motor control disorders ect ppt2 (same lecture) Flashcards

1
Q

what does the concept of “hierarchical organisation” of motor control refer to?

A

higher order areas of hierarchy are involved in more complex tasks

(PROGRAMME and DECIDE ON movements, COORDINATE muscle activity)

lower level areas of hierarchy: lower level tasks (EXECUTION of movement)

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2
Q

what does the concept of functional segregation refer to?

A

motor system organised in a number of different areas that control different aspects of movement

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3
Q

where does the motor cortex (primary and non primary) receive information from? where does it send info to?

A

-from other cortical areas (thalamus)

-sends to thalamus and brainstem and spinal cord

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4
Q

what areas sometimes mediate transfer of info from motor cortices to brainstem and thalamus?

A

basal ganglia (for thalamus)
cerebellum (for both)
they adjust the commands sent

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5
Q

where does the brainstem send info to?

A

spinal cord to stimulate muscles of body, or straight to muscles of face head and neck to move these regions

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6
Q

2 major types of descending tracts

A

pyramidal and extrapyramidal (refers to whether they pass through pyramids in medulla)

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7
Q

which are the extrapyramidal tracts ?

A

vestibulospinal
tectospinal
reticulospinal
rubrospinal

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8
Q

role of extrapyramidal tracts?

A

involuntary (automatic) movements FOR BALANCE, POSTURE and LOCOMOTION

think of EXTRA: einai ta extra, fine tuning, isoropia klp)

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9
Q

where do extrapyramidal tracts start and end?

A

start brainstem nuclei end spinal cord

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10
Q

which are the pyramidal tracts

A

corticospinal (Body)
coritcobulbar (face)

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11
Q

role of pyramidal tracts

A

voluntary movements of body and face (think of pyramidal: pyrinika: basics)

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12
Q

pathway of corticospinal tract of UPPER motor neurons up to where they link to lower motor neurons;

A

1) upper motor neurons (in primary motor cortex)
2) midbrain (cerebral peduncle)
3) medulla in pyramids
4) 85-90% decussate in medulla BEFORE they enter spinal cord : forming lateral corticospinal tract in spinal cord
(going to limb muscles)

  • the rest doesnt cross- stays as it is and forms anterior corticospinal tract in spinal cord
    (going to trunk muscles)

5) then they link to lower motor neurons once in spinal cord

(Note; pyramids are only in medulla, dont continue in spinal cord thats why the tracts turninto anterior and lateral and not called pyramidal anymore)

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13
Q

what is the homunculus?

A

Represents the proportional amount of brain (in somatosensory or motor cortices -theres a diffirent humunculus for each) devoted to that part of body

(think H for HUMUNGUS HANDS): BECAUSE the sketch has huge hands einai san terataki see slide 10

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14
Q

what is somatotopy

A

Represents location of part of body on brain NOT AMOUNT devoted to it

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15
Q

role of corticobulbrar tract

A

Principal motor pathway for voluntary movements of the face (and neck)

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16
Q

what are some areas/ types of nuclei in brain that are components of the basal ganglia?

A

caudate nucleus + putamen nucleus
(these two make the “striatum”)
globus pallidus
thalamus

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17
Q

what does a nucleus in neuro terms refer to (just for my understanding not from slide)

A

In neuroanatomy, a nucleus typically refers to a collection of neurons (nerve cells) located within the central nervous system that have a similar structure and function.
These nuclei are often grouped together based on their anatomical location

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18
Q

what do motor nerves from these nuclei do?:
1)occulomotor nuc, throchlear, 2)trigeminal motor nucleus,
3)abducents,
4)facial,
5)hypoglossal

A

eye movements
muscles of jaw
eye movements
muscles of face
tongue

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19
Q

role of vestibulospinal tract

A

Stabilise head during body movements, or as head moves
Coordinate head movements with eye movements
Mediate postural adjustments

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20
Q

role of reticulospinal tract

A

Changes in muscles tone associated with voluntary movement
(ex. Standing one leg, when walking, reaching, its controlling trunk muscles so you stay stable)

Postural stability

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21
Q

role of tectospinal tract

A

orientation of head and nech during spine movements

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22
Q

rubrospinal tract role

A

In humans mainly taken over by corticospinal tract
but one thing it does:
Innervate lower motor neurons of FLEXORS (thats a unique thing) of the upper limb

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23
Q

where do each of the extrapyramidal tracts originate in (in brainstem as seen previously) but where specifically for each

A

tectospinal tract: superior colliculus of midbrain
reticulospinal: medulla and pons
red nucleus of midbrain for rubrospinal

didnt find smth for vestibulospinal in my flashcards, chatgpt : medulla and pons

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24
Q

which is the most primitive descending tract? (develops first in babies ect)

A

reticulospinal

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25
Q

what does it mean in general to have negative signs of upper motor neuron lesions?

A

Loss of voluntary motor function:

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26
Q

what are the types of negative signs of upper motor neuron lesions?

A

1) Paresis: graded weakness of movements
2) Paralysis (plegia): complete loss of voluntary muscle activity

NOTE:”graded” implies that the weakness is not uniform but can range from mild to severe,

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27
Q

what does it mean in general to have positive signs of upper motor neuron lesions?

A

generally: abnormal increased motor function due to loss of inhibitory descending inputs

28
Q

specific positive signs of upper motor neuron lesions

A

Spasticity: increased muscle tone
Hyper-reflexia: exaggerated reflexes
Clonus: abnormal oscillatory muscle contraction
Babinski’s sign (sharp object on sole thing) normal adult is fingers to curl down

29
Q

what is apraxia

A

A disorder of skilled movement. Patients are not paretic but have lost information about how to perform skilled movements

30
Q

LESION IN which area gves you apraxia

A

supplementary motor area - SMA)
- is basically in premotor cortex
- in terms of lobes its a little on inferior parietal and on frontal

31
Q

what are the most common causes of disease in these areas that can cause apraxia? (go to ppt to see mri)

A

stroke and dementia

32
Q

lower motor neuron lesion symptom type in general

A

weakness

33
Q

specific symptoms of lower motor neuron lesion

A

Hypotonia (reduced muscle tone)
Hyporeflexia (reduced reflexes)
Muscle atrophy
Fasciculations:
Fibrillations:

(remember: lower motor: hypo hypo Motor ff)

34
Q

what is the difference between muscle fasciculations and fibrilations

A

Fasciculations are VISIBLE twitches of a motor unit after it has been DAMAGED and produces a spontaneous action potential.

fibrillations are NON VISIBLE twitches on individual muscle FIBRES (only with needle electromyography) that are SPONTANEOUS

35
Q

difference between spasticity (thing seen in positive sign UPPER motor neurons) vs fasciculations

A

Spasticity: Spasticity refers to increased muscle tone or stiffness, often accompanied by involuntary muscle contractions.
Fasciculations are involuntary muscle twitches or contractions that can occur in SMALL BUNDLES of muscle fibers. - see a little twitch under skin type thing

36
Q

what is motor neuron disease (MND) + most common form

A

Progressive neurodegenerative disorder of the motor system

Most common/ characteristic type: Amyotrophic Lateral Sclerosis

37
Q

start- finsish of upper motor neurons

A

from motor cortex to brainstem

38
Q

two types of lower motor neurons and what they innervate - only relevant areas to MND

A

brainstem lower motor neurons (innervate tongue/ face, upper limb, intercostal muscles (:through axon bundles)

and spinal cord lower motor neurons (innervate lower limb muscle)

39
Q

MND upper motor neuron signs

A

Spasticity (increased tone of limbs and tongue)
Brisk limbs and jaw reflexes
Babinski’s sign
Loss of dexterity (dexiotita)

Dysarthria (difficulty speaking) (facial muscles)
Dysphagia (difficulty swallowing)

40
Q

MND lower motor neuron signs

A

Weakness!!
Muscle wasting!!
Tongue fasciculations and wasting!!
Nasal speech!!
Dysphagia

!!: unnique compared to upper

41
Q

what is the physiological problem in parkinsons disease

A

Degeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum

42
Q

what are the symptoms of parkinsons disease

A

bradykinesia
akinesia
hypomimic face
rigidity
tremor at rest (hand and then can spread to other areas later in disease)

43
Q

what is akinesia parkinsons

A

difficulty initiating movement internally

44
Q

what is rigidity parkinsons

A

increased muscle tone causing resistance to extenraly impose djoint movements

45
Q

what is hypomimic face pakrinsons

A

face - expressionless, mask-like (absence of movements that normally animate the face)

46
Q

what is the physiological pathology in huntington’s disease?

A

Degeneration of GABAergic neurons in the striatum (caudate and then putamen).

*(striatum is the name for caudate and putamen nuclei)

47
Q

what is the cause of huntingtons disease? what kind of disease is it

A

Genetic neurodegenerative disorder

48
Q

what chromosome is the issue in in huntingtons? what is the mutation? is it dominant or reccessive?

A

chromosome 4
so its autosomal + dominant
CAG repeat

49
Q

what are the main presenting symptoms of huntingtons?

A

choreic movements
rapid jerky involuntary movements (hands and face affected first thne legs and resto of body)

unsteady gait

speech impairment
difficulty swallowing

50
Q

what are some huntingtons symptoms in later stages?

A

cognitive decline
dementia

51
Q

what part of the NS has usally been damaged in balism and how?

A

Usually from stroke affecting the subthalamic nucleus.

52
Q

what is the main symptom of ballism
and what does the side of symtmtom onset tell you about pathology location

A

Sudden uncontrolled flinging of the extremities
(remember pic of ppt)
symptoms occur contralaterally

53
Q

location of cerebellum in skull

A

posterior cranial fossa

54
Q

what structure separates cerebrum from cerebelum

A

tentorium cerebelli

55
Q

role of cerebellum and what happens when its damaged

A

Not thaaaat important just that it mediates the signals sent fromo brain down so harm in cerebellum is usually loss of skilled movement!!! Eg playing guitar, piano ext: loss of coordination and prediciton of movement: that’s what skills are about

56
Q

what is the role of the cerebellum

A

Regulation of gait, posture and equilibrium
Coordination of head movements with eye movements

57
Q

what is the result of vestibulocerebellum damage?

A

causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)

58
Q

role of spinocerebellum

A

Coordination of speech
Adjustment of muscle tone
Coordination of limb movements

59
Q

usual cause of vestibulocerebellum damage

A

tumour

60
Q

usual cause of spinocerebellum damage

A

degeneration and atrophy

61
Q

what happens when spinocerebellum is damaged

A

affects mainly legs, causes abnormal gait and stance (wide-based) (people have legs more spread than. normal

62
Q

cerebrocerebellum role

A

Coordination of skilled movements
Cognitive function, attention,
processing of language
Emotional control

63
Q

what is the consequence of damage in cerebrocerebellum

A

affects mainly skilled coordinated movements of the arms (tremor) and speech

64
Q

when are the signs of cerebellar dysfuncitno apparen?

A

only on movement

65
Q

what are the signs of cerebellar dysfunction

A

Ataxia
General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait

Dysmetria
Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)

Intention tremor
Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)

Dysdiadochokinesia
Inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)

Scanning speech
Staccato, due to impaired coordination of speech muscles