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MD4001 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Brain makes up __% of body weight but __% of cardiac output?

A
  • 2%

- 15%

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2
Q

Can brain cells store nutrients & have alternatives to aerobic respiration?

A

NO

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3
Q

What happens when blood flow is restricted to the brain?

A

Unconsciousness follows within 15 seconds

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4
Q

When does nerve cell damage/death start after blood flow to the brain stops?

A

3 mins

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5
Q

At the core of the brain focal ischaemic lesions are ______, at the edge (penumbra) ______ can occur?

A
  • Irreversible

- Recovery

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6
Q

What are the 4 arteries supplying the brain?

A
  1. x2 Internal carotid arteries (ant)

2. x2 Vertebral arteries (post)

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7
Q

Where does the vertebral artery branch from?

A

1st part of the subclavian artery

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8
Q

Whats the location of the vertebral artery?

A
  • Ascends through foramina in transverse processes (upper 6 cervical)
  • Enters skull via foramen magnum
  • Pierces meninges to enter subarachnoid space
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9
Q

How/where is the Basilar artery formed?

A

Union of the 2 vertebral arteries at the lower border of the ventral pons

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10
Q

How does the basilar artery terminate?

A

Dividing into 2 posterior cerebral arteries

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11
Q

List all 7 vertebral arteries which join to form the basilar artery?

A
  1. Posterior cerebral
  2. Superior cerebellar
  3. Pontine
  4. Labyrinthine
  5. Anterior inferior cerebellar
  6. Posterior inferior cerebellar
  7. Anterior spinal artery
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12
Q

What are the 3 arteries which supply the cerebellum?

they also supply parts of the brainstem

A
  1. Superior cerebellar
  2. Anterior inferior cerebellar
  3. Posterior inferior cerebellar
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13
Q

Where does the internal carotid artery begin?

A

Bifurcation of the common carotid artery

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14
Q

How does the internal carotid artery ascend?

A
  • In neck & passes into skull through carotid canal in temporal bone
  • Passes through cavernous sinus
  • Pierces the dura at anterior clinoid process & enters subarachnoid space
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15
Q

What does the internal carotid artery divide into?

A

Anterior & middle cerebral arteries

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16
Q

What is the Carotid Syphon?

A

Curve in the cavernous segment (C4)

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17
Q

What is the Circle of Willis?

A

Anastomosing system of arteries at the base of the brain

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18
Q

What are the 6 arteries anastomosing in the circle of Willis?

A
  1. Anterior cerebral
  2. Anterior communicating
  3. Posterior communicating
  4. Posterior cerebral
  5. Internal carotid
  6. Middle cerebral
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19
Q

What 4 structures is the circle of Willis closely related to?

A
  1. Cerebral peduncles
  2. Optic chiasma
  3. Pituitary stalk
  4. Oculomotor nerves
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20
Q

What does the anterior cerebral artery (ACA) supply?

A

Structures near the midline

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21
Q

Where does the middle cerebral artery (MCA) pass through?

A

Lateral fissure & emerges onto lateral surface of cerebral hemisphere

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22
Q

What are the Lenticulostriate (lateral striate) arteries?

A

Group of small arteries which arise at the commencement of the middle cerebral artery

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23
Q

What are the symptoms for Middle Cerebral artery (MCA) stroke?

A
  • Contralateral hemiplegia (paralysis)
  • Hemi-sensory loss
  • Contralateral hemianopia (visual pathway)
  • Dysphasia (dominant hemisphere)
  • Anosognosia (neglect/impaired perception defects, non dominant hemisphere)
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24
Q

What are the symptoms for Anterior Cerebral artery (ACA) stroke?

A
  • Weak contralateral leg & arm
  • Sensory loss in contralateral foot & leg
  • Gait apraxia (difficulty in walking movement)
  • Akinetic mutism (paucity of movement and speech)
  • Urinary incontinence
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25
Q

What are the symptoms for Posterior Cerebral artery stroke?

A
  • Contralateral Homonymous hemianopia (same sided visual loss on opposite side of lesion)
  • Macula sparing
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26
Q

What is the blood supply of basal ganglia & internal capsule?

A
  • Medial striate branches of ACA
  • Lateral striate branches of MCA
  • Anterior choroidal
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27
Q

What is the blood supply of the thalamus?

A

Branches of PCA/ posterior communicating

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28
Q

What is the blood supply of the midbrain?

A

PCA/ posterior communicating

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29
Q

What is the blood supply of the Pons?

A
  • Basilar
  • Superior cerebellar (SCA)
  • Anterior inferior cerebellar (AICA)
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30
Q

What is the blood supply of the medulla?

A
  • Vertebral/anterior spinal
  • Inferior cerebellar
  • Basilar
  • Posterior spinal
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31
Q

Where is the arterial lesion for signs of right sided tongue deviation & left sided weakness?

A

Right medial medulla

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32
Q

Where does the circle of willis lie?

A

Subarachnoid space

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33
Q

What can a berry aneurysm in the circle of willis cause?

A

Subarachnoid haemorrhage

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34
Q

Where is a frequent site for a berry aneurysm in the circle of willis?

A

Posterior communicating artery arises from the ICA

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35
Q

What forms the diffusion barrier in the BBB?

A

Endothelial cell + tight junction

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36
Q

Is depression just “feeling blue”?

A
  • NO

- Its not a sign of weakness and people cannot merely “pull themselves together” and get better

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37
Q

What does the World Health Organisation say about depression?

A

“Common mental disorder. Globally, more than 300 million people of all ages suffer from depression”

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38
Q

What is Major depression?

A
  • Unipolar depression (old term)
  • Loss of interest & enjoyment
  • Low mood
  • Emotional, cognitive, physical & behavioural symptoms
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39
Q

What is Dysthymia?

A

Long-term chronic symptoms that do not disable but keep one from functioning well or feeling good

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40
Q

What is Bipolar disorder?

A
  • Called manic-depressive illness

- Severe highs (mania) & lows (depression)

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41
Q

What are the 3 key symptoms for assessing depression via the criteria in DSM-IV (nice guidelines)

A
  1. Persistent sadness or low mood
  2. Marker loss of interest or pleasure
  3. At least 1 of these, most days, most of the time for at least 2weeks
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42
Q

What are the other associated symptoms you ask about when the patient has any one of the 3 key symptoms in DSM-IV?

A
  • Disturbed sleep
  • Appetite/weight
  • Fatigue/loss of energy
  • Agitation/slowing of movements
  • Poor concentration/indecisiveness
  • Worthlessness/excessive inappropriate guilt
  • Suicidal thoughts/acts
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43
Q

What else do you ask about when assessing depression & its severity via DSM-IV?

A
  • Duration
  • Associated disability
  • Past & Family history of mood disorders
  • Availability of social support
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44
Q

What is CG90 (?

A

NICE clinical guidelines appendix C for assessing depression & its severity

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45
Q

What’s the definition of Anhedonia?

A

Loss of interest or pleasure in hobbies & activities that were once enjoyed

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46
Q

What are the cognitive symptoms of depression?

A
  • Negative view of self
  • Poor concentration & reduced attention, difficulty making decisions
  • Mental slowing or rumination
  • Suicidal ideation
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47
Q

What are the biological/behavioural symptoms of depression?

A
  • Lowered appetite, weight loss/gain
  • Insomnia, early-morning, feeling worse in morning
  • Low energy, fatigue
  • Loss of libido
  • Social withdrawal
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48
Q

What 2 questions (according to CG90) should you ask people who may have depression?

A
  1. “During the last month, have you often been bothered by feeling down, depressed or hopeless?”
  2. “During the last month, have you often been bothered by having little interest or pleasure in doing things?”
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49
Q

What are risk factors for depression (combination of factors)?

A
  • Genetic & family
  • Early life experiences
  • Stressful life events
  • Gender
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50
Q

What evidence is there for genetic & family factors of depression?

A
  • “~3 fold increase in 1st-degtree relatives of individuals with major depression”
  • Twin & adoption studies show genetic component
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51
Q

What study shows there is a genetic & family factor for depression?

A

Fava & Kendler (2000)

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52
Q

What early life experiences can increase a person’s vulnerability to depression (Fava & Kendler, 2000)

A
  • Poor parent-child relationship
  • Marital discord & divorce
  • Neglect
  • Physical & sexual abuse
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53
Q

What did the interview that Brown & Harris (1978) did with Women in Camberwell show?

A
  • 15-20% of women were mod-severely depressed with no treatment
  • Rate 3x higher in those who lost their mother before 11 & also experienced severe recent loss
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54
Q

What 3 factors (according to Brown & Harris) contribute to low self-esteem, sense of mastery & hopelessness?

A
  1. Lack of intimate, supportive relationships
  2. Lack of employment
  3. Household >3 children
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55
Q

Most depressions are preceded by a __________?

A

Recent stressful event

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56
Q

According to Fava & Kendler, how does gene-by-environment interaction affect depression?

A

Genetic factors influence overall risk of illness BUT also influence sensitivity of individuals

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57
Q

Do genes on their own cause depression?

A

NO

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58
Q

What factors contribute to why major depression seems to be more common in women?

A
  • They express/report symptoms more
  • Hormones
  • Early life stress (sexual abuse)
  • Additional stresses (responsibilities home/work)
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59
Q

What does NICE guideline CG91 say about depression & chronic illness?

A
  • 2x / 3x more common with chronic physical health problem
  • Occurs in 20% with chronic physical health problem
  • Can both cause & exacerbate depression
  • Depression can be a risk factor in range of physical illnesses
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60
Q

What factors in medical patents cause depression to more regularly appear?

A
  • Life threatening conditions
  • Unpleasant treatments
  • Pain & disability
  • Low social support t& adverse social circumstances
  • Personal/family history
  • Alcohol/substance abuse
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61
Q

Why can assessment of depression in chronically ill patients be problematic?

A
  • Signs of depression (fatigue, insomnia, weight loss) also expression of disease
  • Drug treatments can cause depression (hypertensives, corticosteroids, chemo)
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62
Q

What is the relation of depression & coronary heart disease (CHD)?

A
  • Major depression associated with 2- to 4 fold increase cardiac mortality in MI patients
  • Depressed without cardiac disease have increased risk of cardiac mortality
  • Higher prevalence of smoking, diabetes, reduced exercise
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63
Q

What can depression trigger which contributes to CHD?

A

Dysregulation of neurohormonal system (cortisol & catecholamine secretion)

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64
Q

What are the 4 treatment options for depression?

A
  1. Pharmacological
  2. Psychological
  3. Exercise (mild/mod depression)
  4. Electroconvulsive (severe & complex depression)
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65
Q

What is the model for treatment of depression?

A

Stepped care model (page 16 on CG90)

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66
Q

What are 3 different low-intensity psychosocial interventions for depression?

A
  1. Individual guided self-help based on the principles of cognitive behavioural therapy (CBT)
  2. Computerised cognitive behavioural therapy (CCBT)
  3. Structured group physical activity programme
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67
Q

What is Cognitive behavioural therapy (CBT)?

A
  • Short-term psychological treatment
  • Role of thinking in how we feel & what we do
  • Identifying & challenging unhealthy modes of thinking
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68
Q

What 2 psychological interventions should people with depression & risk of relapse be offered?

A
  1. Individual CBT (relapsed despite antidepressants)

2. Mindfulness-based cognitive therapy (currently well with >3 previous episodes)

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69
Q

In high income countries _ x as many men die of suicide than women.
In low & middle income, ratio _ men to women.

A
  • 3x

- 1.5

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70
Q

What are the 2 myths about suicide?

A
  1. People who talk of suicide do not do it

2. Talking openly about topic of suicide puts “the idea in their head”

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71
Q

What are 4 tips to talking to someone who is suicidal?

A
  1. Address motivation for suicide & develop alternatives
  2. Listen non-judgementally
  3. Don’t be critical
  4. Don’t say “cheer up”, “pull yourself together”
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72
Q

What are the 3 NICE guidelines 90, page 15 for taking a history from someone who there is a risk of self-harm or suicide?

A
  1. Assess whether the person has adequate social support & is aware of sources of help
  2. Arrange help appropriate to the level of risk (primary care staff/specialist)
  3. Advise the person to seek further help if the situation deteriorates.”
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73
Q

Describe the dura mater?

A
  • Tough & fibrous
  • Bridges crevices
  • Attached to skull
  • Includes branches of middle meningeal artery
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74
Q

Describe Arachnoid mater?

A
  • Delicate
  • Sealed bag for CSF
  • Bridges crevices
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75
Q

Describe Arachnoid trabeculae?

A

“Ropes” across subarachnoid space

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76
Q

Where is the Cerebral artery branch embedded in?

A

Pia mater

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77
Q

Describe Pia mater?

A
  • Delicate

- Dips into crevices

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78
Q

What are spaces filled with CSF called?

A

Cisterns

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79
Q

Name the 4 different cisterns in the brain?

A
  1. Superior cistern
  2. Cisterna magna (cerebellomedullaris)
  3. Cisterna pontis
  4. Interpeduncular cistern
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80
Q

What ligaments come off the pia mater?

A

Denticulate ligaments

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81
Q

Why are roots long at cord end?

A

Because spinal column grows faster & longer than spinal cord (S1 root exits well below its origin in cord)

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82
Q

Where can you safely perform a lumbar puncture to sample CSF?

A

Subarachnoid space well below L2, usually L4/5

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83
Q

Describe the veins which drain the brain?

A
  • Thin walls, no valves
  • Lie in subarachnoid space
  • Drain into cranial venous sinuses
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84
Q

What are the 2 groups of veins which drain the brain?

A
  1. External cerebral veins

2. Internal cerebral veins

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85
Q

Name the 3 sinuses that the great cerebral vein drains into?

A
  1. Transverse sinus
  2. Straight sinus
  3. Superior sagital sinus
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86
Q

Whats another name for the great cerebral vein?

A

Vein of Galen

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87
Q

What are the 5 deep veins above the thalamus?

A
  1. Thalamostriate vein
  2. Choroidal vein
  3. Internal cerebral vein
  4. Basal vein
  5. Great cerebral vein
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88
Q

What are the 3 different dural folds called inside the skull?

A
  1. Falx cerbri
  2. Tentorium cerebelli
  3. Tentorial notch
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89
Q

What is the rate of cerebrospinal fluid production?

A

150ml produced at 0.5ml/min & turns over 4x a day

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90
Q

What are the different ventricles of the brain?

A
  • Lateral x2
  • Interventricular foramen
  • 3rd ventricle
  • 4th ventricle
  • Aqueduct
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91
Q

Hows the CSF formed?

A

In choroid plexus and flows out of ventricle system into subarachnoid space via apertures in 4th ventricle

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92
Q

What are the 3 apertures in the 4th ventricle?

A

1 median

2 lateral

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93
Q

What are Arachnoid granulation’s?

A

Projections of the arachnoid membrane into the dural sinuses that allow CSF entrance from subarachnoid space into venous system (superior sagittal sinus)

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94
Q

What is a Subdural haemorrhage?

A
  • Haematoma, usually associated with traumatic brain injury.
  • Blood gathers between inner layer of dura mater & arachnoid mater
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95
Q

How does hydrocephalus occur?

A

Blocked transport, or overproduction/blocked absorption of CSF which dilate the ventricles and cause brain compression

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96
Q

What is a medical treatment for hydrocephalus?

A

Shunt from frontal horn of lateral ventricle into the peritoneum

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97
Q

What does CT stand for?

A

Computerised Tomography

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98
Q

How much more radiation is there in a CT head with contrast compared to a normal chest x-ray?

A

200x more than Chest X-ray

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99
Q

What are the technical points of viewing a CT image?

A
  • Caudal view: looking from patients feet (left on image is the right on patient)
  • More sulci, white bolbs and atrophy as you get older (age effect)
  • Diagonal image plane to avoid too much exposure to the eyes
  • Image is generated by absorption
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100
Q

What is greyer in CT scan- white/grey matter?

A

White matter

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101
Q

What colour does bone and air appear on CT scan?

A
  • BONE: white

- AIR: black

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102
Q

Describe the ABC’S system for head CT & MRI interpretation?

A

A- adequacy, alignment, artifact
B- bones, blood, brain
C- cisterns, ventricles
S- subcutaneous, surfaces, soft tissue

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103
Q

What to look for at “A” in the ABC’S system for CT interpretation?

A
  • Alignment: see if its symmetrical, midline shift

- Artifact: see if there is any metal ruining image or motion when taking the image

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104
Q

What to look for at “B” in the ABC’S system for CT interpretation?

A
  • Bones: fractures
  • Blood: extradural/subdural/subarachinoid haematoma
  • Brain: look for any diffuse axonal injury, infarction, oedema, masses
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105
Q

What to look for at “C” in the ABC’S system for CT interpretation?

A

Cisterns & Ventricles: atrophy, hydrocephalus, oedema, intracranial hypertension, infection

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106
Q

What to look for at “S” in the ABC’S system for CT interpretation?

A

Subcutaneous, Surface & Soft tissue: subdural haematoma, cerebral oedema, compression, lesions, meningioma

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107
Q

What are the technical points of head/neck MRI?

A
  • Caudal view: looking from patients feet (left on image is the right on patient)
  • Age effect
  • Any plane
  • Image generated by emission
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108
Q

When (3) can you not perform a head/neck MRI?

A
  • Pacemaker
  • Cochlear implant
  • Metal around eye/head
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109
Q

How do you know when the MRI image is taken at T1 or T2?

A
  • T1: spinal fluid is black

- T2: spinal fluid is white

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110
Q

What are the 8 different MRI variants?

A
  1. Diffusion weighted
  2. Apparent diffusion coefficient (ADC)
  3. Fluid attenuated inversion recovery (FLAIR)
  4. Gradient echo imaging (GRE)
  5. Echo planar imaging (EPI)
  6. Perfusion
  7. Angiography
  8. Functional spectrography
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111
Q

What does SPECT stand for?

A

Single Photon emission tomography

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112
Q

What does PET stand for?

A

Positron emission tomography

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113
Q

What is the Anterolateral system composed of (3)?

A
  1. Spinothalamic pathways
  2. Spinomesencephalic pathway
  3. Spinoreticular pathway
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114
Q

What are the 2 pathways in the Spinothalamic pathways called?

A
  1. Neospinothalamic (discriminating)

2. Paliospinothalamic (undiscriminating)

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115
Q

What is the purpose of the thalamus in the brainstem?

A
  • Connects reciprocally with every part of the cortex
  • Receives “input” from all of cortex
  • “Gatekeeper” for sensory info
  • Control arousal & somnolence of cortex
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116
Q

What is the purpose of the Mesencephalon (midbrain)?

A
  • Reflexes associated with hearing & vision
  • Fine control of skeletal movement through red nucleus
  • Habituation & motivation via dopaminergic centres
  • Contains cerebral peduncles (ascending/descending info)
  • Contains periaquaductal grey matter (pain modulator)
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117
Q

Where does the Neospinothalamic tract terminate in the anterolateral system?

A

Ventral posterior lateral nucleus (VPL) which is somatotropic so there is locational discrimination

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118
Q

Where does Paliospinothalamic tract terminate in the anterolateral system?

A

Dorsomedial (DM) & intra laminar areas which provide generalised location of pain

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119
Q

What is the Neospinothalamic tract mainly composed of?

A

Aδ fibres (sharp pain)

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120
Q

What is the Paliospinothalamic tract mainly composed of?

A

C fibres (dull pain)

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121
Q

Where is the spinal cord origin of the Spinothalamic & Spinomesencephalic tracts?

A

Laminae 1 & 5 (pain modulation from descending pathways)

122
Q

Where is the spinal cord origin of the Spinoreticular tract?

A

Diffusely in intermediate zone & ventral horn laminae 6-8

123
Q

What is the main function of the anterolateral system?

A

Pain basis for avoidance behaviours that protect us from harm

124
Q

What is the Anterolateral system linked to and why?

A

Strong memory forming circuit via the hippocampus & amygdala

125
Q

Describe what happens in prolonged stimulation of the Paliospinothalamic pathway?

A

Hardest pains to bear & can affect mood & outlook

126
Q

Why does anterolateral system synapse with brainstem nuclei?

A

Increase arousal & pain prevents sleep

127
Q

What is the outcome of the anterolateral system stimulating hypothalamic autonomic circuitry?

A

Pain makes you sweat & feel sick

128
Q

The anterolateral system is positively associated with the ______ system, giving an _______ component?

A
  • Limbic

- Emotional

129
Q

What is the outcome of lesions in the neospinothalamic tract?

A

Decreased pain & temperature on the contralateral side of the body, always 1 or 2 dermatomes below level of lesion (Lissauers tract)

130
Q

What is Cervical Cordotomy?

A

Surgical procedure in which left anterolateral portion of the cord is lesioned using electrical current for terminal disease pain (pain returns ~1yr)

131
Q

What is the feeling when spinothalamic tract lesions, rarely, cause paraesthesia?

A

Searing shooting or burning pain

usually pain/temp deficit

132
Q

What 4 sensations travel in the trigeminal nerve?

A
  1. Pain
  2. Temperature
  3. Discriminatory touch
  4. Proprioception
133
Q

What are the 3 divisions of the Trigeminal brainstem nuclei?

A
  1. Mesencephalic nucleus of V
  2. Main sensory nucleus of V
  3. Spinal nucleus & tract of V
    (motor nucleus of V)
134
Q

What is the function of the trigeminal mesencephalic nucleus?

A

Proprioception from mouth/jaw

135
Q

What is the function of the pontine (main) sensory nucleus?

A

Discriminating touch, vibration & conscious proprioception from face

136
Q

What is the function of the trigeminal motor nucleus?

A

Controls muscles of mastication

137
Q

What is the function of the trigeminal spinal nucleus?

A

Pain & temperature sensation from face, back of tongue, pharynx, larynx & ear

138
Q

What does the spinal trigeminal pathway consist of?

A

Aδ & C fibres which enter the brainstem at mid-pontine level

139
Q

What happens to the Aδ & C fibres in the trigeminal pathway?

A
  • Travel ipsilaterally down cord to spinal trigeminal nucleus (C1) & synapse 2nd neuron
  • Cross midline & ascend in trigeminal lemniscus (trigeminothalamic)
  • Branches come off as trigeminoreticular & trigeminomesencephalic
  • 2nd order neurons synapse with tertiary neurons in VPM lobe of thalamusq
140
Q

What are the sensory symptoms of lesions in the trigeminal pathway?

A

Loss of touch, pain, temp, joint proprioception (conscious), vibrations

141
Q

What are the motor symptoms of lesions in the trigeminal pathway?

A

Loss of control of muscles of mastication, tensor tympani muscle

142
Q

What is Trigeminal neuralgia?

A
  • Common form of trigeminal dysfunction, intense shooting sharp pain in areas innervated by trigeminal nerve often response to light touch
143
Q

What causes Trigeminal neuralgia?

A

Intense quasi-ectopic firing of the nerve either proximal or within the brainstem induced by normally low frequency action potentials

144
Q

What is often associated with Trigeminal neuralgia?

A

De-myelination of the nerve which can lead to reverberation firing in the axon, or other forms of damage

145
Q

What is the treatment for Trigeminal neuralgia?

A

Voltage sensitive sodium channel blockers (phenytoin)

146
Q

What are the 2 types of information fed to the cerebellum?

A
  1. Joint proprioception, cutaneous, muscle spindle & Golgi tendon organ information= real time information about position of limb
  2. All of 1, but integrated with descending modulatory & reflex arc messages= information about how body is moving & how CNS proposes to move limbs
147
Q

How does real time proprioceptive information enter the cerebellum?

A

At inferior peduncle via 2 ipsilateral pathways:

  1. Posterior spinocerebellar tract
  2. Cuneocerebellar tract
148
Q

How does information about how the body is moving & how the CNS proposes to move limbs enter the cerebellum?

A

At superior or both the superior/inferior peduncles via 2 pathways:

  1. Anterior spinocerebellar tract
  2. Rostral spinocerebellar tract
149
Q

How does the posterior Spinocerebellar tract carry non-integrated (real time) proprioceptive information to the cerebellum?

A
  • Sensory axon from lower limbs enter dorsal horn & synapse in Clarkes Column
  • Then ascend to cerebellum & enter inferior peduncle
150
Q

How does the Cuneocerebellar tract carry non-integrated (real time) proprioceptive information to the cerebellum?

A
  • Sensory axon from upper limbs & neck enter dorsal horn, ascend ipsilaterally to accessory Cuneate nucleus & synapse
  • Then secondary neurones enter cerebellum via inferior peduncle
151
Q

How does the Anterior Spinocerebellar tract carry integrated (future movement) proprioceptive & motor information to the cerebellum?

A
  • Sensory axon from lower limb enter dorsal horn & synapse in interneurons (spinal border cells) with collaterals from descending modulatory motor output & local reflex arcs
  • Then cross contralaterally & enter cerebellum via superior peduncle & recross back to ipsilateral side
152
Q

How does the Rostral Spinocerebellar tract carry integrated (future movement) proprioceptive & motor information to cerebellum?

A
  • Sensory axons from upper limbs & neck enter dorsal horn, project to anterolateral portion of ant horn & synapse on spinal border cells with reflex arc collaterals & descending modulatory motor output
  • Then enter cerebellum ipsilaterally via both superior & inferior peduncles
153
Q

What is Friedreich’s ataxia?

A

Inherited disease where spinocerebellar tract becomes increasingly ineffective due to repeats of gene for protein Frataxin

154
Q

What is the function of protein Frataxin?

A

Iron metabolism in mitochondria

155
Q

What are the 3 signs/symptoms of Friedreich’s ataxia?

A
  1. Progressively uncoordinated arm & leg movements
  2. Wide based “reeling” gait
  3. Intention tremor
156
Q

Describe the location of Upper Motor Neuron cell bodies?

A

In brain/brainstem and do NOT project outside the CNS

157
Q

Describe the location of lower motor neuron cell bodies?

A

In motor nuclei of brainstem/ventral horn of spinal cord & project OUTSIDE the CNS to muscle

158
Q

Where does the medial pathways in the lower motor neurons project to?

A

Proximal & axial muscles

159
Q

Where does the lateral pathways in the lower motor neurons project to?

A

Distal muscles

160
Q

What is the function of the Ventromedial (medial) descending pathways from brain to motor centres?

A
  • Mainly control posture & locomotion
  • Control axial & proximal muscles
  • Mainly controlled by brainstem
161
Q

What is the function of the Lateral descending pathways from the brain to motor centres?

A
  • Control voluntary movements
  • Control distal muscles
  • Mainly controlled by cerebral cortex (via corticospinal tracts)
162
Q

Describe the posture control in the ventromedial pathways?

A
  • Vitally important in balance

- Adjusted by involuntary movement driven by predictively (postural set) & reflexively (compensation)

163
Q

What is posture & why do we need it?

A
  • Position of a body & its parts relative to each other
  • The interplay between voluntary/involuntary movement is vital for seamless movement & adaptation to the environment
164
Q

Compensatory responses are based on information sent from what 3 things?

A
  1. Muscle proprioceptors (changes in muscle length/tension)
  2. Sense of balance from movements of head relative to earths gravitational field (vestibular apparatus)
  3. Visual inputs (movements in visual field)
165
Q

Where is the postural set generated?

A

Nuclei in the brainstem which received sensory inputs & feed forward info from voluntary circuit collaterals

166
Q

What does the medial vestibular nucleus give rise to?

A

Bilateral medial vestibular tracts to cervical MNs to provide control over head position

167
Q

What does the lateral vestibular nucleus give rise to?

A

Ipsilateral tract to spinal MNs which although relatively lateral, is still part of involuntary medial system

168
Q

What is the principle effect of lateral vestibulospinal pathway?

A

Ipsilateral extensor motor neurones & inhibit flexor motor neurones innervating the proximal & axial muscles

169
Q

What is the overall effect of the lateral vestibulospinal pathway?

A

Increase tone to antigravity muscles when the vestibular system signals a loss of postural stability

170
Q

What do the vestibulocollic reflexes (medial vestibulospinal) act on?

A

Neck to keep the head stable

171
Q

Describe the symmetrical tonic neck reflex in infancy?

A

Neck flexion induces extension of lower limbs & flexion of upper limbs

172
Q

What are non-vestibulospinal neck reflexes?

A

Cervicocollic reflex

173
Q

What are cervicocollic reflexes mediated by?

A

Proprioceptively by muscle spindles in neck muscles & receptors in joints of cervical vertebrae

174
Q

What does cervicocollic reflexes do?

A

Contraction of muscles in stretched muscles to oppose action & stabilise the head (returning it to normal position)

175
Q

What pathway controlling limb posture is linked to the same sensory apparatus as the cervicocollic reflex?

A

Cervicospinal pathway

176
Q

Describe the cervicospinal asymmetric tonic neck reflex?

A
  • Mediates limb movement as a function of head on trunk position & augments vestibular reflexes
  • Sends messages via vestibular nucleus along vestibulospinal tracts
177
Q

What does decerebrate mean?

A

No cerebral or vestibular input

178
Q

What is the function of the reticulospinal pathway?

A

Co-ordinates movement for maintenance of posture based on feed forward info

179
Q

How does the reticulospinal pathway (medial) work?

A

Excitatory part (pontine reticular nucleus) & inhibitory part (medullary reticular nucleus) receive ascending & descending info from multiple sources & both project to axial antigravity & limb extensor muscles

180
Q

What 4 places does information for integration in the reticulum come from?

A
  1. Principally cortical areas (corticoreticular)
  2. Vestibular nuclei
  3. Proprioception (ascending spinal), vision
  4. Cerebellar output
181
Q

What is processed in the reticulum?

A

Information about how to counter any postural instability

182
Q

What 2 neurons is the corrective output in the reticulospinal pathway routed via?

A
  1. Alpha motor neurons innervating trunk & proximal limb effectors (correct for shift in centre of gravity)
  2. Excitation/inhibition of gamma motor neurons which increase muscle tone (correct for shift in weight bearing)
183
Q

What effect does the influence of the limbic system have on the reticular pathway?

A
  • Physical expression of emotion (depressed= sluggish stance, appear sad)
  • BODY LANGUAGE
184
Q

Describe the Tectospinal pathway (colliculospinal pathway)?

A
  • Contralateral
  • Raises in superior colliculus (receives input from retina)
  • Projects as far as cervical spinal segments
185
Q

What is the function of the Tectospinal pathway?

A
  • Coordinate eye movements to head & neck movements

- Move neck/head so points of visual interest can be focused on

186
Q

What is the thought cause of depression?

A

Reduction in serotonin receptors in hippocampus

187
Q

What does MAOI stand for?

A 
Mono amine oxadase inhibitors 
(1st class of antidepressants)
188
Q

Describe the function of MAOI?

A

Inhibit activity of MAO enzymes which increases level of norepinephrine/serotonin & dopamine

189
Q

Give 3 examples of MAOI’s (antidepressants)?

A
  1. Phenelzine
  2. Selegiline (also used in Parkinsons)
  3. Tranylcypromine
190
Q

What 4 drugs should not be used in combo with MAOI antidepressants & why?

A
  • SSRI/Tricyclic/Morphine/Tramadol - Increase serotonin to dangerous levels causing confusion, hypertension, tremor, death ie. neuroleptic malignant syndrome
191
Q

What “washout” period should you give MAOI before starting other antidepressants?

A

14 days

192
Q

What foods interact with MAOI antidepressants?

A

High in tyramine ie. cheese, venison, alcohol, green veg due to hypertensive crisis

193
Q

What is Moclobeminde?

A

Reversible inhibitor of monoamine oxidase A (RIMA) drug

194
Q

How do tricyclic antidepressants work?

A
  • Inhibiting reuptake of norepinephrine & serotonin by blocking transports responsible for re-uptake
  • Increasing conc of neurotransmitters in synapse & triggering neurotransmission
195
Q

What are some of the uses of Tricyclic antidepressants?

A
  • Depression
  • Anxiety
  • Chronic pain
  • IBS
  • Neuralgia
  • OCD
  • Nocturnal enuresis
  • PTSD
196
Q

What are the potential side effects of Tricyclic antidepressants?

A
  • Risk of arrythmias
  • Antimuscarinic that block acetylcholine receptor & reduce intestinal mobility
  • Bradycardia followed by tachycardia
  • Reduce bronchial secretions
  • Urinary retention
  • Dry mouth & confusion
197
Q

What are 5 common Tricyclic antidepressants?

A
  1. Amitriptyline
  2. Nortriptyline
  3. Clomipramine
  4. Imipramine
  5. Lofepramine
198
Q

What is the concern with Tricyclic antidepressants?

A

Very dangerous in overdoes so beware of how much prescribed esp with high risk of suicide

199
Q

How does Selective Serotonin reuptake inhibitors (SSRI) work?

A

Increasing levels of neurotransmitter serotonin by limiting reabsorption & pure SSRI have weak affinity for norepinephrine & dopamine transmitterss

200
Q

What are serotonin receptors also known as?

A

5-hydroxytryptamine (5-HT)

201
Q

What are some of the uses of SSRI’s?

A
  • Depression
  • Anxiety
  • OCD
  • Panic disorder
  • PTSD
  • Eating disorder
202
Q

What 5 neurotransmitters do 5-HT receptors (in PNS & CNS) modulate the release of?

A
  1. GABA
  2. Dopamine
  3. Epinephrine
  4. Norepinephrine
  5. Acetylecholine
203
Q

What are the potential side effects of SSRI’s?

A
  • Reduced libido
  • QT interval prolongation (esp citalopram)
  • Affects anticoagulants & increases risk of GI bleed
  • Increased risk of suicide
  • Reduce fit threshold
  • Nausea, rash, muscle aches, insomnia, sweating
204
Q

What are the 5 different SSRI’s ranging from most toxic to least?

A
  1. Citalopram (QT interval)
  2. Escitalopram
  3. Paroxetine
  4. Sertraline
  5. Fluoxetine
205
Q

What are the uses of Duloxetine antidepressant (SNRI)?

A
  • Depression
  • Neuropathic pain (diabetes, fibromyalgia)
  • Stress urinary incontinence
206
Q

What are the uses of Mirtazapine antidepressant (alpha2-adrenoreceptor antagonist & NaSSA)?

A
  • Depression
  • Anxiety
  • PTSD
207
Q

What does NaSSA stand for?

A

Noradrenergic & Specific serotonergic antidepressant

208
Q

What are the side effects of Mirtazapine antidepressant with low/high dose?

A
  • Low dose= drowsiness

- High dose= stimulant effect

209
Q

What are the uses of Venlafaxine antidepressant (SNRI)?

A
  • Major depressive disorder
  • Anxiety
  • Panic
  • Social phobia
  • Resistant depression
210
Q

What does SNRI stand for?

A

Serotonin- norepinephrine reuptake inhibitor

211
Q

What does the body metabolise Venlafaxine into?

A

Desvenlafaxine by cytochrome P206 isoenzyme in liver

212
Q

What are 2 other drugs with antidepressant properties?

A
  1. Antipsychotics (Risperidone)

2. Lithium for bipolar stabilisation

213
Q

What are 3 commonly used antidepressants for pain?

A
  1. Amitriptyline
  2. Nortriptyline
  3. Duloxetine
214
Q

What is Duloxetine also licensed for?

A

Diabetic neuropathy

215
Q

What can prolongation of the QT interval lead to?

A

Life threatening arrhythmia known as “torsades de pointes”

216
Q

What people have more risk factors for QTc prolongation & so are particularly vulnerable to drug-induced LQTS?

A
  • Major psychiatric disorders
  • Cardiovascular disease
  • Elderly
  • Women
217
Q

What does each phase (integration, planning, execution) of voluntary movements involve?

A

Distinct areas of the cerebral cortex & feedback from basal ganglia & cerebellum

218
Q

Describe the organisation of the cortical motor areas?

A
  • Somatotopic homunculus organisation with disproportionate size
  • “Cortical magnification” reflec precise movement in that part of the body
219
Q

What is enlarged in the motor homunculus?

A
  • Hands & fingers

- Lips & tongue

220
Q

How does the premotor areas & association areas help the primary motor cortex?

A
  • Electrical stimulation of area infront produces movement (area 6)
  • Stronger/prolonger stimuli are necessary
  • Movements usually more complex (1+ joint, bilateral)
221
Q

What are the premotor areas functionally subdivided into?

A
  1. Premotor cortex

2. Supplementary or secondary motor cortex

222
Q

What happens to the premotor areas if the primary motor area is destroyed?

A

Electrical stimulation of premotor areas has NO effect, principle actions mediated via primary motor cortex

223
Q

What happen when you damage the premotor areas?

A

APRAXIA- cannot perform tasks involving complex sequence of movements

224
Q

How can you demonstrate the role of the supplementary motor area?

A

Measure cerebral blood flow (fMRI)

225
Q

What 2 areas are used for simple finger flexion?

A
  1. Primary motor area

2. Somatic sensory cortex

226
Q

What area is used for mental rehearsal of sequence finger movements?

A

Supplementary motor area

227
Q

What areas are used for actual sequence of finger movements?

A
  1. Supplementary motor areas
  2. Primary motor cortex
  3. Somatic sensory cortex
228
Q

Where does the premotor cortex project fibres to?

A
  1. Brainstem motor nuclei

2. Spinal circuits controlling proximal & axial muscles (postural mainly)

229
Q

What is the function of the premotor cortex?

A
  • Plasticity of complex sequences of movements based on prior experiences, influenced by memory & limbic
  • Orienting body in prep for voluntary movement
230
Q

What 2 cortex’s send projections to premotor area & supplementary motor cortex?

A
  1. Parietal cortex

2. Prefrontal cortex

231
Q

What information does the parietal cortex receive?

A

Somatosensory cortex & visual cortex

232
Q

What 5 motor outputs is the parietal cortex information integrated into?

A
  1. Somatic sensory area (limb position)
  2. Vestibular system (head position)
  3. Premotor areas (motor plans)
  4. Visual system
  5. Limbic cortex (motivational state)
233
Q

During a movement the impulse frequency of neurons in the primary motor cortex is directly related to what?

A

Force required, do NOT code for distance of the movement

234
Q

What is direction coded by?

A

Different populations of neurons, however individual neurons can be active for a range of
angles of movement

235
Q

What are the 3 main sources of input to the corticospinal output that fine tune movement?

A
  1. Sensory receptors
  2. Cerebellum
  3. Basal ganglia
236
Q

What should you remember about all movement-related inputs to the cortex coming from other parts of the brain/spinal cord?

A

They also pass through the thalamus

237
Q

What does the cerebellum input do for the corticospinal output?

A

Planning (feed forward) movement & corrective feedback from proprioception

238
Q

What does the basal ganglia input do for the corticospinal output?

A

Initiating complex movement & correction from the reward system. Overlay of emotional component from limbic circuits

239
Q

What do the axons in the corticospinal tract do?

A
  • Most decussate at ventral pyramids in brainstem & control distal contralateral muscles
  • 10% remain ipsilateral until they innverate bilaterally at level of ventral root & control bilateral axial muscles
240
Q

Describe the Rubrospinal pathway?

A
  • Originate in brainstem (red nucleus)
  • Projects to upper limb (flexor activity)
  • Info from corticospinal collaterals & cerebellum
241
Q

Why is corticospinal neuron (upper motor neurons) lesions relatively common?

A

Axon are very long & therefore vulnerable

242
Q

What are lesions of the corticospinal neutrons commonly caused by?

A

Infarcts related to cerebrovascular incidents (middle cerebral artery v vulnerable)

243
Q

What can also damage the corticospinal system?

A
  • Trauma
  • Tumors
  • Demyelinating diseases
244
Q

What is a negative sign of lesions in corticospinal neuron?

A

Loss of function (weakness or paralysis)

245
Q

What is a positive sign of lesions in corticospinal neuron?

A

Abnormal response ie. extensor planter reflex (Babinski sign)

246
Q

Describe Upper motor neuron syndrome?

A
  • Pyramidal muscle weakness (Caveman escape)
  • No muscle atrophy
  • No fasciculations
  • Increased muscle tone (spasticity)
  • Increased stretch reflexes
  • Abnormal reflexes (Babinski)
247
Q

Describe how lower motor neurone lesions present?

A
  • Muscle weakness
  • Muscle atrophy
  • Fasciculations
  • Reduced muscle tone
  • Reduced stretch reflexes
248
Q

What is the presentation of Upper motor neurone disease from lesions of the internal capsule?

A

Hypotonia precedes hypertonia

249
Q

What does ALS stand for?

A

Amyotrophic lateral sclerosis

250
Q

Describe ALS?

A
  • Affects both UMN & LMN
  • LMN affected in the anterior horn & brainstem nuclei
  • UMN affected in the cerebral cortex
251
Q

What happens to the neurons in ALS?

A

Die at the periphery first & move inwards

252
Q

Describe the physical results of ALS?

A
  • As LMNs die muscles atrophy

- As axons in descending tracts die, hard scar tissue forms (sclerosis)

253
Q

What is spared/stays normal in ALS?

A
  • Ocular motility
  • Sacral parasympathetic neurons (bladder)
  • Motor coordination systems
  • Intellectual capabilities
254
Q

What is the brainstem?

A

Part of the brain lying between spinal cord, cerebellum & cerebral hemisphere

255
Q

Where is the brainstem?

A

Posterior cranial fossa

256
Q

What lies anterior to the brainstem?

A
  • Clivus

- Nerves & vessels

257
Q

What lies posterior to the brainstem?

A

Cerebellum & Attachments

258
Q

What lies inferior to the brainstem?

A
  • Foramen magnum

- Spinal cord

259
Q

What lies superior to the brainstem?

A
  • Tentorium

- Diencephalon

260
Q

What links to the cerebellum in the midbrain of the brainstem?

A

Superior cerebellar peduncle

261
Q

What links to the cerebellum in the pons of the brainstem?

A

Middle cerebellar peduncle

262
Q

What links to the cerebellum in the medulla of the brainstem?

A

Inferior cerebellar peduncle

263
Q

What 4 different classifications of nuclei which lie within the brainstem?

A
  1. Motor co-ordination
  2. Reticular formation
  3. Cranial nerves
  4. Vital & Non vital centres
264
Q

Describe the pain-temperature pathway?

A

Decussates quickly & goes up the contralateral pathway –> spinothalamic tract in brainstem –> Thalamus –> Cerebral cortex (sensory)

265
Q

Describe the proprioception-stereognosis (conscious) pathway?

A

Goes up ipsilateral posterior column –> decussates at medulla –> medial lemniscus in contralateral pathway –> thalamus –> cerebral cortex (sensory)

266
Q

Describe the light touch pathway?

A

Can either travel up posterior column or decussate quickly & go up contralateral pathway –> Decussates to contralateral spinothalamic tract –> thalamus –> cerebral cortex (Sensory)

267
Q

Describe the unconscious proprioception pathway?

A

Lies on the right pathway & travels up spinocerebellar tract ipsilaterally –> cerebellum from brainstem

268
Q

Describe the motor (Corticospinal) tract?

A

From motor cortex –> Decussates at medulla –> Travels down contralateral corticospinal tract —> Synpase at UMN –> Synapse at LMN –> Muscle

269
Q

What are 2 examples of upper motor neurone lesions occurring?

A
  • Cerebral infarction

- Corticospinal tract lesion

270
Q

What are 2 examples of lower motor neurone lesions occurring?

A
  • Lesion of peripheral nerve

- Lesion at nerve level

271
Q

What happens to the central grey matter as you go from spinal cord to brainstem?

A

Goes from vertical to more horizontal & “opens up dorsally”

272
Q

Whats the location of the 12 cranial nerves?

A
  • 4 from midbrain & above
  • 4 from pons
  • 4 from medulla
273
Q

What will a brainstem lesion usually produce?

A

Ipsilateral cranial nerve defects (horner’s syndrome)

274
Q

Somatic motor is ____ in brainstem?

A

Medial

275
Q

What cranial nerves innervate somatic orbital muscles?

A
  • III, IV (midbrain)

- VI (pons)

276
Q

What cranial nerve innervates the tongue?

A

XII (medulla)

277
Q

Somatic sensory spans the whole brainstem & its mainly ____?

A

Lateral

278
Q

Describe the location of the V trigeminal nerve in brainstem?

A
  • From posterior horn of spinal cord to midbrain
279
Q

What different head somatic innervations does the V trigeminal nerve supply?

A
  • Midbrain: proprioception
  • Pons: discriminative touch
  • Medulla: pain & temp
280
Q

What is compression on the 3rd nerve usually due to?

A

Aneurysm

281
Q

What is the sympathetic output from the hypothalamus?

A
  • Facial sweating
  • Eyelid elevation
  • Vasomotor & pupil dilation
    (descends mainly uncrossed)
282
Q

What are the special somatic afferent cranial nerves for hearing, balance & sight?

A

VIII, II

283
Q

What are examples of descending tracts?

A
  • Corticobulbar (motor)
  • Corticospinal (motor)
  • Sympathetic (ipsilateral)
284
Q

What are examples of ascending tracts?

A
  • Spinocerebellar
  • Spinothalamic (contralateral)
  • Medial lemniscus
285
Q

What are examples of linking tracts?

A
  • Cerebellar peduncles

- Medial longitudinal fasciculus

286
Q

Where does corticobulbar tract fibres exit?

A

Appropriate level of brainstem to synapse on the lower motor neurons of the cranial nerves

287
Q

Where do the corticospinal fibres cross?

A

90% cross in medulla

288
Q

What will a brainstem lesion in the corticobulbar/corticospinal tracts (pyramidal tracts) produce?

A

Contralateral UMN signs

289
Q

What is the spinal equivalence of the medial lemniscus pathway?

A

Continuation of the dorsal column

290
Q

What is the function of the medial lemniscus pathway (contralateral)?

A

Carry proprioception (JPS) & some touch to thalamus

291
Q

What do the fibres in medial lemniscus pathway do?

A

Cross over & ascend as medial lemniscus in medulla

292
Q

What can a brainstem lesion affecting the medial lemniscus pathway cause?

A

Contralateral loss of JPS

293
Q

What is the spinal equivalence of the spinal lemniscus pathway?

A

Continuation of the spina-thalamic tract

294
Q

What is the function of the spinal lemniscus pathway?

A

Carries pain, temp, course touch to the thalamus

295
Q

What happens to the fibres in the spinal lemniscus pathway?

A

Synapse & cross over the spinal cord & ascend through the brainstem

296
Q

What will a brainstem lesion affecting the spinal lemniscus pathway cause?

A

Contralateral loss of pain & temp

297
Q

What is the function of the spinocerebellar pathway (ipsilateral)?

A

Carries proprioceptive info to the cerebellum

298
Q

What does a brainstem lesion affecting the spinocerebellar pathway cause?

A

Ipsilateral spinocerebellar tract defect

299
Q

What is the function of the medial longitudinal fasciculus (contralateral)?

A

Carries info about direction that the eyes should move

300
Q

What is the medial longitudinal fasciculus (MLF)?

A
  • 1 of a pair of crossed fiber tracts, on each side of the brainstem
  • These bundles of axons are situated near midline of brainstem & both composed of ascending & descending fibers that arise from different sources & terminate in different areas
301
Q

What is the relation of Multiple sclerosis & the medial longitudinal fasciculus (MLF)?

A

Multiple sclerosis causes de-myelination of axons in MLF = internuclear ophthalmoplegia

MD4001 (11 decks)

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