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Year 2 - Semester 1 > Neuro- week 3 > Flashcards

Neuro- week 3 Flashcards

1
Q

describe attention

A

part of executive function

reflective of frontal lobe function, especially prefrontal cortex

dysfunction is the main sign in delirium

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2
Q

types of attention

A

focused - respond discretely to specific stimuli

sustained - maintain attention during sustained or repetitive activity

selective - attention in the face of distracting stimuli

alternating - switch between tasks which have different cognitive requirements

divided - may not exist and just be people very good at alternating seamlessly

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3
Q

what does damage to the hippocampus cause

A

inability to form declaritive memories
anterograde amnesia
this is because the hipocampus is important in encoding short term memories into long term

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4
Q

what are the five stages of completing goals

A

1 - a best guess at what reality is
2- a commitment to some goal
3- hypothesis generation on how to achieve the goal
4- action in the world
5- dynamic monitoring on whether the goal is getting closer or further away

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5
Q

what are the parts to having a best guess at what reality is

A

self vs other - separating ourselves from the environment

agent vs object - things capable of action vs inanimate objects

agent intentionality - thinking about what something else might be planning
i. Mirror neurons which mirror what others are doing to get insight into their intentions

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6
Q

where do bottom up goals come from

A

limbic system

goals essential to survival such as reproduction

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7
Q

where do top down goals come from

A

prefrontal cortex

higher functions determining complex, non-essential goals

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8
Q

how do we monitor if a goal gets closer or further away after an action

A

in absense of knowledge, all actions are equal

dopamine in mesolimbic and mesocortical pathways have a role in reward and prefrontal cortex processing

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9
Q

where are language centres in the human brain

A

85% on the left
10% on the right
5% split

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10
Q

what does damage to broca’s area lead to?

A

difficulty expressing language

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11
Q

what does damage to wernicke’s area lead to?

A

difficulty understanding language

speech becomes jumbled and difficult to understand because they don’t understand what they are saying

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12
Q

what connects broca’s area and wernicke’s area?

A

the arcuate fasciculus

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13
Q

what does damage to the arcuate fasciculus lead to?

A

innability to repeat things said to you

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14
Q

describe fluent language problems

A

able to speak a lot.

damage to wernicke’s

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15
Q

describe non-fluent language problems

A

broca’s or arcute fasciculus damage

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16
Q

what is the definition of stroke

A

rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin

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17
Q

what is the definition of TIA

A

brief episodes of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction

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18
Q

what does the left carotid come off of

A

aortic arch

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19
Q

what does the right carotid come off of

A

the brachiocephalic trunk

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20
Q

what do the vertebral arteries come off of

A

the subclavian arteries

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21
Q

where do the vertebral arteries travel?

A

in the transverse processes of the spine

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22
Q

what do the vertebral arteries join to become

A

the basilar artery

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23
Q

what does the basiar artery split into?

A

the right and left posterior cerebral arteries

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24
Q

what is the definition of infarction

A

morphological entity; a large, localised area of tissue necrosis brought about by reduced blood flow

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25
Q

what is the definition of ischaemia?

A

perfusion below the metabolic needs of the tissue

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26
Q

what subcategories of stroke are there and what are the proportions of each one

A

5% subarachnoid haemorrhage
15% intracerebral haemorrhage
80% ischaemic stroke.

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27
Q

what subcategories of ISCHAEMIC stroke are there and what are the proportions of each one

A
  • 50% artherothromboembolism
  • 25% small artery disease
  • 20% cardiac source of embolism
  • 5% rare causes
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28
Q

what kinds of infarct are there

A
  • Occlusion of a vessel; infarction
  • Hypoperfusion; watershed infarct
  • Cardiac arrest; selective vulnerability and global ischaemic injury
29
Q

what can cause strokes

A 
–	Atherosclerotic plaques
–	Arterial dissection
–	Emboli
        •	Atherosclerotic material
        •	Cardiogenic
        •	Fat emboli
        •	Rare cause; neoplasms, air bubbles
30
Q

what does a small infarct in internal capsule cause

A

weakness of opposite side of body, no damage to cortical structures or other tracts. Low mortality but can be very disabling

31
Q

what are water shed infarcts

A

seen when the systemic blood pressure falls to such a level that cerebral blood flow cannot be maintained. Brain is most affected where there is overlap from anterior and posterior perfusion.
After 20-30 minutes of global cerebral ischaemia, the brain is irreversibly damaged.
This causes laminar necrosis – lines running through the grey matter.

32
Q

where are common places for intracerebral haemorrhage

A

basal ganglia, cerebellum and brain stem

33
Q

why is hypertension a risk factor for intracerebral haemorrhage

A

• Causes small vessel disease
• lipohyalinosis - Degenerative process initiated
by fibrinoid necrosis.
• Arteriolosclerosis - Concentric hyaline wall
thickening of small arteries and arterioles

34
Q

what can cause intracerebral haemorrhage

A
  • Hypertension
  • Vascular malformation
  • Neoplasia
  • Trauma
  • Cerebral amyloid angiopathy
  • Iatrogenic, other blood dyscrasias
35
Q

whats the most common cause of lobar haematoma (one lobe)

A

cerebral amyloid angiopathy – amyloid accumulate in the blood vessels and predispose them to rupture.

36
Q

describe subarachnoid haemorrhage

A

Often due to a vascular malformation – aneurysms – shown as white ring in CT

common sites of aneurysm include at the bifurcation of the middle cerebral artery and at the joining points of communicating arteries with either anterior cerebral, posterior cerebral or internal carotid arteries.

Rarely an aneurysm will rupture into the brain parenchyma itself so diagnosis would be intracerebral haemorrhage instead of sub arachnoid.

37
Q

what are some causes of venous infarction

A

• Sagittal sinus thrombosis
o Oral contraceptives
o Dehydration
o Meningitis

• Cortical vein thrombosis
o Meningitis

38
Q

what happens in persistent high BP

A

• Autoregulatory range reset at a higher level
• Curve shifts to right
• Unwise to rapidly lower high blood pressure to ‘normal’,
• When BP falls below 90 mm Hg:
– autoregulation fails
– CBF drops
ischaemic brain damage can occur

39
Q

what is in the lateral grey horn

A

preganglionic fibres of the sympathetic nervous system

40
Q

where does the sympathetic trunk receive fibres from

A

T1 - L2

runs above and below this but only receives fibres from here

41
Q

what joins the ventral rami to the sympathetic chain

A

the white and grey rami communicantes

42
Q

what is the enteric system

A

Intrinsic collections of neurones within the wall of the digestive tract, and can function independently of the CNS or PNS

43
Q

what happens to sympathetic fibres coming from the spinal cord

A

some will synapse with second neurone in sympathetic chain.
Some will run through sympathetic chain without synapsing to prevertebral ganglia.

Prevertebral ganglia occur only in abdomen and pelvis
They lie anterior to the vertebral column

44
Q

what are the main prevertebral ganglia

A

Coeliac
superior mesenteric
inferior mesenteric
inferior hypogastric ganglia

45
Q

what do alpha 1 receptors do

A

in smooth muscle in arterioles causing vasocontriction

46
Q

what do alpha 2 receptors do

A

on coronary arteries causing vasodilation

47
Q

what do beta 1 receptors do

A

on cardiac muscle causing increased contractility

48
Q

what do beta 2 receptors do

A

found in sino-atrial node to increase heart rate, in some smooth muscle in arterioles (esp. skeletal muscle ) causing vasodilation and in smooth muscle of bronchi causing bronchodilation

49
Q

what are the parts of the parasympathetic division

A

cranial outflow
o Comes from the brain
o Innervates organs of the head, neck, thorax, and
abdomen

sacral outflow
o Supplies remaining abdominal and pelvic organs

50
Q

in what nerves do preganglionic fibres run in the cranial outflow

A
  • Oculomotor nerve (III)
  • Facial nerve (VII)
  • Glossopharyngeal nerve (IX)
  • Vagus nerve (X)
  • Cell bodies located in cranial nerve nuclei in the brain stem
51
Q

describe the outflow via the vagus nerve

A

Fibers innervate visceral organs of the thorax and abdomen
• Stimulates - digestion, reduction in heart rate and blood pressure

Preganglionic cell bodies
• Located in dorsal motor nucleus in the medulla

Ganglionic neurons
• Confined within the walls of organs being innervated

52
Q

describe the sacral outflow

A

Emerges from S2-S4
Innervates organs of the pelvis and lower abdomen
Preganglionic cell bodies
Located in visceral motor region of spinal gray matter
Form splanchnic nerves

53
Q

what is the pharmacology of the parasympathetic NS

A

Ach binding to nicotinic and muscarinic receptors

54
Q

describe the functions of ANS neurones

A

• Sympathetic and parasympathetic afferents very similar to somatic sensory pathways.
• Mostly free nerve endings in viscera, axons passing to ganglion (dorsal root ganglion or cranial nerve sensory ganglion). 2nd order neuronal cell body found in dorsal grey matter of spinal cord.
• Sensory innervation of viscera
o Usually not consciously perceived (except hunger, fullness)
o Visceral reflexes (coughing, vomiting, swallowing etc)
• In pathological conditions may result in pain and nausea- referred pain

55
Q

compare somatic motor system and the ANS

A

Somatic motor system
• One motor neuron extends from the CNS to skeletal muscle
• Axons are well myelinated, conduct rapidly

Autonomic nervous system
•	Chain of two motor neurons
o	Preganglionic neuron
o	Postganglionic neuron
•	Conduction is slower due to thinly or unmyelinated axons
56
Q

what are the anatomical differences between sympathetic and parasympathetic

A

• Arise from different regions of the CNS
o Sympathetic – also called the thoracolumbar
division
o Parasympathetic – also called the cranio-
sacral division
• Length of postganglionic fibres
o Sympathetic – long
o Parasympathetic – short
• Branching of axons
o Sympathetic - highly branched
• Affects many organs
o Parasympathetic – few branches

57
Q

what neurotransmitter is released by preganglionic axons

A

acetylcholine for cholinergic and nicotinic branches

58
Q

what neurotransmitter is released by post ganglionic axons

A
  • Sympathetic – most release noradrenaline (adrenergic)

* Parasympathetic – release acetylcholine (muscarinic receptors)

59
Q

describe the adrenal medulla

A

Major organ of the sympathetic nervous system
Secretes great quantities adrenaline (some NA)
Stimulated to secrete by pre-ganglionic sympathetic fibers

60
Q

where is the central control of the ANS

A

Control by the brain stem and spinal cord
• Reticular formation exerts most direct influence
o Medulla oblongata
o Periaqueductal gray matter
Control by the hypothalamus and amygdala
• Hypothalamus – the main integration center of the ANS
• Amygdala – main limbic region for emotions
Control by the cerebral cortex

61
Q

describe horner’s syndrome

A

Miosis (small pupil)
Ptosis (drooping eyelid)
Loss of sweating same side of face
Redness of conjunctiva

May result from interruption of sympathetic fibres centrally (anywhere between hypothalamus and upper thoracic level of spinal cord) or peripherally (cervical sympathetic chain)

Causes include:
Carotid artery dissection, brainstem stroke, syringomyelia

62
Q

describe syncope

A
  • Vasovagal syncope: simple faint, seen commonly in young people with no underlying illness
  • Sudden vasodilatation occurs often caused by strong emotion.
  • Peripheral resistance decreases in arterioles and blood pressure falls. Cardiac rate fails to increase. Vagal stimulation may then occur leading to further bradycardia and to perspiration, increased peristalsis, yawning, nausea, pallor and salivation
63
Q

describe orthostatic hypotension

A
  • Like vasovagal syncope but brought on by getting up from reclined position or standing still for long period
  • Often person stands up and then has steady fall in blood pressure but without compensatory rise in HR. Mild staggering or falling may precede loss of consciousness
64
Q

describe bladder control problems

A
  • Prime example of autonomic dysfunction.
  • Common symptom of Multiple sclerosis patients.(75% of MS patients)
  • Main symptoms are urgency, frequency and urge incontinence.
  • Main cause is overactivity of detrusor muscle. Involuntary bladder contraction gives rise to feeling of need to void immediately despite bladder volume being low.
65
Q

what are some tests for ANS dysfunction

A
  • Pupil reactions
  • Postural blood pressure – abnormal fall when getting up
  • Variation of HR with deep breathing
  • Lacrimal function - tears
66
Q

describe schizophrenia

A

0.5% prevalence
• Disorder of PFC function
• Excess dopamine hypothesis
• Treated with dopamine antagonists

67
Q

describe depression

A 
12-20% prevalence
•	Disorder of Limbic function (?)
•	Monoamine deficiency hypothesis
•	Treated with 
•	Diet, exercise
•	Drugs: SSRI, SNRI, TCA, MAOI, ‘Atypical antidepressants’ 
•	Psychotherapy
•	ECT (rarely)
68
Q

describe anxiety

A 
prevalence – 33%
•	Disorder of Limbic function (?)
•	Central role of amygdala
•	Treated with 
•	Psychotherapy can be very effective
•	Drugs: SSRI, SNRI, TCA, Others
69
Q

describe personality disorders

A 
– prevalence 12%
•	A  - odd/eccentric 
       o	Paranoid
       o	Schizoid
       o	Schizotypal
•	B – dramatic/emotional/erratic
       o	Antisocial
       o	Borderline
       o	Histrionic
       o	Narcissistic 
•	C – anxious/fearful
       o	Avoidant
       o   	Dependent
       o	Obsessive-compulsive

Year 2 - Semester 1 (13 decks)

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