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Imperial > 21. Motor Systems > Flashcards

21. Motor Systems Flashcards

1
Q

What is the collective term given to the basal ganglia and cerebellum?

A

Extrapyramidal system

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2
Q

Broadly speaking, what is the role of the extra-pyramidal system?

A
  • It checks that the movement selected by the motor cortex is correct
    • They are responsible for the involuntary and automatic control of all musculature:
      • Muscle tone
      • Balance
      • Posture
      • Locomotion
  • Both parts of the extrapyramidal system has functions aside from modulating motor control
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3
Q

Where is the basal ganglion located?

A

White matter in the middle of the brain

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4
Q

What are the different parts of the basal ganglia?

A
  • Striatum
    • Caudate nucleus
    • Putamen
  • Globus Pallidus
    • External segment (GPext)
    • Internal segment (GPint)
  • Substantia nigra
    • Pars compacta (SNc)
    • Pars reticulata (SNr)
  • Subthalamic nucleus
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5
Q

What is the function of the basal ganglia?

A
  • It is involved in planning and coordinating movement
  • It elaborates associated movements
    • e.g. swinging arms when walking
  • Contribute to the smoothness of complex action Involved in moderating and coordinating movements
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6
Q

Describe the structure of the direct pathway in the basal ganglia.

A

Fibres initially come from the motor cortex to the striatum (caudate and putamen)

  • Direct Pathway: putamen –> internal segment (GPi) + pars reticulata (SNr)
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7
Q

Describe the structure of the indirect pathway in the basal ganglia.

A
  • Fibres initially come from the motor cortex to the striatum (caudate and putamen)
  • Putamen –> globus pallidus external segment –> subthalamic nucleus –> globus pallidus internal segment
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8
Q

What is the difference in the function of the direct and indirect pathways?

A
  • Direct Pathway = excitatory on the motor cortex
  • Indirect Pathway = inhibitory on the motor cortex
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9
Q

What extra component modulates the function of the direct and indirect pathways?

A

Nigro-striatal pathway

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10
Q

Where do the projections go after leaving the basal ganglion structures?

A
  • They go to the thalamus
  • From the thalamus they go to the cortex
    • Primary motor area (BA4) and supplementary motor area (BA6)
      • ​ two regions involved in movement preparation and planning
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11
Q

Describe how the basal ganglia are involved in choosing correct motor programmes to carry out particular functions

A
  • The basal ganglia and cortex form a processing loop
    • The basal ganglia enable proper motor programmes (stored in the cortex) via the direct pathway (excitatory)
    • The basal ganglia inhibit the competing motor programmes via the indirect pathway
  • In summary, the basal ganglia and its direct and indirect pathways make sure that appropriate motor commands get transmitted down the hierarchy.
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12
Q

Connections with which parts of the brain allow the basal ganglia to have a role in enabling various cognitive, executive and emotional programmes?

A
  • Prefrontal cortex
  • Limbic system
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13
Q

What causes Parkinson’s disease?

A
  • Parkinson’s disease is the neuronal degeneration of dopaminergic neurones in the pars compacta (SNc)
  • It is caused by the progressive depletion of dopaminergic neurones
  • NOTE: symptoms only appear when 80% of the dopamine cells in the substantia nigra have died
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14
Q

What are the consequences of Parkinson’s with regards to the circuitry of the basal ganglia?

A
  • The loss of nigro-striatal dopaminergic axons in the caudate and putamen mean that the connection between the striatum and pars compacta (SNc) is lost.
    • Striatum = caudate nucleus and putamen
  • This means that the direct pathway is reduced and so the excitation of the motor cortex is reduced
  • The lack of excitatory input interferes with the ability of the motor cortex to generate commands for voluntary movement, resulting in poverty of movement.
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15
Q

State the main signs of Parkinson’s disease.

A
  • Bradykinesia
    • slow movement
  • Akinesia
    • ​difficulty in the initiation of movements
  • Hypomimic face
    • expressionless face
  • Tremor
  • Rigidity
    • ​increase in muscle tone
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16
Q

Describe the Parkinsonian gait.

A
  • Walking slowly
  • Small steps
  • Shuffling feet
  • Reduced arm swing
  • Stooped posture with head and body bent forwards and downwards
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17
Q

What is Huntington’s disease caused by?

A
  • Abnormality on chromosome 4 (autosomal dominant)
  • Caused by the degeneration of GABAergic neurones in the striatum
    • ​Firstly the caudate and then the putamen
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18
Q

What are the consequences of Huntington’s disease with regards to the circuitry of the basal ganglia?

A
  • The inhibitory effect of the indirect pathway no longer keeps the direct pathway under control so the cortex will be hyperexcitable
  • Patients will continuously have abnormal movements because the cortex is continuously sending involuntary commands for movements
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19
Q

What are the main signs of Huntington’s disease and how does the disease progress?

A
  • Chorea = brief, semi-directed, irregular movements that are not repetitive or rhythmic, but appear to flow from one muscle to the next
  • Choreic movements
    • Rapid, jerky, involuntary movements of the body
    • Hands and face are affected first
    • Chorea gradually increases over time until the patients are totally incapacitated by it
  • Later on the patients will develop cognitive decline and dementi
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20
Q

State the 3 lobes of the cerebellum.

A

Anterior Posterior Flocculonodular

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21
Q

The cerebellum is divided sagitally into 3 zones. What are these zones?

A

Vermis (midline) Intermediate hemisphere (closest to vermis) Lateral hemisphere

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22
Q

State the 3 layers of the cerebellar cortex.

A

Granule cell layer Purkinje cells Molecular layer

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23
Q

Name the 3 deep nuclei that are involved in the connections of thecerebellum with other parts of the body. Include their function.

A

Fastigial = involved in control of balance and connected with vestibular nuclei Interposed + Dentate = both involved in voluntary movement and are connected to the thalamus and the red nucleus

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24
Q

What are the 3 sources of input into the cerebellum and what do they connect with?

A

Mossy Fibres – from the cortex and pons (corticopontine fibres) Mossy Fibres – from the spinocerebellar tract Climbing Fibres – from the inferior olive

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25
Q

Functionally, the cerebellum can be divided in three. What are these three divisions?

A

Vestibulocerbellum Spinocerebellum Cerebrocerebellum

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26
Q

What is the role of the vestibulocerebellum?

A

Vestibulocerbellum is the flocculonodular lobe It is connected to vestibular nuclei Involved in balance, posture and regulation of gait It is also involved in coordination of head movements with eye movements

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27
Q

Which parts of the cerebellum are part of the spinocerebellum?

A

Vermis and intermediate hemisphere

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28
Q

From where does the spinocerebellum receive inputs?

A

Afferents from axial portions of the body, visual, auditory and trigeminal inputs –> vermis Afferents from limbs –> intermediate hemisphere

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29
Q

What are the roles of the spinocerebellum?

A

Coordination of speech Adjustment of muscle tone Coordination of limb movement

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30
Q

Which part of the cerebellum is part of the cerebrocerebellum?

A

Lateral hemisphere

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31
Q

From where does the cerebrocerebellum receive inputs and what are its main functions?

A

It receives projections from the cortex Main functions are:  Coordination of skilled movements  Cognitive function  Attention  Processing of language  Emotional control

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32
Q

In summary, what are the four main functions of the cerebellum?

A

Maintenance of balance and posture Coordination of voluntary movements Motor learning Cognitive functions

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33
Q

State three syndromes caused by dysfunction of different parts of the cerebellum.

A

Vestibulocerebellar syndrome/Flocculonodular lobe syndrome Spinocerebellar syndrome Cerberocerebellar syndrome

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34
Q

What are the symptoms of vestibulocerebellar syndrome?

A

This syndrome is similar to vestibular disease Patients tend to lose their balance with gait ataxia and a tendency to fall.

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35
Q

What behavioural habit is spinocerebellar syndrome associated with?

A

Chronic alcoholism

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36
Q

Describe the symptoms of spinocerebellar syndrome.

A

Mainly affects the legs It causes abnormal gait and a wide-based stance

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37
Q

Describe the symptoms of cerebrocerebellar syndrome.

A

Damage mainly affects the arms It affects coordinated movements Speech becomes very hesitant and slow (staccato)

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38
Q

What are the main signs of cerebellar disorders?

A

Ataxia– general impairments in movement coordination and accuracy Dysmetria– inappropriate force and distance for target-directed movements Intention tremor– increasingly oscillatory trajectory of a limb in a target directed movement (nose-finger tracking) Dysdiadochokinesia– inability to perform rapid alternating movements Scanning speech– staccato, due to impaired coordination of speech muscles

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39
Q

State a hereditary and acquired cause of the symptoms listed above.

A

Hereditary – Friedreich’s Ataxia Acquired – Multiple Sclerosis

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40
Q

What is volition?

A

Motor systems produce movements that are adaptive and accomplish a certain goal

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41
Q

Describe the hierarchical organisation of motor control.

A

Association Cortex Motor Cortex Brainstem Spinal Cord

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42
Q

What are postural adjustments and unconscious processing?

A

Postural Adjustments – the motor system has to compensate for changes in the body’s centre of mass during movements Unconscious Processing – many of the postural adjustments occur without our awareness

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43
Q

What are the three parts of the motor cortex?

A

Primary Motor Cortex Premotor Cortex Supplementary Motor Area

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44
Q

What is volition?

A

Motor systems produce movements that are adaptive and accomplish a certain goal

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45
Q

Describe the hierarchical organisation of motor control.

A

Association Cortex Motor Cortex Brainstem Spinal Cord

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46
Q

What are postural adjustments and unconscious processing?

A

Postural Adjustments – the motor system has to compensate for changes in the body’s centre of mass during movements Unconscious Processing – many of the postural adjustments occur without our awareness

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47
Q

What are the three parts of the motor cortex?

A

Primary Motor Cortex Premotor Cortex Supplementary Motor Area

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48
Q

What makes up the association cortex?

A

Frontal Cortex Parietal Cortex NOTE: this is not exactly part of the motor pathway but it influences the planning and execution of movements

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49
Q

What are the two parts of the pyramidal (descending) system?

A

Corticospinal Tract – starts in the cortex and exits and innervates the muscles in the arms and legs Corticobulbar Tract – starts in the cortex then exits and innervates the muscles in the face

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50
Q

Describe the side loops of this descending pathway and their role.

A

The descending pathway also has two side loops that go to the cerebellum and basal ganglia The cerebellum and basal ganglia check the motor information before ittravels to the muscles and has its effect

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51
Q

Which lobe are the three parts of the motor cortex found in? Describe their arrangement.

A

Frontal (anterior to the central sulcus) The primary motor cortex is on the precentral gyrus The premotor cortex and the supplementary motor area are anterior to the primary motor area

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52
Q

What is another name given to the three parts of the motor cortex?

A

Primary Motor Cortex = Broadmann’s Area 4 Premotor + Supplementary Motor Area = Broadmann’s Area 6

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53
Q

What are the most important cells in the primary motor cortex?

A

Betz Cells (pyramidal cells)

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54
Q

Where are these cells located within the grey matter and which tracts originate from here?

A

They are found in the 5th layer of grey matter The corticospinal tracts originate from here

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55
Q

Describe what happens to the upper motor neurones that come from the primary motor cortex.

A

They travel through the brainstem to the pyramidal decussation in themedulla where 90% of the axons cross the midline. These axons continue down the spinal cord and synapse with a lower motor neurone and exit into a peripheral nerve to the reach the skeletal muscle. The pathway of the corticobulbar tract is somewhat similar – upper motor neurones go down into the brainstem and synapse with a lower motor neurone and they exit to the muscles of the face

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56
Q

What are the two types of descending pathway?

A

Lateral and Medial

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57
Q

Which tracts fall into each of these types?

A

Lateral  Lateral corticospinal tract  Rubrospinal tract Medial  Anterior corticospinal tract  Reticulospinal tract  Vestibulospinal tract  Tectospinal tract

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58
Q

What is the function of each of these types of pathway?

A

Lateral  Control of proximal and distal musculature  Voluntary movements or arms and legs Medial  Control of axial muscles  Balance and posture

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59
Q

Describe the structure and function of the lateral corticospinal tract.

A

The lateral corticospinal tract originates in the primary motor cortex from the Betz cells. Their axons pass down through the brainstem and decussate at the pyramidal decussation in the medulla. It then passes down the spinal cord and synapses with a lower motor neurone. It goes onto control mainly the distal musculature. NOTE: 90% of axons from the primary motor cortex decussate at the medulla (these are the lateral corticospinal tract axons). The 10% that don’t decussate form the anterior corticospinal tract.

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60
Q

Where does the rubrospinal tract originate?

A

Red nucleus of the midbrain

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61
Q

What is the function of the rubrospinal tract?

A

It is an alternative pathway that allows voluntary motor commands to be sent down the spinal cord meaning that the body can compensate for a lesion in the primary motor cortex. It also has a role in movement velocity.

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62
Q

Describe the structure and function of the vestibulospinal tract.

A

The lateral vestibulospinal tract originates at the lateral vestibular nucleus. The medial vestibulospinal tract originates at the medial vestibular nucleus. They mediate postural adjustments and head and eye movements

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63
Q

Describe the structure and function of the reticulospinal tract.

A

It originates in the reticular formation in the brainstem then goes down the spinal cord to innervate muscle. It is involved in complex actions:  Orienting  Stretching  Maintaining a complex posture

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64
Q

Describe the structure and function of the tectospinal tract.

A

It originates in the superior colliculus (brainstem) Its function is not known but is most likely involved in reflexive turning of the head to orient to visual stimuli.

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65
Q

Describe the structure and function of the anterior corticospinal tract.

A

The anterior corticospinal tract is made up of the upper motor neurone axons coming from the primary motor cortex that do not decussate at the pyramidal decussation. These fibres cross the midline at the level of the spinal cord It controls proximal musculature.

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66
Q

What diagram depicts the somatotopic organisation of the primary motor cortex?

A

Penfield’s Motor Homunculus

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67
Q

How can the cortical representation of a muscle in the motor cortex change?

A

The more we use a muscle, the bigger the representation of that muscle in the cortex.

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68
Q

What is the function of the premotor cortex?

A

Plans movements and assembles movements into coordinated actions NOTE: premotor cortex is anterior to the primary motor cortex

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69
Q

What is the function of the supplementary motor area?

A

Planning complex internally driven voluntary movements e.g. speech It also becomes active when you are thinking about movement before movement (e.g. rehearsing a dance)

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70
Q

What are the two parts of the association cortex that are involved in motor control? State their functions.

A

Posterior Parietal Cortex – ensures movements are targeted accurately to objects in external space Prefrontal Cortex – involved in the selection of appropriate movements for a particular course of action

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71
Q

Describe the features of upper motor neurone lesions.

A

Initially you get loss of function of the motor neurones leading to:  Paresis = graded weakness of movement  Paralysis = complete loss of muscle activity After a few weeks, the loss of descending inhibitory pathways leads to increased abnormal motor activity such as:  Spasticity (increased muscle tone)  Hyperreflexia (exaggerated reflexes)  Clonus (abnormal oscillatory muscle contraction)  Babinski’s Sign  NO muscle atrophy

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72
Q

What is Babinski’s Sign?

A

You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards) In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.

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73
Q

Why is muscle atrophy not seen in upper motor neurone lesions?

A

The lower motor neurones are still in tact and they have a role inproviding nutrients to the muscle. There will still be partial atrophy due to muscle disuse.

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74
Q

Define apraxia.

A

A disorder of skilled movement not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea). It is caused by the loss of information on how to perform skilled tasks rather than loss of motor command to the muscles.

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75
Q

Lesions in which part of the brain tend to cause apraxia?

A

Inferior parietal lobe Frontal lobe (premotor cortex and supplementary motor area)

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76
Q

What are the two most common causes of apraxia?

A

Stroke and Dementia

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77
Q

Describe the features of lower motor neurone lesions.

A

It is generally the opposite of upper motor neurone lesions.  Hypotonia  Hyporeflexia  Weakness  Muscle Atrophy– the metabolic trophic support to the muscles is lost  FASCICULATIONS– damages motor units produce spontaneous action potentials, resulting in a visible twitch  Fibrillations – twitch of individual muscle fibres (aren’t visible to the naked eye but are picked up on EMG)

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78
Q

What is motor neurone disease?

A

A progressive neurodegenerative disorder of the motor system – it is a spectrum of disorders. MND can affect upper motor neurones, lower motor neurones or both

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79
Q

What is the term given for upper AND lower motor neurone disease?

A

Amyotrophic Lateral Sclerosis (ALS)

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80
Q

Describe how the symptoms of ALS change as the disease progresses.

A

Some patients may present with only upper motor lesion symptoms or only lower motor lesion symptoms but as the disorder progresses, both upper and lower motor neurone signs will be coexistent.

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81
Q

List some signs of ALS.

A

 Increased muscle tone (spasticity in the limbs and tongue)  Brisk limb and jaw reflexes (hyperreflexia)  BABINSKI’s SIGN  Loss of dexterity  Dyarthria – difficulty speaking  Dysphagia – difficulty swallowing

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82
Q

Which lower motor neurone controls the tongue?

A

Hypoglossal Nerve (CN XII)

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83
Q

What might you see in the tongue of an MND patient?

A

Fasciculations and spasticity

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84
Q

What makes up the association cortex?

A

Frontal Cortex Parietal Cortex NOTE: this is not exactly part of the motor pathway but it influences the planning and execution of movements

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85
Q

What might you see in the tongue of an MND patient?

A

Fasciculations and spasticity

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86
Q

Which lower motor neurone controls the tongue?

A

Hypoglossal Nerve (CN XII)

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87
Q

List some signs of ALS.

A

 Increased muscle tone (spasticity in the limbs and tongue)  Brisk limb and jaw reflexes (hyperreflexia)  BABINSKI’s SIGN  Loss of dexterity  Dyarthria – difficulty speaking  Dysphagia – difficulty swallowing

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88
Q

Describe how the symptoms of ALS change as the disease progresses.

A

Some patients may present with only upper motor lesion symptoms or only lower motor lesion symptoms but as the disorder progresses, both upper and lower motor neurone signs will be coexistent.

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89
Q

What is the term given for upper AND lower motor neurone disease?

A

Amyotrophic Lateral Sclerosis (ALS)

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90
Q

What is motor neurone disease?

A

A progressive neurodegenerative disorder of the motor system – it is a spectrum of disorders. MND can affect upper motor neurones, lower motor neurones or both

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91
Q

Describe the features of lower motor neurone lesions.

A

It is generally the opposite of upper motor neurone lesions.  Hypotonia  Hyporeflexia  Weakness  Muscle Atrophy– the metabolic trophic support to the muscles is lost  FASCICULATIONS– damages motor units produce spontaneous action potentials, resulting in a visible twitch  Fibrillations – twitch of individual muscle fibres (aren’t visible to the naked eye but are picked up on EMG)

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92
Q

What are the two most common causes of apraxia?

A

Stroke and Dementia

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93
Q

Lesions in which part of the brain tend to cause apraxia?

A

Inferior parietal lobe Frontal lobe (premotor cortex and supplementary motor area)

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94
Q

Define apraxia.

A

A disorder of skilled movement not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea). It is caused by the loss of information on how to perform skilled tasks rather than loss of motor command to the muscles.

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95
Q

Why is muscle atrophy not seen in upper motor neurone lesions?

A

The lower motor neurones are still in tact and they have a role inproviding nutrients to the muscle. There will still be partial atrophy due to muscle disuse.

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96
Q

What is Babinski’s Sign?

A

You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards) In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.

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97
Q

Describe the features of upper motor neurone lesions.

A

Initially you get loss of function of the motor neurones leading to:  Paresis = graded weakness of movement  Paralysis = complete loss of muscle activity After a few weeks, the loss of descending inhibitory pathways leads to increased abnormal motor activity such as:  Spasticity (increased muscle tone)  Hyperreflexia (exaggerated reflexes)  Clonus (abnormal oscillatory muscle contraction)  Babinski’s Sign  NO muscle atrophy

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98
Q

What are the two parts of the association cortex that are involved in motor control? State their functions.

A

Posterior Parietal Cortex – ensures movements are targeted accurately to objects in external space Prefrontal Cortex – involved in the selection of appropriate movements for a particular course of action

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99
Q

What is the function of the supplementary motor area?

A

Planning complex internally driven voluntary movements e.g. speech It also becomes active when you are thinking about movement before movement (e.g. rehearsing a dance)

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100
Q

What is the function of the premotor cortex?

A

Plans movements and assembles movements into coordinated actions NOTE: premotor cortex is anterior to the primary motor cortex

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101
Q

How can the cortical representation of a muscle in the motor cortex change?

A

The more we use a muscle, the bigger the representation of that muscle in the cortex.

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102
Q

What diagram depicts the somatotopic organisation of the primary motor cortex?

A

Penfield’s Motor Homunculus

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103
Q

Describe the structure and function of the anterior corticospinal tract.

A

The anterior corticospinal tract is made up of the upper motor neurone axons coming from the primary motor cortex that do not decussate at the pyramidal decussation. These fibres cross the midline at the level of the spinal cord It controls proximal musculature.

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104
Q

Describe the structure and function of the tectospinal tract.

A

It originates in the superior colliculus (brainstem) Its function is not known but is most likely involved in reflexive turning of the head to orient to visual stimuli.

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105
Q

Describe the structure and function of the reticulospinal tract.

A

It originates in the reticular formation in the brainstem then goes down the spinal cord to innervate muscle. It is involved in complex actions:  Orienting  Stretching  Maintaining a complex posture

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106
Q

Describe the structure and function of the vestibulospinal tract.

A

The lateral vestibulospinal tract originates at the lateral vestibular nucleus. The medial vestibulospinal tract originates at the medial vestibular nucleus. They mediate postural adjustments and head and eye movements

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107
Q

What is the function of the rubrospinal tract?

A

It is an alternative pathway that allows voluntary motor commands to be sent down the spinal cord meaning that the body can compensate for a lesion in the primary motor cortex. It also has a role in movement velocity.

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108
Q

Where does the rubrospinal tract originate?

A

Red nucleus of the midbrain

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109
Q

Describe the structure and function of the lateral corticospinal tract.

A

The lateral corticospinal tract originates in the primary motor cortex from the Betz cells. Their axons pass down through the brainstem and decussate at the pyramidal decussation in the medulla. It then passes down the spinal cord and synapses with a lower motor neurone. It goes onto control mainly the distal musculature. NOTE: 90% of axons from the primary motor cortex decussate at the medulla (these are the lateral corticospinal tract axons). The 10% that don’t decussate form the anterior corticospinal tract.

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110
Q

What is the function of each of these types of pathway?

A

Lateral  Control of proximal and distal musculature  Voluntary movements or arms and legs Medial  Control of axial muscles  Balance and posture

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111
Q

Which tracts fall into each of these types?

A

Lateral  Lateral corticospinal tract  Rubrospinal tract Medial  Anterior corticospinal tract  Reticulospinal tract  Vestibulospinal tract  Tectospinal tract

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112
Q

What are the two types of descending pathway?

A

Lateral and Medial

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113
Q

Describe what happens to the upper motor neurones that come from the primary motor cortex.

A

They travel through the brainstem to the pyramidal decussation in themedulla where 90% of the axons cross the midline. These axons continue down the spinal cord and synapse with a lower motor neurone and exit into a peripheral nerve to the reach the skeletal muscle. The pathway of the corticobulbar tract is somewhat similar – upper motor neurones go down into the brainstem and synapse with a lower motor neurone and they exit to the muscles of the face

114
Q

Where are these cells located within the grey matter and which tracts originate from here?

A

They are found in the 5th layer of grey matter The corticospinal tracts originate from here

115
Q

What are the most important cells in the primary motor cortex?

A

Betz Cells (pyramidal cells)

116
Q

What is another name given to the three parts of the motor cortex?

A

Primary Motor Cortex = Broadmann’s Area 4 Premotor + Supplementary Motor Area = Broadmann’s Area 6

117
Q

Which lobe are the three parts of the motor cortex found in? Describe their arrangement.

A

Frontal (anterior to the central sulcus) The primary motor cortex is on the precentral gyrus The premotor cortex and the supplementary motor area are anterior to the primary motor area

118
Q

Describe the side loops of this descending pathway and their role.

A

The descending pathway also has two side loops that go to the cerebellum and basal ganglia The cerebellum and basal ganglia check the motor information before ittravels to the muscles and has its effect

119
Q

What are the two parts of the pyramidal (descending) system?

A

Corticospinal Tract – starts in the cortex and exits and innervates the muscles in the arms and legs Corticobulbar Tract – starts in the cortex then exits and innervates the muscles in the face

120
Q

What are the two enlargements in the spinal cord and what is their significance?

A

Cervical enlargement (C4-T1) – has extra motor neurons that go to the muscles of the upper limb Lumbosacral enlargement (L2-S3) – has extra motor neurons that go to the muscles of the lower limb

121
Q

What are the little protrusion of pia mater around the spinal cord called?

A

Denticulate ligaments

122
Q

Which space is present in the spinal meninges but not in the cranial meninges?

A

Epidural space – this can be used for injecting anaesthetics

123
Q

What are the three most important tracts in spinal cord injury? State their roles.

A

Lateral corticospinal tract – fine motor movements Dorsal columns – touch, pressure, vibration, proprioception Spinothalamic tract – pain and temperature

124
Q

What are the two stages of lateral corticospinal tract damage?

A

SPINAL SHOCK – you get loss of reflexes below the level of the lesion leading to flaccid paralysis. The limbs become floppy and there is little muscle tone RETURN OF REFLEXES – you get hyperreflexia and spasticity. The patient experiences spontaneous muscle contraction and there is very high muscle tone – rigid paralysis

125
Q

Where do the upper motor neurons within the lateral corticospinal tract decussate?

A

Pyramidal decussation in the medulla

126
Q

If you have a unilateral lesion of the lateral corticospinal tract in the mid-thoracic region, where will the deficit be?

A

Ipsilateral – on the same side as the lesion because the fibres decussate at the pyramidal decussation in the medulla

127
Q

Where do the sensory fibres of the dorsal columns decussate?

A

Sensory decussation in the medulla

128
Q

How are pain neurons arranged differently to other sensory and motor neurons?

A

The first order neurons synapse in the dorsal horn and then the second order neuron crosses to the contralateral side immediately (at the level of the synapse with the first order neurone) The second order neurons then ascend on the contralateral side

129
Q

What is syringomyelia? Describe and explain its features.

A

Enlargement of the central canal (the space is called a syrinx) This selectively affects the spinothalamic fibres that are crossing at the level of the lesion and it does not affect fibres that have alreadycrossed So if the enlargement of the central canal is in the region of the cervical enlargement, you could get loss of pain/temperature sensation in the arms but not the legs (because those fibres would already have crossed and would be ascending in the spinothalamic tract away from the central canal)

130
Q

Spinothalamic anterior

A

-consicous sensation -crude touch, pressure first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus-third order neurons synapse in primary sensory cortex

131
Q

Spinothalamic lateral

A

-consicous sensation -pain, temperature -first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus -third order neurons synapse in primary sensory cortex

132
Q

Posterior column

A

-consicous sensation -fine touch, pressure, vibration, proprioreception -first order synapses at the medulla -decussates at the medulla -second order synapses in thalamus -third order synapses with primary sensory cortex

133
Q

Spinocerebellar posterior

A

-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -NO decussation second order synapse at cerebellum -NO 3rd order

134
Q

Spinothalamic anterior

A

-consicous sensation -crude touch, pressure first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus-third order neurons synapse in primary sensory cortex

135
Q

Spinothalamic lateral

A

-consicous sensation -pain, temperature -first order synapse in dorsal root of spinal column -decussation happens with second order neuron in spinal column -second order synapses on ventral nuclei of thalamus -third order neurons synapse in primary sensory cortex

136
Q

Posterior column

A

-consicous sensation -fine touch, pressure, vibration, proprioreception -first order synapses at the medulla -decussates at the medulla -second order synapses in thalamus -third order synapses with primary sensory cortex

137
Q

Spinocerebellar posterior

A

-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -NO decussation second order synapse at cerebellum -NO 3rd order

138
Q

Spinocerebellar anterior

A

-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -DECUSSATION -second order (interneurons) synapse at cerebellum -NO 3rd order

139
Q

Spinocerebellar anterior

A

-subconscious sensation -proprioceptive info about position of skeletal muscles, tendons and joints -DECUSSATION -second order (interneurons) synapse at cerebellum -NO 3rd order

140
Q

What is the morphology of somatic sensory neurons?

A

Pseudounipolar - they do not have any dendrites

141
Q

What is the equivalent of astrocytes in the PNS?

A

Satellite cells

142
Q

Describe the packaging of nerve axons into larger structures.

A

Axons are packaged into fascicles and the fascicles are packaged into nerves.

143
Q

What are the three layers of connective tissue found in nerves?

A

Endoneurium - wraps around individual axons Perineurium - wraps around fascicles Epineurium - wraps around nerves REMEMBER: unmyelinated axons also have Schwann cells wrapped around them, the difference is that they only have one layer of membrane around them and one Schwann cell can accommodate many axons.

144
Q

Describe the arrangement of autonomic motor neurons.

A

Autonomic motor neurons have a preganglionic neuron and a postganglionic neuron with an autonomic ganglion in the middle. The location of the autonomic ganglion varies depending on whether it is sympathetic or parasympathetic.

145
Q

Which roots do motor and sensory nerves go out of?

A

Motor = ventral Sensory = dorsal

146
Q

Where do autonomic sensory neurons have their cell bodies?

A

In the dorsal root ganglion

147
Q

What is a myotome?

A

The muscle that a spinal nerve innervates

148
Q

What spinal nerves make up the brachial plexus?

A

C5-T1

149
Q

What are the nerves called that are leaving the brachial plexus?

A

Peripheral nerves

150
Q

Describe the differences in the dermatomes of spinal nerves and peripheral nerves.

A

Spinal nerves = stripey Peripheral nerves = patchy

151
Q

Describe the process of regeneration following peripheral nerve injury.

A

With compression injuries, the axoplasm is separated but the endoneurium is still in tact. The axon distal to the compression (further away from the cell body) degenerated - macrophages invade and phagocytose the cell debris. Axons sprouts then grow down the endoneurium. There is competition between the axonal sprouts to reach the target organ. When the first axon sprout reaches the target cell, the other axon sprouts regress. The axon then widens and a myelin sheath forms. The only difference is that the internodal distance is reduced so the conduction speed is reduced.

152
Q

What could happen if the damage to the neuron is so severe that there are no guidance cues at all for the axonal sprouts?

A

A neuroma could form which is very painful and needs to be surgically removed.

153
Q

What are the two types of peripheral neuropathy? Describe them.

A

Segmental Demyelination - loss of a Schwann cell hear and there. This will not kill the cell but it will slow down the action potential. Axonal Degeneration - once you already have degeneration of an axon, the myelin also degenerates and you get a conduction block

154
Q

What are two techniques of diagnosing peripheral neuropathy?

A

Conduction velocity Nerve biopsy

155
Q

What are the three main dopaminergic pathways in the brain?

A

Nigrostriatal Mesolimbic Tuberoinfundibular system

156
Q

Where are each of these pathways found?

A

Nigrostriatal– projecting from the substantia nigra pars compacta to the striatum Mesolimbic– projecting from the ventral tegmental area to the nucleus accumbens, frontal cortex, limbic cortex and olfactory tubercle Tuburoinfundibular system– projecting from the arcuate nucleus in the hypothalamus to the median eminence and pituitary gland

157
Q

What are the roles of these pathways?

A

Nigrostriatal – control of movement Mesolimbic – involved in emotion Tuburoinfundibular system – regulate hormone secretion

158
Q

What are the two families of dopamine receptors and which receptors fall into each of these families?

A

D1 family – D1 + D5 D2 family – D2, D3 + D4

159
Q

Describe dopamine synthesis.

A

Tyrosine is converted by tyrosine hydroxylase to DOPA DOPA is converted by DOPA decarboxylase to Dopamine

160
Q

Is Parkinson’s disease more common in males or females?

A

Males – 4:1

161
Q

What percentage of all cases of Parkinson’s disease is accounted for by familial Parkinson’s disease?

A

8% The rest are idiopathic

162
Q

What are the possible causes of idiopathic Parkinson’s disease?

A

Possibly a combination of environmental, oxidative stress, altered protein metabolism and risk genes

163
Q

What are the cardinal signs of Parkinson’ disease?

A

Resting tremor (pill-rolling tremor) Rigidity (stiffness – limbs feel weak and heavy) Bradykinesia (slowness of movement) Postural abnormality

164
Q

What are the presenting symptoms of Parkinson’s disease?

A

Pill-rolling resting tremor Difficulty with fine movements (micrographia) Poverty of blinking Hypomimic face Monotony of speech and loss of volume of voice Disorders of posture – flexion of the neck and trunk Lack of arm swing Loss of balance – lack of righting reflex, retropulsion Short steps, shuffling gait

165
Q

Describe the initial distribution of symptoms across the body.

A

Unilateral onset Symptoms spread to both sides Generally symptoms worsen with some patients becoming severely disabled

166
Q

What are some non-motor symptoms of Parkinson’s disease?

A

Depression Pain Taste/smell disturbances Cognitive decline/dementia Autonomic dysfunction (constipation, postural hypotension, urinary frequency/urgency, impotence, increased sweating)

167
Q

What is the main area of the brain that is affected by Parkinson’s disease?

A

Substantia nigra Other brain areas affected: locus coeruleus, dorsal vagus nucleus, nucleus basalis of Mynert

168
Q

Describe the neuropathology of Parkinson’s disease.

A

Putamen-projecting pathways degenerate significantly Lewy bodies (large circular structure with bright core and white surrounding, packed with alpha-synuclein) also present – this is probably a defensive mechanism to protect against toxic altered proteins

169
Q

What are the stages of Parkinson’s disease?

A

1-2 = dorsal motor nucleus of vagus, raphe nucleus, locus coeruleus 3 = substantia nigra pars compacta 4 = amygdala, nucleus of Meynert, hippocampus 5-6 = cingulate cortex, temporal cortex, frontal cortex, parietal cortex, occipital cortex

170
Q

What is the main biochemical change seen in Parkinson’s disease?

A

Marked reduction in the caudate nucleus/putamen dopamine content

171
Q

What proportion of dopaminergic neurones of the nigrostriatal dopaminergic pathway must be lost before symptoms occur?

A

80-85% of dopaminergic neurones and 70% of striatal dopamine must be depleted before symptoms appear

172
Q

What is the reason for this?

A

There are compensatory mechanisms e.g. neurone overactivity and increase in dopamine receptors

173
Q

What other type of drug has to be given with L-DOPA in dopamine replacement therapy and why?

A

Peripheral DOPA decarboxylase inhibitor This prevents the conversion of L-DOPA to dopamine by peripheral DOPA decarboxylase (this can cause nausea and vomiting)

174
Q

State two different preparation of dopamine replacement therapy.

A

Sinamet = Carbodopa + L-DOPA Madopar = Benserazide + L-DOPA

175
Q

What does L-DOPA treat?

A

Hypokinesia Tremor Rigidity

176
Q

Describe how the dosage of L-DOPA is changed with continued treatment.

A

It is started low and increased until maximum benefit of drug is achieved without side effects Effectiveness of L-DOPA declines with time

177
Q

What are the acute side effects of L-DOPA?

A

Nausea (prevented by domperidone) Hypotension Psychological effects (schizophrenia like syndrome with dellusions, hallucinations, confusion, disorientation and nightmares)

178
Q

What are the chronic side effects of L-DOPA?

A

Dyskinesias (abnormal movement of limbs and face – can occur within 2 years of treatment – disappear with reduced dose) Rapid fluctuations in clinical state (off periods may last for minutes to hours

179
Q

Name three dopamine agonists.

A

Bromocriptine Ropinerol Pergolide

180
Q

Which receptors do they act on?

A

D2 receptor

181
Q

What are the benefits of dopamine agonists over L-DOPA?

A

Longer duration of action Smoother and more sustained response Actions independent of dopaminergic neurones Incidence of dyskinesias is less NOTE: L-DOPA is still the gold standard

182
Q

What are the adverse effects of dopamine agonists?

A

Common – confusion, dizziness, nausea/vomiting, hallucinations Rare – constipation, headache, dyskinesia

183
Q

What structure used to be present in older dopamine agonists that caused quite serious clinical problems?

A

Ergot ring This caused problems with heart valves

184
Q

What has been the consequence of the removal of this structure within dopamine agonists?

A

Development of addictive behaviour e.g. gambling

185
Q

Name two MAO inhibitors.

A

Deprenyl (selegiline) Rasagiline

186
Q

What are the effects of Deprenyl?

A

Selective for MAO-B (this predominates in dopaminergic areas of CNS) Does NOT have the peripheral side effects of non-selective MAO inhibitors Can be given in combination with L-DOPA (reduce dose of L-DOPA by 30-50%)

187
Q

What are the side effects of Deprenyl?

A

RARE Hypotension Nausea/vomiting Confusion and agitation

188
Q

What are the effects of Rasagiline?

A

It has neuroprotective properties by inhibiting apoptosis (promotes anti-apoptosis genes) NOTE: early clinical trials show this drug might slow down the progression of disease but subsequent studies haven’t been so promising

189
Q

Name two COMT inhibitors.

A

Tolocapone (CNS + PNS) Entacapone (PNS)

190
Q

What are the effects of COMT inhibition in the CNS?

A

Prevents breakdown of dopamine in the brain

191
Q

What are the effects of COMT inhibition in the peripheral nervous system?

A

Peripheral COMT converts L-DOPA to 3-O-methyl DOPA (3-OMD) 3-OMD competes with L-DOPA for the transport system that transports it across the BBB COMT inhibitors stop 3-OMD production and hence there is less competition for L-DOPA Result: REDUCE L-DOPA DOSAGE

192
Q

What are the side effects of COMT inhibitors?

A

Cardiovascular complications

193
Q

What percentage of the general population is affected by schizophrenia?

A

1%

194
Q

What are the symptoms of schizophrenia?

A

Positive Symptoms (overt symptoms that should NOT be present)  Hallucinations  Delusions  Disorganised thoughts Negative Symptoms (lack of characteristics that SHOULD be present)  Reduced speech  Lack of emotional and facial expression  Diminished ability to begin and sustain activity  Decreased ability to find pleasure in everyday life  Social withdrawal Cognitive deficits  Memory  Attention  Planning  Decision making

195
Q

What appears to have quite a strong contribution to the development of schizophrenia?

A

Genetics

196
Q

Once schizophrenia has been diagnosed, what are the four main outcomes for patients?

A

1 – illness resolves completely, with or without treatment and never returns (10-20%) 2 – illness recurs repeatedly with full recovery between episodes (30-35%) 3 – illness recurs repeatedly with incomplete recovery and a persistent defective state develops, becoming more profound with each successive relapse (30-35%) 4 – illness pursues down a downhill course from the beginning (10-20%) NOTE: most cases are relapsing and remitting

197
Q

Describe the involvement of dopamine in schizophrenia.

A

Positive symptoms – results from excessive dopamine transmission in the mesolimbic and striatal region (D2-mediated) Negative symptoms – results from dopamine deficit in the pre-frontal region (D1-mediated)

198
Q

What evidence has arisen that supports this hypothesis?

A

Dopamine agonists can induce various psychotic reactions Typical antipsychotics are dopamine receptor antagonists (blocking D2 receptors)

199
Q

Describe the involvement of glutamate in schizophrenia.

A

NMDA is a glutamate receptor Glutamate exerts an excitatory influence over the GABA-ergic striatal neurones and dopamine exerts an inhibitory influence These GABA-ergic striatal neurones project to the thalamus and constitute a sensory ‘gate’ Too little glutamate or too much dopamine disables this gate, allowing uninhibited sensory input to reach the cortex NOTE: you find reduced glutamate concentration and reduced glutamate receptors in post-mortem schizophrenic brains. Also NMDA receptor antagonists can produce psychotic symptoms

200
Q

What is the most robust gene associated with schizophrenia?

A

Neuregulin-1

201
Q

What are all the susceptibility genes for schizophrenia associatedwith?

A

Dopamine and glutamate neurotransmission

202
Q

What type of drug are all neuroleptics?

A

Dopamine receptor antagonists (D2 receptors) NOTE: most neuroleptics block other receptors

203
Q

Which symptoms do neuroleptic drugs treat?

A

Positive symptoms ONLY

204
Q

What are the initial effects of neuroleptic drugs?

A

Initial increase in dopamine synthesis and neuronal activity – this declines with time

205
Q

What is meant by an atypical antipsychotic?

A

Newer antipsychotics are given this term – they have fewer extrapyramidal side effects

206
Q

Name an atypical antipsychotic.

A

Clozapine

207
Q

Name a typical antipsychotic.

A

Haloperidol

208
Q

What is an important other action of neuroleptics?

A

Anti-emetic Because they block dopamine receptors in the chemotactic trigger zone Phenothiazine is a neuroleptic that is really good at preventingnausea/vomiting caused by drugs NOTE: many neuroleptics also block histamine receptors – this is effective at controlling motion sickness

209
Q

What are the extrapyramidal side effects of antipsychotics caused by?

A

Blockade of dopamine receptors in the nigrostriatal system can induce Parkinson-like side effects

210
Q

What are the two main extra-pyramidal side effects? Acute Dystonia

A

 Involuntary movements  Muscle spasm, protruding tongue, fixed upward gaze, neck spasm etc.  Often accompanied by Parkinson’s like features  Occur in the FIRST FEW WEEKS and often decline with ongoing therapy  Reversible with withdrawal of the drug or anti-cholinergics Tardive Dyskinesias  Involuntary movements  Involving the face and tongue, but also trunk and limbs  Occur in 20% of patients after SEVERAL MONTHS/YEARS of therapy  Made WORSE by drug withdrawal or anti-cholinergics

211
Q

What are the unwanted effects of antipsychotics?

A

Endocrine effects – loss of inhibition of prolactin secretion leads to hyperprolactinaemia (can lead to breast swelling and sometimes lactation) Blocking alpha-adrenoceptors – postural hypotension Blocking 5-HT receptors – weight gain Blockade of muscarinic receptors – typical anti-muscarinic effects e.g. blurring of vision, increased intra-ocular pressure, dry mouth, constipation, urinary retention

212
Q

What test is used to see if someone has peripheral neuropathy?

A

Monofilament test

213
Q

What is the most common site of ulcers on the foot?

A

Ball of the foot

214
Q

What three arms of neuropathy are involved in causing foot ulceration and how are they involved? Motor Sensory Autonomic

A

Motor– causes imbalance between extensors and long plantar flexors causing an abnormal shape of the foot. This means there will be increased pressure being applied on the ball of the foot and knuckles ofthe toes. Sensory Autonomic– can lead to abnormal blood flow (increase pulse pressure in the foot). It also reduces sweating, which normally protects the foot from minor disease.

215
Q

What effect can sugar binding to haemoglobin have on the feet?

A

Makes the tendons less flexible – limits joint mobility

216
Q

What are the three types of diabetic feet?

A

Neuropathic Foot Ischaemic Foot Neuro-ischaemic Foot

217
Q

Describe the neuropathic foot. Where is the most common site of ulceration in these feet?

A

Numb Warm (because blood flow isn’t regulated properly) Dry Palpable foot pulses Ulcers – at points of high-pressure loading

218
Q

Describe the ischaemic foot. Where is the most common site of ulceration in these feet?

A

Cold Pulseless Ulcers – at foot margins

219
Q

What is Charcot foot?

A

The neuropathy leads to joint overuse and misuse This leads to bones losing their normal articulations The abnormal foot shape makes it at extreme risk of ulceration

220
Q

What can ulceration of the foot lead to?

A

Osteomyelitis

221
Q

State the three main sites of microvascular complications.

A

Retinal arteries (retinopathy) Glomerular arterioles (nephropathy) Vasa vasorum (neuropathy)

222
Q

What factors correlate with risk of microvascular and macrovascular complications?

A

Glycaemic control (HbA1c) Hypertension Other factors such as glycaemic memory and genetics can contribute

223
Q

Describe the mechanism of glucose damage to blood vessels.

A

Hyperglycaemia leads to oxidative stress and hypoxia This triggers an inflammatory cascade, which leads to damage

224
Q

What instrument is used to look into the eye?

A

Fundoscope

225
Q

Where is the optic disc relative to the macula on the back of the eye?

A

The optic disc is nasal to the macula

226
Q

What are the 4 types of diabetic retinopathy?

A

Background Pre-proliferative Proliferative Maculopathy

227
Q

What three features do you see in background diabetic retinopathy?

A

Hard exudates Microaneurysms Blot haemorrhages

228
Q

What are hard exudates caused by?

A

Leakage of lipid contents makes the back of the eye look a cheesy colour

229
Q

Describe pre-proliferative diabetic retinopathy.

A

Soft exudates (cotton wool spots) There will be some haemorrhages

230
Q

What do soft exudates indicate?

A

Retinal ischaemia

231
Q

Describe proliferative diabetic retinopathy.

A

Involves the formation of new vessels (in response to retinal ischaemia) The new vessels are generally more fragile and can bleed at any time

232
Q

Describe maculopathy.

A

Presence of hard exudates in the macula This is the same disease as background diabetic retinopathy, it’s just that the hard exudates are in the macula This can threaten direct vision

233
Q

What are the steps taken in managing background diabetic retinopathy?

A

Improve blood glucose control

234
Q

What is the treatment for pre-proliferative and proliferative diabetic retinopathy?

A

Pan-retinal photocoagulation

235
Q

Describe the treatment of maculopathy.

A

You need a grid of photocoagulation in the affected area (aim to limit damage to the macula so you don’t do pan-retinal photo coagulation)

236
Q

State some histological features of diabetic nephropathy.

A

Mesangial expansion Basement membrane thickening Glomerulosclerosis (hardening of the capillaries)

237
Q

In diabetic nephropathy you get over production of matrix. Whatcan this be caused by?

A

Effects of prolonged exposure to high glucose or glycosylated proteins A rise in pressure within the glomerular capillaries Angiotensin II

238
Q

State 3 clinical features of diabetic nephropathy.

A

Progressive proteinuria Increased blood pressure Deranged renal function

239
Q

What is the normal range for proteinuria?

A

< 30 mg/24hr

240
Q

Why do patients with diabetic nephropathy get oedematous?

A

Increased proteinuria means that they are losing albumin through their urine This decreases serum albumin hence decreases the osmotic potential of the plasma so less fluid is drawn back into the circulation

241
Q

Describe some strategies for intervention of patients with diabetic nephropathy.

A

Improve blood glucose control Blood pressure control Inhibition of the activity of the renin-angiotensin system Stopping smoking

242
Q

What effect does angiotensin II have on endothelial cells?

A

It makes endothelial cells more rigid

243
Q

Where is renin produced?

A

Juxtaglomerular apparatus

244
Q

What can stimulate renin release?

A

Low renal perfusion (i.e. low blood pressure)

245
Q

Where is ACE found?

A

Lungs

246
Q

State some drug target sites in the renin-angiotensin system.

A

Drugs blocking renin activity ACE inhibitors Angiotensin II receptor blockers (ARBs)

247
Q

What causes diabetic neuropathy?

A

Occlusion of the vasa vasorum

248
Q

State 6 different types of diabetic neuropathy.

A

Peripheral polyneuropathy Mononeuropathy Mononeuritis multiplex Radiculopathy Autonomic neuropathy Diabetic amyotrophy

249
Q

What can peripheral neuropathy lead to and how can it be tested?

A

Loss of sensation can lead to damage going unnoticed It also leads to loss of ankle jerks and loss of vibrational sense Inappropriate use of joints can lead to Charcot joints Test – monofilament examination

250
Q

What is mononeuropathy?

A

Usually sudden motor loss e.g. wrist drop or foot drop Can also cause cranial nerve palsy

251
Q

Why is the pupil spared in pupil sparing third nerve palsy?

A

The parasympathetic fibres, that are responsible for the diameter of the pupil, run on the outside of the main nerve so they don’t lose their blood supply in diabetes

252
Q

How would an aneurysm causing third nerve palsy present differently to third nerve palsy caused by diabetes?

A

There would be fixed pupil dilation This is because the parasympathetic fibres would also be affected

253
Q

What is mononeuritis multiplex?

A

A random combination of peripheral nerve lesions

254
Q

What is radiculopathy?

A

Pain over SPINAL nerves Usually affecting a dermatome on the abdomen or chest wall

255
Q

What are the effects of autonomic neuropathy on the GI tract?

A

Difficulty swallowing Delayed gastric emptying Constipation/nocturnal diarrhoea NOTE: it can also lead to bladder dysfunction

256
Q

What are the effects of autonomic neuropathy on the CVS?

A

Postural hypotension There have been reports of sudden cardiac death

257
Q

How can you check for autonomic neuropathy?

A

Measure changes in heart rate due to Valsalva manoeuvre Look at an ECG and compare the R-R intervals

258
Q

What four factors affect the force generation in muscle contraction?

A

Recruitment of motor units Filament overlap Velocity and direction of movement Frequency of stimulus

259
Q

What is a motor unit?

A

One motor neuron and all the muscle fibres it innervates

260
Q

What happens if all the motor units are recruited for muscle contraction?

A

You get maximum voluntary contraction (MVC)

261
Q

Where are lower motor neurons found?

A

In the anterior horn of the grey matter

262
Q

What is a tetanus?

A

Prolonger contraction of a muscle due to rapidly repeated stimuli

263
Q

What causes unfused tetanus?

A

If the frequency is not high enough for fused tetanus - there is enough time in between action potentials for the force of contraction to drop slightly before the next action potential causes the next contraction.

264
Q

What is the difference between concentric and eccentric contraction?

A

Eccentric contraction generates more force

265
Q

How does velocity and direction of movement affect force of contraction?

A

The greater the velocity the lower the force of contraction

266
Q

Why is ATP needed for in muscle contraction?

A

ATP is needed for the detachment of myosin from actin ATP is also needed for the reabsorption of calcium into the sarcoplasmic reticulum

267
Q

What hydrolyses phosphocreatine and how much ATP does this generate?

A

Creatine Phosphokinase 1 ATP

268
Q

Why is tetanus not possible in cardiac muscle?

A

There is a very long absolute refractory period meaning that the once the heart muscle is available to be restimulated, it is already quite a long way through the contraction process.

269
Q

Describe the excitation-contraction coupling of smooth muscle.

A

Depolarisation causes the opening of voltage gated calcium channels so calcium ions move into the cell. The calcium ions bind to calmodulin and form a Ca-CaM complex. The Ca-CaM complex activates myosin light chain kinase (MLCK), which then phosphorylates myosin light chains and leads to contraction.

270
Q

The axons from which cells int eh motor cortex form the corticospinal and corticobulbar tracts?

A

Pyramidal cells

271
Q

How do the coritcospinal and corticobulbar tracts descend from the motor cortex to the brainstem?

A
  • Via the corona radiata, internal capsule and cerebral peduncle
272
Q

How do upper motor neurone (UMN) syndromes arise?

A
  • When the descending motor pathways are damaged at the level of the motor cortex or at any point of the descending pathway prior to the final synaps eiwth the motor neurones of the spinal cord or cranial enrve nculei
273
Q

How do lower motor neurone syndromes arise?

A
  • When damage occurs at the level of the motor neurones in the ventral horn of the spinal cord
  • In the case of the spinal cord, this menas damage to the ventral roots and peripheral nerves leding to the muscles
274
Q

What will a subcortical lesion (tumor, hematoma, infarct etc) result in?

A

Contralateral paresis of hand or arm.

275
Q

What will a internal capsule lesion reuslt in?

A

Contralateral spastic hemiplagia

276
Q

What will a peduncle lesion result in?

A
  • Contralateral spastic hemiplegia, which may be associated with ipsilateral paralysis of the oculomotor nerve - Weber syndrome.​
277
Q

What will a pons lesion result in?

A

Contralateral and possibly bilateral hemiplegia.

278
Q

What will a pyramidal lesion result in?

A

Flaccid contralateral hemiparesis

279
Q

What will a cervical lesion result in?

A

Ipsilateral spastic hemiplegia

280
Q

What will a thoracic lesion result in?

A

Unilateral: Spastic ipsilateral monoplegia. Bilateral: Spastic paraplegia.

281
Q

What will an anterior root lesion result in?

A

The palsy resulting from this lesion is ipsilateral and flaccid as a result of the damage of the peripheral of lower motoneurons.

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