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Neuroscience > Brain supply and Stroke > Flashcards

Brain supply and Stroke Flashcards

1
Q

What are the 4 main risk factors for stroke?

2 others?

A

HBP
Diabetes
Smoking
High Cholesterol

Alcohol
Lifestyle

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2
Q

What is the relative risk of stroke with diabetes?

A

2.0

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3
Q

What is the relative risk of stroke in smokers and what is a specific effect that causes this increased risk?

A

RR for stroke ~ 1.5
Risk declines after smoking cessation
Association between carotid disease and smoking

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4
Q

What is the direct cause of most stroke pathology?

A

Emboli to the distal circulation what causes most pathology - (circle of willis is often still effective if blocked in one place)

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5
Q

What is the extensor plantar reflex and when is it significant?

A

Extension and speeding of the toes in response to stimulation of the sole. AKA. Babinski’s sign. Appears after stroke due to damage of upper motor neurones
Extensor plantar stays in children for a few years until fibres myelinated

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6
Q

What is the medical research councils grading scale for power?

A
  1. Normal power
  2. Diminished power
  3. Movement against gravity
  4. Movement with gravity eliminated
  5. Flicker when attempting movement movement
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7
Q

Can you see changes to the white matter tracts in the internal capsule on CT images after stroke?

A

Yes

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8
Q

When is a CT scan done after stroke and what are physicals looking to eliminate?

A

ASAP
Ruling out haemorrhage
(Looking for blood - bright white on the scan
- if haemorrhage - thrombolysis can cause catastrophic haemorrhage)

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9
Q

What are the 2 types of stroke?

A

Ischaemic

Haemorrhagic

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10
Q

Why are hemicraniotomies sometimes performed after stroke?

A

To allow for the swelling of the brain to prevent its compression and coning
(Cytotoxic oedema and reactive hyperaemia)

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11
Q

When is it beneficial to remove blood surgically after haemorragic stroke?

A

Only in very superficial bleeds

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12
Q

What is a thrombolytic drug which is proven to improve stroke outcomes?
And when should it be given?

A

rTPA
Best under 1.5 hours but can be benefit up to 6 hours
(Aspirin also used as an anti platelet agent)

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13
Q

What is the FAST assessment?

A

Face Arm Speech Test Face

Facial Palsy - affected side
Arm Weakness - affected side
Speech Impairment

93% paramedic admitted strokes have FAST deficit
Paramedic Training Package available on request

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14
Q

At rest, what percentage of the human glucose and oxygen intakes does the brain take?
How much glucose does it use per day?
How much energy does it use per day?

A

 60% of glucose utilisation of human at rest

 20% of oxygen utilisation

 120 g of glucose a day

 1760 kJ / day = 20 Watts = dim light bulb

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15
Q

What % of body weight does the brain make?

What % of cardiac output and % of oxygen consumed by whole body does the brain take?

A

Brain is 2% of body weight
Receives 17% of cardiac output
Uses 20% of oxygen consumed by whole body
(Rapid loss of consciousness if bloody supply is interrupted)

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16
Q

Why is the central artery of the retina essential?

A

It is the only arterial supply to the retina

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17
Q

What is the carotid arteries course into the cranium?

A

Internal carotid enters cranium via the carotid canal into the middle cranial fossa
Very sinuous course lateral to body of sphenoid bone emerging adjacent to optic chiasm

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18
Q

What is the course of the vertebral arteries into the cranium?

A

Vertebral arteries enter cranium via the foramen magnum
Run along the lateral surface of the medulla before fusing together on the ventral surface of the pons to form the basilar artery

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19
Q

What does the Circle of Willis encircle?

A

Circle of Willis surrounds the optic chiasm and pituitary on base of brain

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20
Q

Name 5 specific areas of the brain supplied by the middle cerebral artery

A 
Primary motor cortex
Primary sensory cortex
Broca's expressive speech area
Auditory area
Speech receptive area
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21
Q

Give an overview of the course of the middle cerebral artery and what parts of the brain it supplies

A

The middle cerebral artery is the largest of the three cerebral arteries and its cortical territory is the most extensive. It passes laterally from its origin to enter the lateral fissure within which it subdivides, its branches supplying virtually the whole of the lateral surface of the frontal, parietal and temporal lobes. This territory includes the primary motor and sensory and the insula within the depths of the lateral fissure

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22
Q

What does occlusion of the MCA lead to?

A

Contralateral paralysis and sensory deficits of lower face, arm

Aphasia if dominant hemisphere

Hemianopsia of contralateral visual fields (thalamo‐visual cortex tract

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23
Q

Give an overview of the course of the ACA and the parts of the brain that it supplies

A

It course medially above the optic nerve
Then into the longitudinal fissure between the two frontal lobes
Within the GLF it follows the dorsal curvature of rue corpus callosum
Branches rammify over the medial surface of the frontal and parietal lobes, which it supplies
Territory therefore includes the motor and sensory cornices for the lower limb
Fine terminal branches also extend out of the GLF to a narrow lateral band of the frontal and parietal cortices

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24
Q

What does occlusion of the ACA lead to?

A

Paralysis and sensory deficits to contralateral leg and perineum

Mental confusion and dysphasia

Sometimes contralateral face, tongue and upper limb due to internal capsule

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25
Q

Give and overview of the PCA and the parts of the brain that it supplies

A

The PCA curves round the midbrain to supply the visual cortex of the occipital lobe and the inferno medial aspect of the temporal lobe

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26
Q

What would occlusion of the PCA lead to?

A

Blindness in contralateral visual field

Hippocampal memory may be affected but usually temporary

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27
Q

Which arteries supply the medial rim of lateral surface of cerebral hemispheres?

A

ACA and PCA

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28
Q

What do the anterior perforating arteries supply?
Where to they arise and enter the brian?
What can result from their rupture or occlusion?

A
  • basal ganglia, internal capsule, optic chiasm, hypothalamus
  • arise from the ACA, anterior communicating artery and region of origin of MCA.
    They enter the brain between the optic chiasm and the end of the olfactory tract in the anterior perforating substance

contralateral motor and sensory deficit (lec)

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29
Q

Way do the Posterior perforating arteries supply and where do they arise?
We’re do they enter the brain?

A
  • ventral midbrain (and parts of subthalamus and hypothalamus)
  • arise form the PCA and posterior communicating arteries
  • enter the brain in the region between the two crura cerebri of the midbrain (posterior perforating substance)
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30
Q

What can result from occlusion of the vertebral and basilar arteries?

A

Instantly fatal due to coma (reticular formation) and loss of respiratory control

Cerebellar defects

Cranial nerve defects

Deafness if labyrinthine artery affected

Infarction of ventral pons, leads to loss of all voluntary movements except eyes, the senses are spared.

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31
Q

What is the blood supply of the spinal cord?

A

Posterior spinal arteries, from vertebrals or posterior inferior cerebellar

Anterior spinal artery, from vertebrals

Radicular arteries, from ascending cervical, intercostal, lumbar and sacral arteries

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32
Q

The middle meningeal artery is a branch of which artery, enters the cranium where and supplies what?

A
  • maxillary artery
  • foramen spinosum
  • bones of the vault
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33
Q

What is extradural haemorrhage?

A

between skull and dura, e.g. from meningeal arteries may be higher pressure, more prolonged, push onto brain

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34
Q

What is subdural haemorrhage?

A

between dura and arachnoid, e.g. from superior cerebral vein, low pressure, slow accumulation, clots in subdural space and pushes on brain

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35
Q

What is Sub‐arachnoid haemorrhage?

A

– between arachnoid and pia, e.g. from ruptured aneurysms in Circle of Willis, sudden, very painful, neck stiffness, one cause of a “stroke”, bleeds into sub‐arachnoid space

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36
Q

What is intracerebral haemorrhage?

A

within brain tissue itself, another cause of stroke

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37
Q

He is nervous repolarisation achieved?

A

Na+/K+ATPase
Requires ATP for energy
Net REMOVAL of cations from cell - ELECTROGENIC

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38
Q

Why is effective removal of glutamate from the synapse essential?

A

 Highly active at receptors

 Depolarises post-synaptic cells

 they can not pass on new messages

 Can swell and die

 Gives rise to major energy use (75% in primates)

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39
Q

What takes up glutamate from the synapse and how?

A

Astrocytes

NA+/K+ATPase

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40
Q

What happens to glutamate after it is taken up by astrocytes?

A

Glutamate is converted in Glutamine

 Requires another ATP

 Glutamine exported and taken-up pre-synaptically

 Converted and packed into vesicles - requires ATP

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41
Q

Why glutamergic activity lead to increase blood flow?

A

to deliver OXYGEN and GLUCOSE

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42
Q

What happens to glucose in the brain?

A

 Glucose transported from blood into Glial cells (mainly)
 Glucose is the converted into Glucose - 6 - phosphate
 From here is can be either Metabolised or Stored as glycogen
 glycogen stores are small but Have very rapid turnover
- Are an important local energy source
- ‘the brains battery’

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43
Q

What are the results of glycolysis?

A

Overall Glucose (6 carbon) gives

 2 pyruvate (3 carbon each)

 2 ATP

 BUT uses 2 NAD+

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44
Q

What happens after glycolysis in the absence of oxygen?

A 
 In the ABSENCE of Oxygen
 Pyruvate -> LACTATE
 NADH -> NAD+
 Allows glycolysis to continue
 Hence 2 ATP per glucose
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45
Q

What happens after glycolysis in the presence of oxygen?

A

 Pyruvate feeds in Citric Acid cycle for conversion to CARBON DIOXIDE and NADH.

 NADH feed into Oxidative phosphorolation to give phosphorolation to givepi 34 ATP molecules and water

 Overall in the brain this gives 36 ATP per glucose molecule.

 Efficiency of the process is about 40%

 On average an adult makes 70kg ATP per day.

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46
Q

What three parts of glutamergic nervous function require ATP?

A

 Membrane repolarisation

 Glutamate uptake

 Glutamate repackaging

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47
Q

What are the 2 ‘fail safes’ of blood supply to the brain?

A
  1. Circle of Willis

2. Surface network: the leptomeningeal collateral circulation

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48
Q

Why is normal BP essential for minimal damage after an occlusion of the MCA?

A

The brain’s circulation failing:
the “leptomeningeal collateral circulation” does its best if the middle cerebral artery is occluded
But depends on normal blood pressure

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49
Q

How effective is the leptomeningeal collateral circulation in perusing the brain adequately when a stroke (eg. Occlusion of the MCA occurs)?

A

“leptomeningeal collateral circulation” does its best but cannot reach the infarct “core”

the “leptomeningeal collateral circulation” does its best: But it’s best is not enough…. and over 12-48 hours the penumbra deteriorates until it has been “recruited” into the expanding core.

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50
Q

What is meant by ‘core ischaemia’?

A

 Perfusion below the survival threshold

 All cells start to die – neurones and astrocytes

 Capillaries damaged

51
Q

Explain what is meant by the penumbra

A

 The “grey” area around the core, nearer the collaterals

 Perfusion partly reduced, below the function threshold only

 Neuronal and synaptic function suppressed

 Responds to EARLY reperfusion

 Depends on glucose + glycolysis, which increases to generate the required ATP

 Without reperfusion, will mature into core over a day or two

52
Q

Why does the core expand (no fall in blood pressure to reduce the collaterals)?

A

Spreading depolarisations

53
Q

In the normal brain what is the perfusion response to functional activity or to a spreading depolarisation?

A

hyperaemia – increase in blood flow: spreads like ripples from a splash in a pond. Up to 400% for a depolarisation

54
Q

What are the effects of one NORMAL (hyperaemic) depolarisation on brain lactate and glucose?

A

Decreases lactate and increases glucose

55
Q

What is the effect of spreading depolarisation vulnerability of cells and those already vunerable?

A

A depolarisation kills the most vulnerable cells and increases the vulnerability of others.

56
Q

How do spreading depolarisations kill cells?

A

Cytotoxic oedema:

Build up of Na+, Ca2+ and Cl- in the cells - osmotic pressure

57
Q

What is the circulatory response to the spreading depolarisation/cytotoxic oedema?

A

Reactive hyperaemia Whole territory dilates, so.. More capillaries open, so Increase in brain volume.. Capillaries weak, and leak… Haemorrhagic conversion

58
Q

Why does the brain swell with reperfusion after stroke?

A

Cytotoxic oedema

vasogenic oedema and haemorrhage (reactive hyperaemia)

59
Q

Why can repercussion too late be dangerous?

A

Can cause swelling and bleeding

60
Q

What happens to the penumbra if there is no reperfusion?

A

function may recover with reperfusion (without this, the core will gradually expand into the penumbra by starting “tsunamis” around itself, so that the

  1. Why did the brain swell soon after the reperfusion?

 Tissue in the ischaemic Core

 Will die unless reperfused “in time”

 May swell and bleed if reperfused too late

gpenumbra area also infarcts)

61
Q

Where do the corticospinal and corticobulbar pathways decussate

A

Decussation of the pyramids in the medulla

62
Q

What are the nuclei for the oculomotor nerve and what fibres do they involve and where abouts are they located?

A

Oculomotor nucleus - motor
Edinger-Westphal - parasymapthetic (pupillary constriction)

Bottom of midbrain/top of pons

63
Q

What is peculiar about the trochlear nerve and what is the name of its nucleus in the brain stem?

A

only cranial nerve except the optic which decussates and which exits the brain stem on the dorsal side
Trochlear nucleus
(Leaves below the inferior colliculus)

64
Q

Where is the abducens nucleus

A

Beneath the floor of the 4th ventricle in the caudal pons

65
Q

A what level do the 3rd and 4th cranial nerves leave the brain stem?

A

cIII and cIV exit the brain stem at the level of the crus cerebri

66
Q

See page 104 of neuro anatomy for a diagram of the nuclei of the trigeminal nerve

A

-

67
Q

Where do the pain/temperature fibres of the trigeminal nerve synapse?
Where are their cell bodies?

A
  • synapse in nucleus of the spinal tract of the trigeminal

- cell bodies in trigeminal ganglion

68
Q

Where do the touch/pressure fibres of the trigeminal nerve synapse?
Where are their cell bodies?

A
  • Synapse in the chief sensory nucleus of the trigeminal

- cell bodies in the trigeminal ganglion

69
Q

Where do the proprioception fibres of the trigeminal nerve synapse?
Where are their cell bodies?

A
  • synapse just after the mesencephalic nucleus (inferior colliculus)
  • cell bodies in the mesencephalic nucleus
70
Q

What are the brain stem nuclei of the facial nerve?

A

Facial motor nucleus

Superior salivatory nucleus - motor

Nucleus solitarius/nucleus ambiguus? - sensory or motor?

71
Q

Where does the facial nerve exit the brainstem?

A

The cerebellar pontine angle (CPA)

72
Q

What are the nuclei of the vestibulocochlear nerve?

Where does it exit the brainstem?

A
  • vestibular & cochlear nuclei
  • Exits brain stem in CPA

(Affected by acoustic neuroma, conditions which swell it - also get Bell’s Palsy)
(Small motor component)

73
Q

What are the brainstem nuclei of the glossy pharyngeal nerve?

A

Inferior salivatory nucleus - parotid (post gang neurones in the optic ganglion)
Nucleus ambiguus - stylopharyngeus, mediating gag reflex
Hypoglossal - mediating gag reflex
Nucleus solitarius - visceral and taste

74
Q

Where does the glosso pharyngeal nerve join the brainstem?

A

Lateral to the olive

75
Q

What are the brainstem nuclei of the vagus nerve?

A
  • Nucleus solitarius - afferent - visceral sensation
  • nucleus ambiguus - muscles of soft palate, pharynx, larynx and upper part of oesophagus
  • dorsal motor nucleus of the vagus
76
Q

What are the equivalents of the brainstem nuclei in the accessory nerve?

A

Cranial root of cXI

Spinal root of cXI

77
Q

What is the brain stem nucleus of the hypoglossal nerve?

A

Hypoglossal nucleus

78
Q

Where do the hypoglossal nerve rootlets emerge?

A

cXII rootlets emerge between the pyramids and the olives

79
Q

What happens in MND?

A
  • chronic degenerative disorder (> 50 ys)
  • degeneration of corticobulbar tracts
  • degeneration of nucleus ambiguus and hypoglossal nucleus
  • dysphonia (difficulties in phonation)
  • dysphagia (difficulties in swallowing)
  • dysarthria (difficulties in articulation)
  • weakness spasticity of tongue weakness, spasticity of tongue
80
Q

What would happen if cranial nerves XI and XII were compressed by a tumour?

A
  • dysphonia (difficulties in phonation)
  • unilateral weakness wasting and fasciculation of tongue
  • suppression of gag reflex
  • unilateral wasting of sternomastoid and trapezius muscles
81
Q

What is the reticular formation and where is it found?

A

Sets of nuclei in the ventral medulla which have various projections to most parts of the CNS
Regulates many function
Noradrenergic, seratonergic and dopaminergic pathways
- The reticular formation has widespread ascending and descending projections and is involved in multiple normal and pathological processes.

82
Q

What are the Noradrenergic nuclei of the reticular formation and what their projections modulate?
What can happen of the problems affect the Noradrenergic projections?

A
  • locus coeruleus, A5, A7, A1, A2
  • arousal
  • attention
  • awareness
  • sleep
  • cognition
  • cardiac reflexes
  • respiration
  • REM sleep
  • depression
  • anxiety
  • stress
  • opiate withdrawal
  • Rett syndrome
83
Q

What are the Serotonergic nuclei of the reticular formation and what their projections modulate?

A 
raphe dorsalis 
raphe pontis centralis superior 
raphe pontis 
raphe magnus
raphe pallidus and obscurus

• reward • sleep • nociception

(• The serotonergic raphe nuclei innervate every major CNS subdivision.)

84
Q

What are the dopaminergic nuclei of the reticular formation and what their projections modulate?
What can happen of the problems affect the dopaminergic projections?

A

ventral tegmental area
substantia nigra (Rich in melanin - degradation product of dopamine)
locus coeruleus

  • reward
  • cognition
  • motivation
  • emotional processing
  • motor control
  • saccadic eye movement
  • addiction
  • schizophrenia
  • insomnia
  • ADHD
  • Parkinson’s disease (degrades first)

• The dopaminergic substantia nigra is affected in Parkinson’s disease

85
Q

What happens in unilateral lesions (stroke, tumour, multiple sclerosis) of the brainstem?

A
  • ipsilateral cranial nerve dysfunction
  • contralateral spastic hemiparesis
  • hyperreflexia
  • ipsilateral incoordination
  • contralateral hemisensory loss
86
Q

What happens in bilateral lesions (trauma, stroke, tumour) of the brainstem?

A

Coma

Death

87
Q

What is a motor strategy?

A

A SET OF MOTOR PROGRAMS SELECTED TO ACHIEVE A FINAL GOAL

- eg. Standing up and shaking someones hand

88
Q

What is a motor program?

A

MOTOR PROGRAM: A SET OF MUSCLE COMMANDS THAT ARE STRUCTURED BEFORE THE MOTOR ACTS BEGIN AND THAT CAN BE SENT TO THE MUSCLES WITH THE

CORRECT TIMING SO THAT THE ENTIRE SEQUENCE CAN BE CARRIED OUT IN THE ABSENCE OF PERIPHERAL FEEDBACK (Keele, 1968).

89
Q

What is a reflex?

A

A RESPONSE, OR PATTERN OF RESPONSES, RELIABLY EVOKED BY A SPECIFIC STIMULUS OR SET OF STIMULI. ALTHOUGH THE RESPONSES MAY VARY IN MAGNITUDE THEIR SPATIAL AND TEMPORAL PATTERN REMAINS STEREOTYPED

90
Q

What is meant by peripheral feedback in the context of a motor program?

A

By peripheral feedback we mean those sensory signals that arise from sensory receptors in the muscles, tendons, and joints and from visual and vestibular mechanisms which allow the nervous system to monitor the progress of a movement

91
Q

How do we make adjustments to motor program’s to accommodate for the unknown or unexpected environmental factors?

A

VOLUNTARY corrections of force and in part by the action of REFLEXES.

92
Q

How many phases are in the emg pattern for everyday movements?

A

Tri-phasic

- (breaks down in Parkinson’s)

93
Q

What area of Brodmann is the pre-central (motor) cortex?

A

Area 4

94
Q

From where do the fibres of the pyramids arise?

A

The proportion of pyramidal fibres arising from area 4 is about 30%. Another 30% arise from area 6 ( the pre-motor and supplementary motor areas) and the remainder arise from the parietal lobes (areas 1,3,5 and 7).

95
Q

Which areas of the body particularly receive motor neurones minsynaptically?

A

especially those controlling the hand and fingers

96
Q

What are the chronic signs of stroke?

A

(usually after 2 or 3 weeks but highly variable) the chronic signs appear)
[1] abnormal distribution of muscle tone with excessive tone in some muscles i.e. SPASTICITY. [2] exaggerated deep reflexes (e.g. knee jerk). [3] loss of superficial reflexes (e.g. abdominal, cremasteric and plantar reflexes). [4] BABINSKI’S SIGN - which appears acutely but is maintained into the chronic stage.
When pure pyramidal tract lesions (ie. without internal capsule) are made experimentally only [3] and [4] are seen together with the acute signs of stroke

97
Q

What are the acute signs of stroke?

A

the loss of muscle tone and weakness on the side contralateral to the stroke i.e. HEMIPLEGIA. Also, BABINSKI’S SIGN appears

98
Q

What do the changes in reflex excitability after stroke show about the effects of the corticospinal tract?

A

the corticospinal tract is involved in regulating spinal interneurones as well as motoneurones

99
Q

When the pyramidal tract is intact, why does the Babinski’s sign not appear?

A

The appearance of Babinski’s sign is an example of a RELEASE PHENOMENON - with an intact pyramidal tract this reflex pathway is depressed by descending control.

100
Q

What are the three major pathways for sensory transmission to the sensorimotor cortex?

A

Sensory inputs are conveyed to area 4 through the nucleus ventralis lateralis (VL) and nucleus ventralis posterolateralis (VPL) of the thalamus.
VL receives excitatory inputs from the deep cerebellar nuclei.
VPL receives excitatory input from the spinothalamic pathway and from the dorsal column pathway

101
Q

What are the 2 motor areas in area 6?
Wat areas are they connected too?
What are there role thought to be?

A

The supplementary motor area receives synaptic input from the nucleus ventralis anterior of the thalamus (VA).
This area is connected to the basal ganglia.
The pre-motor area receives input from VL which is connected to the deep cerebellar nuclei

It is thought that these areas are involved in the selection and activation of specific motor programs.
Both contain a complete and topographic map of the body

102
Q

To what brain areas does cerebral blood flow increase in a simple finger movement?

A

When a simple finger movement is made CBF increases in area 4. It also increases in the sensory cortex because of the peripheral feedback generated by the movement.

103
Q

To what areas of the brain does cerebral blood flow increase when a complex movement is performed?

A

When a simple finger movement is made CBF increases in area 4. It also increases in the sensory cortex because of the peripheral feedback generated by the movement.

When a more complex movement is made which requires thought and planning CBF increases also in the supplementary motor area.

104
Q

To what areas of the brain does the cerebral blood flow increase in when a complex movement is mentally rehearsed but not performed?

A

When the complex movement is mentally rehearsed but not executed CBF increases in the supplementary area but not in area 4.

The supplementary area therefore concerns itself with movement planning.

105
Q

What happens in primary somatosensory cortical damage?

A

somatosensory anaesthesia (loss of touch and conscious proprioception). Pain remains intact (= parieto-insular supplementary area)

106
Q

What happens in damage to supplementary somatosensory cortex - specifically to the Superior parietal lobule?

A

contralateral somatosensory agnosia (inability to recognise common objects by palpation alone: = touch and proprioception)

107
Q

What happens in damage to supplementary somatosensory cortex - specifically to the inferior parietal lobule?

A

in the dominant hemisphere (Left) concerned especially with language (alexia). Damage of non-dominant hemisphere = bizarre disturbances of “body image” known as somatosensory disregard: eg patients ignore parts of their body, believing they belong to someone else (contralateral to lesion) in spite of the fact that the body part is not anaesthetic to any stimulus

108
Q

Where are the hippocampus and the fornix located?

A

N the floor of the lateral ventricle and the medial wall of the lateral ventricle respectively

109
Q

What is the hippocampus important for and what happens to it in Alzheimer’s?

A

Behaviour and memory (emotional aspects - part of limbic system)
Shrinks with associated cortex

110
Q

List the important ascending cortical connections that you must know

A

Somatosensory from the thalamus: - (inputs from spinal cord via VPL, and trigeminal via VPM)

Auditory: - from the thalamus (inputs from the cochlea via the medial geniculate nucleus)

Visual: - from the thalamus (inputs from the retina via the lateral geniculate nucleus)

Smell (direct into the olfactory cortex) and Taste (via VPM)

Complex information from the cerebellum and basal ganglia via the thalamus

111
Q

List the important descending cortical cortical connections that you must know

A
  • Motor to the spinal cord (corticospinal tract)
  • Motor to the brainstem motor nuclei (cortico-bulbar tract)
  • To the motor control centres (targeted to the basal ganglia and cerebellum) )
  • To the limbic system
112
Q

Explain what is meant by ‘connections with in the cortex’

A
  • On same side: association fibres connecting different brain regions
  • On opposite sides: commissures including the corpus callosum
113
Q

How are the visual and supplementary visual cortex areas organised in the occipital lobe?

A

Medial surface of the Occipital lobe - calcarine sulcus - upper and lower lips - visual cortex

Remaining occipital lobe - association visual cortex

Signals from primary to secondary areas
Dorsal stream - assessing spatial area, motion etc
Ventral - colour, shape
Facial recognition

114
Q

What are the following conditions caused by lesions to the supplementary visual areas:
visual agnosia?
Visual disregard?

A

Visual agnosia - inability to recognise everyday objects

Visual disregard - lesion of non-dominant inferior parietal lobule
contralateral hemifield can be seen but is ignored by patient
(cf. somatosensory disregard)

Face recognition – right hemisphere

115
Q

What do you know about Blint’s Syndrome?

A

bilateral lesions of the dorsolateral parieto-occipital association cortex - clinical triad

Simultanagnosia:- impaired ability to perceive parts of the visual scene as a whole. Patient can perceive only one small region of the visual field at a time. This region can shift around unpredictably, often causing patients to loose track of what they were looking at

Optic ataxia:- impaired ability to reach for or point to objects in space under visual guidance. However once an object has been touched, the patient can perform smooth movements back and forth to it even with their eyes closed (cf cerebellar ataxia – loss of proprioception)

Ocular apraxia:- difficulty directing one’s gaze towards objs in the peripheral vision though saccades. Some patients need to move their heads to initiate a voluntary redirection of gaze

116
Q

10 points on the neuro anatomy of language?

A
  1. Sounds processed in mid brain. Spoken language sent to Wernicke’s area in left hemisphere.
  2. Written language processed in visual area; sent to angular gyrus in left hemisphere. Changed to sound; sent to Wernicke’s. 3. Wernicke’s area extracts meaning from language from any source. Thoughts encoded into crude linguistic outline then sent to Broca’s area in left hemisphere where refined into grammatical form.
  3. Broca’s then signals to motor cortex to make speech. Blood flow studies confirm anatomical conclusions from studies of Stroke and brain damage.
  4. Low frequencies sent to Wernicke’s. High frequencies giving emotional information go to right hemisphere.
  5. Damage right hemisphere- loss of ability to interpret emotional content.
  6. Damage Broca’s area- know what to say but can’t do it with grammar
  7. Damage Wernicke’s area- perfect grammar but meaningless.
  8. Same effects seen with sign language
117
Q

What do you know about different types of association fibres?

A

Superior longitudanal fasciculus: connects frontal and occipital (arcuate frontal to temporal)
Inf. long. fascic: occip to temp for visual recognition
Uncinate fascic: ant/inf frontal to temp - regulates behaviour

118
Q

What do you know about commisures and what happens when they fail?

A

Corpus callosum: connects hemispheres.
“Split brain” produces 2 halves. Visual information to Right non-dominant hemisphere gets no verbal response. So can’t name objects or read words presented in left visual field. Tumour of splenium produces alexia without agraphia - speak and write but cannot read - separation visual processing in right hemisphere from language in left dominant (e.g. of a disconnection syndrome).

119
Q

What focal cortical lesion conditions do you know?

A

Focal cerebral lesions:
epilepsy; sensory and/or motor deficits; & psychological deficits. Left frontal lobe lesion produces “Jacksonian seizures”, contralateral hemiplegia, aphasia (alexia & agraphia)

120
Q

What happens in bilateral cortical degeneration?

A

Alzheimer’s degeneration of temporal, parietal, & limbic. Loss of language and memory

121
Q

Left parietal lesion?

A

anomia, acalculia, as well as alexia and agraphia

122
Q

What does a right parietal lesion cause?

A

constructional apraxia (skilled movements)

123
Q

What might a left temporal lesion cause?

A

absences, automatisms, déjà vu, Wernicke’s aphasia.

Superior contralateral visual field loss.

124
Q

What might single and bilateral occipital lesions cause?

A

single - simple visual hallucinations, contralateral field loss bilateral - blindness - complex

Neuroscience (16 decks)

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