior and middle cerebellar peduncles
  • They’re important because they contain all of the axons that transmit information to/from the cerebellum to the rest of the brain.
123
Q

Where is the inferior olive located?

A

*it’s inferior to the cerebellum

124
Q

Why is the cerebellar in-folding significant?

A

*It creates lots of surface area for the wide function of the cerebellum

125
Q

How are neuronal circuits constructed in the cerebellum?

A

*In a uniform manner that consists of 8 cell types

126
Q

What are the 8 cell types in the cerebellum?

A
  • Purkinje cell
  • Granule cell
  • Golgi cell
  • Parallel Fibers
  • Stellate Cell
  • Basket cell
  • Mossy fibers
  • Climbing fibers
127
Q

What cerebellar cells are part of the 2 major afferent inputs?

A

*Mossy and climbing fibers

128
Q

What are the anatomical divisions of the cerebellum?

A

*Anterior, posterior and flocculonodular lobes

129
Q

What are the deep nuclei of the cerebellum?

A
  • Vestibular nuclei
  • Fastigial Nucleus
  • Emoliform nucleus and globose nucleus (interposed)
  • Dentate nucleus
130
Q

What is the vestibulocerebellum?

A

*Flocculonodular lobe

131
Q

What is the input of the vestibulocerebellum?

A

*Starts at the vestibular apparatus which goes to the vestibular nuclei which detects change in linear and angular head position and orientation of the head with respect to gravity then goes to vestibulocerebellum

132
Q

What is the output of the vestibulocerebellum?

A

*Starts at vestibulocerebellum and sends info to vestibular nuclei then to the vestibulospinal tract

133
Q

What are the 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/coordination
  • Equilibrium particularly during rapid changes in body position or in the direction of movement
134
Q

What is the spinocerebellum?

A

*The vermis and intermediate zones

135
Q

What are the inputs of the spinocerebellum in the vermis?

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)
136
Q

What is the difference between the superior and inferior colliculi?

A
  • Superior colliculi: responds to rapid visual stimulation and causes head to turn towards it
  • Inferior colliculi: responds to auditory stimulus and causes head to turn quickly towards it.
137
Q

What are the outputs of the Spinocerebellum in the vermis?

A
  • From the vermis to the fastigial nucleus to the reticular nuclei to the reticulospinal tract (CMRST)
  • From the vermis to the vestibular nuclei to the lateral and medial vestibulospinal tracts
  • From the vermis to the thalamus to the cortex (MI or broadman area 4) then to the anterior CST
138
Q

What tracts make up group A in Kuyper’s classification?

A

*Corticomedullary reticulospinal tract, vestibulospinal tract, anterior corticospinal tract

139
Q

What are the vermis functions associated with?

A
  • Gross motor movements
  • Coordination of axial and girdle proximal musculature (scapula/shoulder and pelvis/hip)
  • Regulates rhythmic walking movements (regulate CPGs of gait)
  • Adjusts the timing of locomotor movements
  • Modulation of interlimb coordination during locomotion
140
Q

What are the inputs of the spinocerebellum of the intermediate zone?

A

*Dorsal spinocerebellar and cuneocerebellar from the extremities like middle joints like elbow, knee, and distal muscles (somatosensory info extremities)

141
Q

what happens if there’s damage in the right intermediate zone?

A

*Then you have problems on the right side of the body

142
Q

What is group B of kuypers classification associated with?

A

*Fine motor coordination

143
Q

What are the outputs of the spinocerebellum of the intermediate zone?

A
  • From the intermediate zone to the interposed nuclei to the red nucleus to the rubrospinal tract
  • From the intermediate zone to the thalamus to the cortex (MI or Broadman area 4 and SMA) to the Lateral CST
  • From the intermediate zone to the reticular nuclei to the reticulospinal tracts (CPRST)
144
Q

What does the rubrospinal tract in humans innervate?

A

*The upper extremities- cervical and thoracic nerve root segments

145
Q

What are the functions of the intermediate zone?

A
  • Fine motor movements

* Coordination of distal musculature of the extremities (hands and feet)

146
Q

What is the neocerebellum?

A

*The lateral zones, also known as the pontocerebellum or cerebrocerebellum

147
Q

What are the inputs of the neocerebellum?

A

*Cerebral cortex (motor, sensory and PMA) (ipsilateral frontal and parietal lobes) then pontine nuclei then the neocerebellum

148
Q

What are the outputs of the neocerebellum?

A

*From the lateral zone to the denate nucleus to the ventral lateral nucleus of the thalamus to the premotor (PMA) and motor (MI) areas of the cerebral cortex

149
Q

What are the functions of the neocerebellum?

A
  • Planning and timing of voluntary movements (ipsilateral) particularly learned and 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 the next.
  • Onset, duration, amplitude, and rate/timing of muscle contraction. Duration, amplitude, and rate of rise of agonist and antagonist muscle bursts (rate, range, force, and direction of movement)
150
Q

What happens if there’s damage to the lateral zone?

A

*A patient may have trouble stringing tasks together and may halt between tasks

151
Q

What are the comparator functions of 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 info 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 motion
  • Instantaneously corrects or attempts to correct the movement if the velocity of movement allows this correction ((100-200 ms needed to make corrections (Processing time))
152
Q

What are the muscle tone functions of the vestibulocerebellum and spinocerebellum?

A
  • They have general excitatory influence on the gamma motor neurons
  • Damage results in decreased excitation of gamma MN’s then reduced sensitivity of the muscle spindles then decreased muscle tone.
  • Hypotonicity
  • This is usually with acute cerebellar damage; hypotonia decreases over time
153
Q

A normal physiological tremor is usually what?

A

*8-12 cycles per second

154
Q

What is a cerebellar intention tremor?

A

*A lower amplitude tremor (3-5 hz) and starts low and gets worse as you get towards the intended target

155
Q

In Music therapy for a PD patient what connection is trying to be found?

A

*The emotional connection in the limbic system that the pt had with music

156
Q

How common is huntington’s chorea?

A

*6.5 per 100,000 people (varies by location)

157
Q

When does Huntington’s occur?

A
  • Autosomal dominant genetic disease = short arm of chromosome 4
  • Onset is usually after 30 yrs old
  • Death: about 15-20 years after onset
158
Q

How does Huntington’s chorea occur?

A
  • Results from degeneration of the striatal neurons to the SNr and LGP
  • End results are that the cerebral cortex is on Over-drive (facilitated)
  • Hyperkinetic disorder
159
Q

What are the symptoms of huntington’s?

A
  • Chorea- involuntary small amplitude, rapid movements (ataxic, dance-like movements)
  • Akinesia and bradykinesia (poverty of movement)
  • Hypotonia
  • Wide, staggering gait
  • Speech-lacks normal timing and rhythm
  • Difficulty swallowing
  • Vision-poor control of saccadic eye movements
160
Q

What are the cognitive symptoms of huntingtons?

A
  • Dementia
  • Poor judgment
  • Loss of long term memory
  • Depression
  • IQ decreases
  • Irritability
161
Q

What are the components of the UHDRS?

A
  1. motor assessment
  2. cognitive assessment
  3. behavioral assessment
  4. independence scale
  5. functional scale
  6. total functional capacity (TFC)
162
Q

What occurs in early stage HD?

A
  • Symptoms become noticeable enough to warrant a diagnosis

* Can generally continue to work, drive and live independently

163
Q

What are the motor symptoms in early stage HD?

A
  • Usually begin in the extremities of the body
  • Involuntary twitches in fingers, toes and face
  • Subtle loss of coordination
164
Q

What are the cognitive symptoms of early stage HD?

A
  • More difficult for people to think through complicated tasks
  • May be harder to work and perform at their usual level
165
Q

What are the behavioral symptoms of early stage HD?

A

*Depression, irritability, and disinhibition (saying whatever is on your mind, no tact, potentially insulting people)

166
Q

what occurs in middle stage HD?

A

*Often lose their ability to work and drive and might be unable to perform household chores

167
Q

What are the motor symptoms in middle stage HD?

A
  • Eating can become challenging, as patients have trouble performing the complicated series of muscle movements needed to swallow
  • Speech becomes slurred
  • Walking becomes staggered, falls likely
  • Involuntary dance-like movements =chorea
  • Trouble swallowing, which leads to the weight loss that begins to become serious in this phase
168
Q

What are the cognitive symptoms in middle stage HD?

A
  • Have more trouble organizing information and thinking clearly
  • Can’t solve problems they were normally capable of working through
169
Q

What are the behavioral symptoms in middle stage HD?

A
  • Continued worsening of behavorial signs noted in early stage
  • Become increasingly apathetic; losing interesting in activities that they used to enjoy
170
Q

What occurs in late stage HD?

A
  • Totally dependent for all care; confined to bed; often SNF
  • Unable to speak
  • Choking is a major concern; tube feeding
171
Q

What are the motor symptoms of late stage HD?

A
  • Severe rigidity, dystonia, and bradykinesia
  • Chorea has usually stopped, although a minority of patients continue to experience severe chorea
  • Cannot initiate movement
172
Q

What are the cognitive symptoms in late stage HD?

A

*debilitating, though patients can usually still understand speech and recognize loved ones

173
Q

What the behavioral symptoms in late stage HD?

A
  • Depression tends to fade int he late stages of HD, possibly since individual has come to terms with the illness or apathetic
  • Psychosis, a rare problem that causes people to have visual and auditory hallucinations, occurs in 3-11% of pts in the late stages of HD
174
Q

What are the medications of HD?

A
  • Cholinergic or GABA - containing agonists
  • Perphenazine
  • Haloperidol
  • Reserpine
  • Riluzole
175
Q

What is the etiology of dystonia?

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.
176
Q

What is the pathogenesis of dystonia?

A
  • Lesions at caudate, putamen, and globus pallidus
  • Overactive direct pathway within the basal ganglia circuitry increases motor acitvity
  • Hyperkinetic disorder
177
Q

What is the definition of dystonia?

A

*Abnormal muscle tone with simultaneous contraction of agonist and antagonist

178
Q

What are the characteristics of Dystonic movements?

A
  • Involuntary 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 or minutes, hours or longer
  • May be increased with stress, during purposeful movements, task-specific (Sx only present during specific tasks, ex: writing, playing instruments)
  • Decreases upon relaxation and disappear during sleep
  • Often painful condition
179
Q

What occurs in pharyngeal dystonia?

A
  • Spasmotic dysphonia
  • Distorted speech; affect vocal cords
  • Treated with Botox injections
180
Q

What occurs in cervical dystonia?

A
  • Most common
  • Hypertrophy of SCM muscle
    • Lateral flexion toward, rotation away; typically painful
  • Is NOT torticollis (a musculoskeletal disorder with muscle fibrosis)
181
Q

What is writer’s/musician’s cramp dystonia?

A
  • Task-specific focal dsystonia

* Spasm affecting certain muscles of the hand and/or fingers

182
Q

What is the disease progression of dystonia?

A

*Onset: generalized = 8 years old
Focal = 30-50 years old
*Progression
-Dystonia is not fatal, but is chronic and often painful and debilitating
-Generalized begins in legs and progresses to rest of body
-Focal dystonia progresses for about 5 yrs then plateu (spontaneous recovery in 30% of cases)

183
Q

What are the medications often used for focal dystonia?

A
  • Botox

- effective for 3-4 months

184
Q

What are common medications for generalized dystonia?

A
  • Baclofen
  • Artane
  • Sinemet
  • Klonopin
185
Q

What surgeries can be done for dystonia?

A
  • Deep brain stimulation of the globus pallidus

* Rhizotomy- resection of anterior (motor) cervical spinal nerve roots

186
Q

What are cerebellar dysfunctions?

A
  • Abnormal movements are ipsilateral to the lesion
  • Hypotonicity
  • Asthenia
  • Intention Tremors
  • Disturbances of posture and balance
  • Dysmetria
  • Dysdiadochokinesia
  • Ataxic gait
  • Movement Decomposition
  • Poor coordination of muscles of speech
  • Eye movements
  • Delays in force production and errors in force maintenance
  • Time-asymmetric velocity profiles
187
Q

What occurs in hypotonicity of a cerebellar dysfunction?

A
  • Ipsilateral to the lesion
  • Reduced firmness to palpation
  • Reduced tone during PROM
  • Pendular DTR’s secondarly to momentum
  • Reduced extensor tone: trouble remaining upright against gravity
188
Q

What occurs in asthenia of a cerebellar dysfunction?

A

*Generalized weakness or decreased activity and easily fatigued

189
Q

What occurs in intention tremors of a cerebellar dysfunction?

A
  • 3-5 hz

* Tremor amplitude increases as effector approaches the target

190
Q

What occurs in disturbances of posture and balance of a cerebellar dysfunction?

A
  • Flexed posture, wide BOS
  • 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
191
Q

What occurs in dysmetria of a cerebellar dysfunction?

A
  • Dysmetria = over or under shooting the range of motion
  • Impaired ability to properly scale movement distance
    • Think in a 3D way
      • Over or under shoot (error in range or force) (“past pointing”, hyper/hypometria”
      • Off to the right or left (direction)
      • Off up or down (direction)
      • Triphasic AG, ANTAG, and AG2 msucles/EMGs are not programmed correctly (amplitude, duration, onset, termination, and rate of rise (slope) of EMG muscle burst)
192
Q

What occurs in dysdiadochokinesia in a cerebellar dysfunction?

A
  • Deficit in coordination btwn agonist- antagonist muscles during rapid alternating movments
  • Resulting in errors in range/amplitude and rate/timing
  • Poor timing between cessation of agonist muscle activity and initiation of antagonist muscle activity
193
Q

What occurs in an ataxic gait during a cerebellar dysfunction?

A

*Disruption in rhythm of gait, wide based gait, unsteady, fall backwards and toward the side of the lesion

194
Q

What occurs in movement decomposition of cerebellar dysfunction?

A
  • disrupted sequences in a multi-step task

* breaking a multi-joint movmement down into a series of separate movements

195
Q

What occurs in poor coordination of muscles of speech in cerebellar dysfunction?

A
  • Dysarthria - slurred speech

* Explosive speech, staccato speech

196
Q

What occurs in eye movements of cerebellar dysfunction?

A
  • Gaze-evoked nystagmus
  • Ocular dysmetria when performing saccades
  • Disrupted smooth pursuit
  • Poor coordination of eye-head movements
197
Q

What is the frequency of cerebellar strokes?

A
  • Less than 5% of all strokes involve the cerebellar arteries
    • Posterior inferior cerebellar artery
    • Anterior inferior cerebellar artery
    • Superior cerebellar artery
  • Best predictor of recovery post CVA but if the deep nuclei are involved then the prognosis is worse
198
Q

What is the etiology and where is the lesion in Friedreich’s Ataxia?

A

*Etiology: Hereditary (autosomal recessive)

  • Lesion:
    • cerebellum
    • Dorsal root ganglia -sensory impairments
    • Dorsal columns = conscious proprioception, vibration, fine touch
    • Spinocerebellar tracts = unconscious proprioception
    • Some corticospinal tract
199
Q

What occurs in mild and severe time asymmetric velocity profiles in cerebellar dysfunctions?

A
  • Mild: Short acceleration, long deceleration

* Severe: Long acceleration, short deceleration

200
Q

What occurs in delays in force production and errors in force maintenance in cerebellar dysfunction?

A
  • The cerebellum appears to play a role in maintaining constant force
  • Pt may have trouble generating enough force or maintaining it over time
201
Q

What are the neuropatholgies of the cerebellum?

A
  1. Friedreich’s Ataxia
  2. Vascular disorders (stroke)
  3. Tumors
202
Q

What occurs in tumors in the cerebellum?

A
  • More common in children than adults
  • Children have good prognosis for recovery since most tumors are benign and can be removed surgically
  • Tumors in adults tend to be more aggressive cancers and have poorer prognosis
203
Q

What is the onset and prognosis of Friedreich’s ataxia?

A
  • Onset: between 5-15 years old
    • 25% of offspring have FA
  • Course: Highly variable
    • Generally lose ability to walk and confined to WC within 10-20 years after onset
  • Prognosis: Some survive into their 60s and 70s IF there’s no heart attack
204
Q

what are the signs and symptoms of Friedreich’s ataxia?

A
  • Most common Sx
  • Gait ataxia is usually the first symptoms
  • 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 spasticity
  • Nystagmus (20% of cases)
  • Impaired smooth pursuit
  • Heart disease
    • Various forms (ex. cardiomyopathy, dysrhythmia)
    • 60% of population
  • Easily fatigued
  • Scoliosis
  • Dysarthria/tongue and oral motor issues

Neuro D&D (4 decks)

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