23. Cortex, Thalamus & Hypothalamus Flashcards

1
Q

What are the three types of fibre that make up white matter?

A

Association Fibres – connect with areas in the same hemisphere Commissural Fibres – connect the two hemispheres Projection Fibres – connect the cortex with lower brain structures (e.g. thalamus)

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2
Q

How many layers of grey matter are there?

A

3-6 (they are usually numbered by roman numerals)

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3
Q

What is the neocortex?

A

A part of the cerebral cortex concerned with sight and hearing in mammals, regarded as the most recently evolved part of the cortex

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4
Q

Describe the different connections of the 6 layers of grey matter.

A

Layers 1-3 = mainly cortico-cortical connections Layer 4 = input from the thalamus Layer 5-6 = connections with subcortical, brainstem and spinal cord

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5
Q

What does layer 1 mainly consist of?

A

Neutropil – an area composed mostly of unmyelinated axons, dendrites and glial cell processes that forms a synaptically dense region containing a relatively low number of cell bodies

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6
Q

What type of neurone is found in layer 4?

A

Stellate neurones

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7
Q

What type of neurone is found in layer 5?

A

Pyramidal neurones

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8
Q

What are the two parts of the visual association cortex and what are they responsible for?

A

Dorsal Pathway – responsible for interpretation of spatial relationships and movements Ventral Pathway – responsible for form and colour

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9
Q

What is the role of the posterior parietal association cortex?

A

It creates a SPATIAL MAP of the body in its surroundings from multi-modality information

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10
Q

What could injury of this part of the association cortex lead to?

A

Disorientation Inability to read a map or understand spatial relationships Apraxia Hemispatial Neglect

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11
Q

Define apraxia.

A

Inability to make skilled movements with accuracy

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12
Q

What is the temporal association cortex responsible for?

A

Language Object Recognition Memory Emotions

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13
Q

What are the two main consequences of injury to the temporal lobe?

A

AGNOSIA – inability for the brain to interpret sensory information although the nerves carrying sensory information to the brain are fine E.g. visual agnosia – patients can see perfectly fine but they can’t interpret sympbols such as letters RECEPTIVE APHASIA –unable to understand language in the spoken or written forms

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14
Q

What are the consequences of visual association cortex lesions?

A

Prosopagnosia – inability to recognise faces

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15
Q

What is the role of the frontal lobe?

A

Executive functions e.g. planning, judgement, foresight, personality

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16
Q

What are the consequences of a prefrontal lobotomy?

A

Change in personality Inappropriate behaviour Lack of ability to remember and relate things over time Attention span and ability to concentrate are diminished

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17
Q

What two areas does the prefrontal cortex receive massive inputs from?

A

Sensory association cortex (somatosensory, visual and auditory) Dorsomedial Nucleus of the thalamus NOTE: lesion of the dorsomedial nucleus will have similar consequences to prefrontal lobotomy

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18
Q

If you give someone with a unilateral parietal lobe lesion something to draw, what will you expect him or her to do?

A

Hemispatial neglect – they will only draw half of it

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19
Q

What effect do temporal cortex lesions have on memory?

A

Impaired short-term memory They are effectively trapped in a 30 second window of memory

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20
Q

Describe hemispheric specialisation.

A

Right hemisphere = creative + artistic Left hemisphere = logical + scientific

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21
Q

What is a callosotomy?

A

A palliative procedure used for the treatment of seizures The corpus callosum is key for the interhemispheric spread of epileptic activity

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22
Q

State a type of imaging that uses the movement of water molecules in the brain to infer the underlying structure of white matter.

A

Diffusion Tensor Imaging – Tractography

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23
Q

State two types of brain stimulation testing and what it can be used for.

A

Transcranial Magnetic Stimulation (TMS)  Magnetic field induces a current in the cortex  This is method of focally stimulating different areas of the cortex and testing what each area is responsible for Transcranial Direct Current Stimulation (TDCS)  This changes the excitability of neurones but does NOT directly induce neuronal firing  Anode = increases neuronal excitability  Cathode = decreases neuronal excitability  TDCS could be used to reduce motion sickness by suppressing the area of the cortex associated with perceiving vestibular information

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24
Q

Describe and explain how PET scans work. What can it be used for?

A

A radioactive tracer is attached to a molecule to locate areas of the brain where that molecule is being absorbed The tracer emits positrons, which are then detected by the receptors It can be used in Parkinson’s disease to see the uptake of dopamine precursors by dopaminergic neurones

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25
Q

What is the difference between MEGs and EEGs?

A

MEGs = magnetoencephalography – measures magnetic fields EEGs = electroencephalography – measures electric fields

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26
Q

What is a major problem with MEGs and EEGs and how is this resolved?

A

It is quite noisy – there is a lot of background activity This is resolved by doing a trial of a large number of participants so that an average can be found Once the average has been found, it can be deducted from the captured signal to see the underlying activity

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27
Q

What is fMRI?

A

Function MRI It detects changes in blood flow in the brain It relies on the fact that blood flow in the brain and neuronal activity are coupled – more active parts of the brain require increased blood flow

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28
Q

Which areas of the brain become more active when participants imagine positive events?

A

Amygdala Rostral anterior cingulate cortex

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29
Q

Where is the thalamus found within the brain?

A

It is right in the middle the brain just under the posterior half of the corpus callosum

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30
Q

What separates the two halves of the thalamus?

A

3rd ventricle Some people have a bridge connecting the two halves

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31
Q

Describe the connections of the thalamus with the forebrain.

A

Each half of the thalamus has ipsilateral connections with the forebrain

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32
Q

What is the main function of the thalamus?

A

It is a relay centre between the cerebral cortex and the rest of the CNS

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33
Q

What is the only function that is not represented within the thalamus?

A

Olfaction

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34
Q

Describe how thalamic nuclei are named.

A

They are named based on their location within the thalamus

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35
Q

What is the classification of thalamic nuclei based on and what are the four different classes?

A

The classification is based on the connections of the thalamic nuclei with the cortex SPECIFIC – connected to primary cortical areas ASSOCIATION – connected to association cortex INTRALAMINAR – connected to ALL cortical areas RETICULAR –not connected to the cortex

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36
Q

Which nuclei connect with the motor cortex (primary, premotorand supplementary)?

A

Ventral lateral Ventral anterior

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37
Q

Which nuclei relay sensory information from different parts of the body?

A

Head – Ventral posteromedial Below the neck – Ventral posterolateral

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38
Q

Which nucleus is connected to the primary visual cortex?

A

Lateral geniculate nucleus

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39
Q

Which nucleus is connected to the primary auditory cortex?

A

Medial geniculate nucleus

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40
Q

The association cortex can be divided into three areas based on thalamic function. What are these three areas?

A

Prefrontal Cortex Parieto-tempero-occipital Cortex Cingulate Cortex

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41
Q

What do the anterior, lateral dorsal and dorsomedial nuclei connect with?

A

Prefrontal and Cingulate Cortex

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42
Q

What do the lateral posterior and pulvinar nucleus connect with?

A

Prefrontal and Parieto-tempero-occipital Cortex

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43
Q

What important system are the intralaminar and reticular nuclei a part of?

A

Reticular activating system – involved in maintaining consciousness

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44
Q

Describe how the reticular nuclei affect cortical activity.

A

The reticular nuclei don’t have any direct connections with the cortex but they do have widespread intrathalamic connections with all other thalamic nuclei so it can influence the flow of information from the othernuclei to the cortex

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45
Q

What is the core of grey matter that runs through the brainstem and is involved in the reticular activating system?

A

Reticular formation

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46
Q

How do the intralaminar nuclei modulate the activity of the cortex?

A

The reticular formation projects up to the thalamus to the intralaminar nuclei and the intralaminar nuclei, because of their diffuse cortical projections, can modulate the activity of the cortex

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47
Q

What is thalamic syndrome?

A

Syndrome that develops after thalamic stroke The symptoms depend on which part of the thalamus has been affected

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48
Q

What three main changes occur in thalamic syndrome?

A

CHANGE IN SENSATION – reduced, exaggerated, altered PAIN – central, non-localised (not easily treated because normal analgesics have no effect – may need to use opioids or anti-convulsants/anti-depressants) EMOTIONAL DISTURBANCE – the nuclei that transmit information to and from the association cortex are associated with the limbic system

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49
Q

Describe the location and structure of the hypothalamus.

A

The hypothalamus is just below the thalamus and is divided by the 3rd ventricle It also has ipsilateral connections with the forebrain

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50
Q

How is the hypothalamus involved in maintaining homeostasis?

A

It coordinates these different mechanisms to maintain homeostasis:  Autonomic nervous system  Endocrine system  Behaviour

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51
Q

State some forebrain structures that the hypothalamus has very close connections with

A

Olfactory system Limbic system

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52
Q

List some structures of the limbic system.

A

Hippocampus Amygdala Cingulate Cortex Septal Nuclei

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53
Q

What does the behavioural control exerted by the hypothalamus include?

A

Eating and drinking Expression of emotion Sexual behaviour Circadian rhythm Memory

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54
Q

Which nucleus is involved in the circadian rhythm?

A

Subrachiasmatic nucleus

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55
Q

How is our behaviour directed towards homeostatic goals?

A

There is a pleasure centre within the limbic system, which, whenever you’ve achieved homeostasis (e.g. eating food when you’re hungry), the activity of the pleasure centre increases

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56
Q

What are the presenting symptoms of hypothalamic tumour?

A

Polydipsia Polyuria Absent menses

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57
Q

What are some later symptoms of hypothalamic tumour?

A

Labile emotions, rage Inappropriate sexual behaviour Memory lapses Temperature fluctuation Thyroid, adrenal cortex and gonadal function decreases Hyperphagia

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58
Q

How common are strokes in US?

A
  • 3rd leading cause of death in US - major cause of adult disability - about 800,000 people in US have a stroke each year - on avg, one American dies from a stroke q 4 minutes
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59
Q

Definition of a stroke? 2 main types?

A
  • alteration of cerebral blood flow either from: brain ischemia: thrombosis, embolism, or systemic hypo perfusion or brain hemorrhage: intracerebral hemorrhage or SAH
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60
Q

source of anterior circulation of the brain?

A
  • from internal carotid - majority of blood flow to the brain
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61
Q

Source of posterior circulation of the brain?

A
  • verterbal-basilar
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62
Q

Cardiac sources of ischemic stroke?

A
  • a fib - ASD/VSD - recent AMI - endocarditis - cardiac tumor - valvular disorder
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63
Q

What is the most common stroke type?

A
  • ischemic stroke
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64
Q

Other etiologies of strokes?

A
  • atherosclerotic plaques (emboli from rupture, lack of perfusion from stenosis of vessels) - vasculitis - prothrombotic state - cerebral hemorrhage (20% of strokes)
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65
Q

How is a-fib a source of a stroke? - how does anticoag help this? aspirin?

A
  • embolization of intracardiac thrombi - most commonly from left atrial appendage - anticoagulation decreases the risk of stroke by up to 70% - aspirin decreases risk by 20-25%
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66
Q

Atrial and ventricular septal defects - source of stroke?

A

atrial: - if assoc with R to L shunt can cause stroke - patent foramen ovale: present in about 25% of general population, surgical or percutaneous closure ventricular: if assoc with R to L shunt can cause stroke

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67
Q

MI - as source of stroke?

A
  • most common in pts after anterior wall infarction - left ventricular wall mural thrombi: large infarctions, LV dilation, CHF
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68
Q

Endocarditis source of stroke?

A
  • emboli from vegetations
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69
Q

Cardiac tumor as a source of stroke?

A
  • obstruction of blood flow - can lead to arrhythmias (like a-fib) - embolization of tumor fragments
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70
Q

Valvular disorders as a source of a stroke?

A
  • native valves: rheumatic mitral stenosis is most commonly assoc with stroke - MVP: may have fibrinious deposits on valve - prosthetic heart valves: mechanical valves require lifelong anticoag - repaired cardiac valves: require only anticoag short term
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71
Q

How common is hemorrhagic stroke?

A

20% of al strokes - spontaneous intracerebral hemorrhage (10%) - SAH - other 10%: intracranial aneurysm, and arteriovenous malformations

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72
Q

What are the causes of spontaneous intracerebral hemorrhage?

A
  • assoc with poorly controlled HTN: commonly located in basal ganglia and less commonly in pons, thalamus, cerebellum or cerebral white matter - lacunar infarcts are assoc with HTN or DM - bleeding disorders - amyloid angiopathy: amyloid deposits lead to weakening of cerebral blood vessels resulting in a stroke
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73
Q

Causes of SAH?

A
  • trauma - spontaneous SAH is usually related to a ruptured AVM or aneurysm - abnorm vascular composition (amyloid angiopathy or dissection) - illict drug use such as cocain or amphetamines - intracranial arterial dissections - 20% may have no ID cause
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74
Q

Most common site for intracranial aneurysm? What determines the risk of rupture?

A
  • most commonly located in circle of willis - aneurysm is usually asx until rupture - size and location determine risk of rupture: in general size over 1 cm carries a high risk of rupture
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75
Q

What is an arteriovenous malformation (AVM)?

A
  • abnormal arterial to venous connection - arteries and veins are tangled up - veins are under high pressure which leads to rupture - also assoc with risk of seizure - occurs in 0.01% of population, 1-2% of all strokes and 9% of SAH - may be assoc with heredirary hemorrhagic telangiectasia (HHT; osler-weber-rendu syndrome)
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76
Q

Subtypes of strokes?

A
  • hemorrhagic: intracerebral hemorrhage SAH - ischemic: anterior circulation posterior circulation lacunar
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77
Q

What is an intracerebral hemorrhage? Major causes?

A
  • arterial bleeding directly into the brain parenchyma - major causes: HTN, trauma, bleeding disorder, amyloid angiopathy, illicit drug use, AVMs - accum of blood over minutes to hours forming a localized hematoma - *** neuro sxs increase gradually as hematoma grows - brain tissue is destroyed as hematoma enlarges, pressure created by blood and surrounding brain edema is life-threatening - large hematomas have a high mortality and morbidity - goal of tx is to contain and limit the bleeding
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78
Q

2 main causes of SAH? What is happening?

A
  • ruptured aneurysm (most common) or AVM - bleeding into CSF and space surrounding brain - aneurysm bleeds into CSF under arterial pressure and increased the ICP (this causes sxs) - bleeding lasts a few seconds but rebleeding is common
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79
Q

Main tx goal of SAH?

A
  • Identification of source of bleeding and tx before rebleeding occurs - other goal of tx is to prevent brain damage due to delayed ischemia related to vasoconstriction of intracranial arteries: blood within the CSF induces vasoconstriction which can be intense and severe (can cause another stroke!)
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80
Q

2/3 of all ischemic strokes affect what circulation in the brain? 2 main arteries of this circulation?

A
  • anterior circulation - MCA and ACA
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81
Q

What is the most commonly affected vessel in ischemic strokes?

A
  • MCA: 96% of all anterior circulation strokes (due to direct flow from internal carotid artery and its large size) - 3% in ACA - 1% in entire ICA distribution
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82
Q

What arteries would be involved in posterior circulation stroke? What areas of the brain does this supply?

A
  • verterbral artery - basilar artery - posterior cerebral artery - blood supply to posterior portion of brain, including occipital lobes, cerebellum, and brainstem
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83
Q

Outcomes of posterior circulation strokes?

A
  • terrible! - 20% of all strokes - 20-60% have unfavorable outcomes - basilar artery occlusion: 90% mortality, 8-14% of all posterior circulation strokes
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84
Q

What are lacunar strokes?

A
  • small lesions (less than 5 mm) that occur in penetrating arterioles in basal ganglia, pons, cerebellum, internal capsule, thalamus, and deep cerebral white matter
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85
Q

Outlook of lacunar strokes? How do these appear on CT?

A
  • less morbidity and mortality than other strokes - on CT sometimes seen as “punched out hypodense areas” but sometimes no abnormalities can be seen
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86
Q

Anterior strokes occur from occlusion off of what artery?

A
  • internal carotid artery or its branches
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87
Q

Posterior strokes occur from occlusion off of what artery?

A
  • vertebral artery or its branches
88
Q

HTN may cause what tpye of strokes?

A
  • intracerebral hemorrhages or lacunar infarcts from small vessel occlusion
89
Q

Stroke RFs?

A
  • HTN - DM - hyperlipidemia - cigarette smoking - cardiac disease - elevated blood homcysteine levels - AIDs - recreational drug abuse - heavy alcohol consumption - family hx of stroke - overweight - ischemic heart disease - PVD - sedentary lifestyle - men older than 45 and women older than 55 - OCPs combined with smoking - hypercoagulopathy - polycythemia - prior stroke - sleep apnea (causes pro-thrombotic state while sleeping) - bleeding disorders
90
Q

What is aphasia?

A
  • acquired communication disorder - impairs ability to process language but doesn’t affect intelligence - impairs ability to speak and understand others - experience diffciculty reading and writing
91
Q

Types of aphasia?

A
  • global - anomic - broca’s - wernicke’s
92
Q

Global aphasia?

A
  • most severe form - produce few recognizable words - understands little or no spoken speech - can neither read or write
93
Q

Anomic aphasia?

A
  • persons who are left with persistent inability to supply words for the things that they want to talk about. - sig in nouns and verbs - understand speech well - read adequately - poor writing ability
94
Q

Broca’s aphasia (expressive)?

A
  • broca’s area supplied by superior division L MCA - speech output severely reduced limited mainly to short utterances of less than 4 words: formation of sounds often laborious/clumsy, and comprehension fair, and cognitively intact - reading and writing also affeted - AKA expressive aphasia
95
Q

Wernickes aphasia (receptive)?

A
  • wernickes area supplied by inferior division of L MCA - fluent but meaningless spontaneous speech - jargon of real words and nonwords - individual unaware of language errors unlike in broca’s aphasia - comprehension is poor - writing, reading also poor - AKA receptive aphasia
96
Q

Dysarthria?

A
  • problem with muscles that produces speech
97
Q

Dysconjugate gaze?

A
  • failure of eyes to turn together in the same direction
98
Q

Apraxia?

A
  • difficulty with motor planning to perform tasks or movements when asked (ex: being asked to put on shoes and tie them)
99
Q

Dystaxia?

A
  • lack of muscle coordination
100
Q

Agnosia?

A
  • inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes or smells
101
Q

FAST campaign?

A

F- facial droop A - arm weakness S - speech difficulties T - time to call 911

102
Q

Diff sxs of a stroke?

A
  • typical: right sided facial droop with weakness of R arm and leg - sudden onset severe HA - severe dizziness, N/V - acute speech deficit - sudden onset impaired consciousness w/o focal neuro deficits
103
Q

Sxs of a SAH?

A
  • Sxs begin abruptly - sudden increase in ICP may cause a cessation of activity (knees may buckle, loss of memory) - sudden, severe HA “thunderclap” followed by vomiting - usually no focal neuro signs - may have signs of meningeal irritation - sxs may be preceded by heavy physical exertion or sex
104
Q

Sxs of an intracerebral hemorrhage?

A
  • sxs slower onset than SAH and increase over minutes to hours - sxs worsen as hematoma enlarges - HA and vomiting occur in about half of pts - sxs may be preceded by heavy physical exertion or sex - neuro sxs will vary depending on location and size of bleed and may be similar to ischemic sxs - with large hematoma - may have decreased LOC
105
Q

Differences and similarities b/t SAH and ICH strokes?

A
  • SAH: sxs at max intensity at onset – ICH: sxs increase with intensity as bleed worsens - both have HA but much worse at onset and more common in SAH - both may lack focal deficits - may have meningeal signs - both may rapidly deteriorate clinically
106
Q

What side of the body is affected by a stroke?

A
  • brain damage in one side results in neuro deficits on opposite side of body
107
Q

General sxs of an anterior circulation stroke? (ACA and MCA)?

A
  • may have one or all of the following sxs: face-hand-arm-leg contralateral hemiparesis aphasia dysarthria
108
Q

ACA occlusion may cause what sxs?

A
  • leg weakness and sensory loss (contralateral side affected) - arm (esp proximal) weakness and sensory loss: contralateral side - pronator drift - urinary incontinence
109
Q

MCA occlusion may cause what sxs?

A
  • contralateral hemiplegia in the face-arm-leg - homonymous hemianopsia - if on L and it is dominant hemisphere = aphasia: wernickes (receptive) brocas (expressive) - nondominant right hemisphere: confusion, spatial disorientation, sensory and emotional neglect of other side of body - apraxia
110
Q

Structures that rely on posterior circulation blood supply?

A
  • structures that rely on posterior circulation blood supply: brainstem thalamus hippocampus cerebellum visual cortex temporal lobes occipital lobe
111
Q

What CNs are housed in midbrain?

A
  • III and IV
112
Q

What CNs are housed in pons?

A
  • V, VI, VII, VIII
113
Q

What CNs are housed in medulla?

A
  • IX, X, XI, XII
114
Q

What cranial nerves can be affected by a stroke affecting the brainstem?

A
  • CNs III-XII
115
Q

Sxs of posterior circulation stroke?

A
  • vertigo - diplopia, dysconjugate gaze, ocular palsy, homonymous hemianopsia - sensorimotor deficits - ipsilateral face and contralateral limbs (crossed findings), drop attack - dysarthria - ataxia
116
Q

What do you have to rule out if a pt presents with vertigo?

A
  • posterior circulation stroke!
117
Q

What are the 5 D’s of posterior stroke sxs?

A
  1. dizziness 2. diplopia 3. dysarthria: difficulty speaking (loss of motor control for speech) 4. dysphagia: diff swallowing 5. dystaxia: difficulty controlling voluntary movement
118
Q

Sxs of lacunar stroke?

A
  • pure motor loss (weakness): most common presentation in up to 2/3 of cases - or pure sensory - many other lacunar snydromes including: senorimotor stroke (2nd most common) ataxic hemiparesis
119
Q

NIH stroke scale?

A
  • use in both clinical trial and as part of clinical care in US - 0 = no stroke - 1-4 = minor - 5-15 = mod - 16-20 = mod to severe - 21-42 = severe
120
Q

Acute eval? what is criticual to know?

A
  • timing of onset of sxs is critical - assessment of stroke risk factors - physical exam looking for stroke sources
121
Q

Blood work for suspected CVA?

A
  • lipid profile - blood sugar - CBC - CMP - PT/PTT - cardiac biomarkers to R/O cardiac ischemia
122
Q

Dx workup of CVA?

A
  • acute workup = noncontrast CT of head (rule out/in hemorrhagic stroke) - later = MRI +/- MRA of brain - EKG - US of carotids - echo
123
Q

Window of opportunity to tx a CVA?

A
  • time is very impt in order to receive medication - window of opportunity to start tx stroke pts is 3 hrs, but to be eval and receive tx, pts need to get to hospital w/in 60 min
124
Q

What is in your medical tool bag for CVA tx?

A
  • ASA - heparin or lovenox - fibrinolytics - percutaneous intracerebral intervention in selected cases
125
Q

Tx of ischemic stroke?

A
  • clot-busters - must give w/in 3-4.5 hrs and within an hour of arrival to hospital
126
Q

Tx of hemorrhagic stroke?

A
  • correct cause of hemorrhage
127
Q

What should be continuously monitored in stroke pts?

A
  • vital signs, neuro status, cardiac and respiratory status - medical support as needed: if they can’t protect airway: support airway - intubate
128
Q

What is tPA?

A
  • tissue plasminogen activator - clot busting drug aka fibrinolytic aka thrombolytic - dissolve clot in ischemic strokes and neuro deficits are more likely to improve - if mistakenly given to hemorrhagic stroke pts = death
129
Q

Inclusion criteria for thrombolytics?

A
  • clinical dx of ischemic stroke causing measurable neuro deficit - onset of sxs less than 4.5 hrs before beginning tx - 18 or older
130
Q

Exclusion criteria for thrombolytics (hx)?

A

-sig stroke or head trauma in previous 3 months - previous ICH - intracranial neoplasm, AVM, or aneurysm - recent intracranial or intraspinal surgery - arterial puncture at a noncompressible site in previous 7 days

131
Q

Exclusion criteria for thrombolytics (clinical)?

A
  • sxs suggestive of SAH - persistent BP elevation (SBP 185 or greater or DBP 110 or greater) - serum glucose less than 50 mg/dl - active internal bleeding - acute bleeding diathesis, including but not limited to conditions defined in hematologic - Head CT scan: evidence of hemorrhage evidence of multilobar infarction with hypodensity involved more than 33% of cerebral hemisphere
132
Q

Exclusion criteria for thrombolytics (hematologic)?

A
  • platelet count below 100,000 mm3 - current anticoag use with INR greater than 1.7, or PT greater than 15 sec - Heparin use within 48 hrs and abnorm elevated aPTT - current use of direct thrombin inhibitor or direct factor Xa inhibitor with evidence of anticoag efect by lab tests
133
Q

Relative exclusion criteria for thrombolytics?

A
  • only minor and isolated neuro signs - spontaneously clearing stroke sxs - major surgery or serious trauma in last 14 days - GI or urinary tract bleedin in previous 21 days - MI in previous 3 months - seizure at onset of stroke with postictal neuro impairments - pregnancy
134
Q

Relative exclusion criteria for tx from 3-4.5 hrs from sx onset?

A
  • age: older than 80 - oral anticoag use regardless of INR - very severe stroke (NIHSS score above 25) - combo of both previous ischemic stroke and DM
135
Q

Medical management for stroke pts?

A
  • dietary - neuro - PT and OT - ST: swallowing eval, and speech retraining - nursing - physical med and rehab Dr. consultation
136
Q

D/C meds for stroke pts?

A
  • ASA - statin - maybe anticoag (for sure if A fib) - plavix? - antiHTNs - assess adequacy of blood sugar control if DM * don’t give anticoag initially after stroke - bleed again, also don’t want to give antiHTNs because need high BP for better perfusion to the brain - d/c pts on these meds though
137
Q

Recovery from aphasia?

A
  • after stroke - if sxs last longer than 2 or 3 months, complete recovery is unlikely: people continue to improve over period of time - slow process - need to learn compensatory strategies for communicating
138
Q

Residual effects of strokes?

A
  • emotional lability (mood swings, depression) - perceptual effects: difficulty recognizing, understanding familiar objects - difficulty planning and carrying out simple tasks - loss of awareness (one sided neglect) - dysphagia (diff swallowing) and aspiration
139
Q

Medical complications of a stroke?

A
  • bladder dysfxn - bowel dysfxn - pressure ulcers - malnutrition - dehydration - falls and injuries - recurrent strokes - DVT - dysphagia - aspiration pneumonia - seizures - spasticity
140
Q

What is a TIA?

A
  • stroke like event lasting less than 24 hrs (usually 20 min) that occurs secondary to cerebral ischemia - sxs resolve completely - all TIAs are ischemic
141
Q

Likelihood of having a stroke after having a TIA?

A
  • more than 1/3 of people will go on to have a stroke - 5% of strokes will occur within 1 month of TIA or first stroke - 12% will occur w/in 1 year - 20% will occur w/in 2 years - 25% will occur w/in 3 years
142
Q

Etiology and RFs of TIA?

A
  • same as ischemic sources - etiologies: from cardiac source: A fib. ASD/AVD, recent MI, endocarditis, cardiac tumor, valvular disorder other sources: atherosclerotic plaques: emboli from rupture or lack of perfusion from stenosis, vasculitis, prothrombotic state, cerebral hemorrhage RFs: HTN, DM, hyperlipidemia, cig smoking, cardiac disease, elev blood homocysteine levels, AIDS, recreational drug abuse, heavy ETOH consumption, family hx of stroke, overweight, ischemic heart disease, PVD, sedentary lifestyle, men older than 45 and women older than 55, OCPs with smoking, hypercoagulopathy, polycythemia, prior stroke, sleep apnea,and bleeding disorders
143
Q

Types of TIA?

A
  • amarosis fugax (transient monocular blindness) - low flow (severe episode of hypotension) - embolic - thrombotic
144
Q

Workup of TIA?

A
  • CT or MRI - carotid US - eval for soruce of emboli or thrombus
145
Q

Tx of TIA?

A
  • consider admission to hosp if seen within 72 hrs of sxs - RF management is same as if pt has had a stroke - be d/c on ASA, statin - maybe anticoag?
146
Q

Why do you want to avoid aggressive BP control in ischemic strokes?

A
  • want to increase cerebral perfusion
147
Q

What are the parts of the adrenal gland from the outside to the inside?

A

Zona Glomerulosa (aldosterone production) Zona Fasciculata (cortisol and sex steroids) Zona Reticularis (cortisol and sex steroids) Adrenal Medulla

148
Q

What is the direction of blood flow in the adrenals?

A

From the cortex towards the medulla

149
Q

What is produced by the adrenal medulla? What are the cells involved called?

A

Catecholamines by the Chromaffin cells

150
Q

What is produced in the adrenal cortex? State the four hormones produced.

A

Corticosteroids: Mineralocorticoids - aldosterone Glucocorticoids - cortisol Sex Steroids - androgens and oestrogens

151
Q

What is androstenedione?

A

It is a weak androgen that can be converted to testosterone and dihydrotestosterone

152
Q

How are corticosteroids transported in the blood?

A

They bind to plasma proteins. There is so much albumin that some corticosteroids will non-specifically bind to albumin. There are more specific plasma proteins - corticosteroid binding globulin

153
Q

Describe the difference in the blood concentrations of cortisol and aldosterone.

A

The concentration of cortisol is 1000 times greater than the concentration of aldosterone.

154
Q

How does cortisol concentration vary?

A

Cortisol concentration changes with the circadian rhythm. It is a stress hormone so is released more at times of stress.

155
Q

What are the effects of aldosterone?

A

Increased potassium and H+ secretion Increase sodium reabsorption

156
Q

Describe the mechanism of action of aldosterone.

A

Aldosterone binds to intracellular receptors and translocates to the nucleus and causes changes in transcription leading to the synthesis of ion channels and pumps.

157
Q

Describe the arrangement of the juxta-glomerular apparatus in the kidneys.

A

The juxta-glomerular cells are in contact with the afferent arteriole. The macula densa cells are next to the juxta-glomerular cells

158
Q

What hormone is stimulated by an increase in plasma osmolality?

A

Vasopressin

159
Q

What is a consequence of increase extracellular fluid volume?

A

Hypertension

160
Q

Describe how the juxtaglomerular apparatus can lead to production of aldosterone.

A

Macula densa detects a decrease in tubular sodium concentration and stimulates the release of renin from the juxta-glomerular cells. Renin stimulates the production of angiotensin II, which upregulates aldosterone release.

161
Q

State three causes of renin release.

A

Decreased renal perfusion pressure Increased renal sympathetic activity Decreased sodium concentration at the top of the loop of Henle

162
Q

Describe the steps in the production of angiotensin II from the angiotensinogen.

A

Renin converts angiotensinogen (produced by the liver) to angiotensin I Angiotensin I is converted by ACE (which is found in high concentration in the lung endothelium) to Angiotensin II

163
Q

What are the effects of cortisol?

A

Increased hepatic gluconeogenesis Increase glycogenolysis Increased fat metabolism Stimulates peripheral protein catabolism Enhances effects of glucagon and catecholamines

164
Q

What are the three effects of large amounts of cortisol?

A

Anti-inflammatory Immunosuppressive Anti-allergic

165
Q

Which receptors do a) aldosterone and b) cortisol bind to?

A

Aldosterone - mineralocorticoid receptors Cortisol - glucocorticoid receptors AND mineralocorticoid receptors

166
Q

Describe the mechanism of action of cortisol.

A

Cortisol binds to intracellular receptors, moves to the nucleus and causes a GENOMIC change.

167
Q

Describe the control of cortisol.

A

There is direct negative feedback by ACTH on the hypothalamus Cortisol also have negative feedback effects on the hypothalamus and on the adenohypophysis

168
Q

What is dehydroepiandrosterone (DHEA)?

A

This is a very weak androgen that peaks around 20-30 years. It is particularly important in post-menopausal women as a precursor for oestrogen.

169
Q

As cortisol has a much higher blood concentration than aldosterone, why doesn’t cortisol constantly bind to mineralocorticoid receptors?

A

The kidneys have an enzyme called 11 beta-hydroxysteroid dehydrogenase 2 that converts cortisol into the inactive CORTISONE.

170
Q

What is a hypothalamic nucleus?

A

A collection of cell bodies that send their axons to a particular place.

171
Q

State the two main hypothalamic nuclei.

A

Supraoptic Paraventricular

172
Q

What is the other hypothalamic nucleus where the biological clock resides?

A

Suprachiasmatic

173
Q

What two molecules are produced by the neurohypophysis?

A

Vasopressin Oxytocin

174
Q

What are the two types of neurone and how do they differ?

A

Parvocellular: Average sized Terminate in the median eminence and other parts of the brain ONLY from paraventricular nucleus Magnocellular: LARGE Terminate in neurohypophysis Nuclei in both paraventricular AND supraoptic nuclei

175
Q

Describe supraoptic neurones.

A

They are ALL MAGNOCELLULAR and terminate in the neurohypophysis They are either oxytocinergic or vasopressinergic. The neurosecretions are hormones because they release directly into the circulation.

176
Q

What is a key feature of magnocellular neurones?

A

Herring Bodies - areas where neurosecretions can be stored on their way down to the neurohypophysis

177
Q

Describe the synthesis of Vasopressin. What other molecules are produced when the prohormone is cleaved?

A

Vasopressin is synthesised from Pre-provasopressin Cleaved to produce: Arginine vasopressin Glycopeptide Neurophysin

178
Q

Describe the synthesis of Oxytocin.

A

Synthesised from pre-prooxytocin Cleaved to produce: Oxytocin Neurophysin (different to that produced from pre-provasopressin) Does NOT produced glycopeptide

179
Q

State the main differences between Arginine Vasopressin and Oxytocin.

A

AVP has PHENYLALANINE instead of ISOLEUCINE AVP has ARGININE instead of LEUCINE

180
Q

State some similarities between Arginine Vasopressin and Oxytocin.

A

They are both nonapeptides They are both synthesised from prohormones Prohormones are cleaved to produce neurophysin

181
Q

What is the main effect of vasopressin?

A

Increased water reabsorption in the kidney collecting ducts

182
Q

What are some other effects of vasopressin?

A

Vasoconstriction Synthesis of blood clotting factors Corticotrophin release Hepatic glycogenolysis

183
Q

What are the different types of vasopressin receptor and which cells express these receptors?

A

V1a MOST IMPORTANT Vasculature Brain V1b Involved in control of corticotrophin release Adenohypophysial cells (corticotrophs) V2 Involved in antidiuretic effect Kidney collecting duct cells

184
Q

Describe how V1 and V2 receptors work.

A

V1 = Gq protein linked receptor (PLC; PIP2 —> IP3 + DAG; increase in [Ca2+]) V2 = Gs protein linked receptor (adenylate cyclase; increase cAMP; PKA)

185
Q

Explain how vasopressin acts on cells in the kidney collecting duct.

A

AVP binds to V2 on collecting duct cells Activates adenylate cyclase —> increase in cAMP —-> activate PKA —> increased synthesis of AQUAPORIN 2 AQP2 —> assembled into aggraphores —> aggraphores migrate to apical membrane —> water moves in —> water moves out of cell down concentration gradient via AQP3 + AQP4

186
Q

What are the two main functions of vasopressin and how is vasopressin release stimulated?

A

Water Reabsorption Vasoconstriction Stimuli: Increase in plasma osmolality Fall in blood pressure

187
Q

What are the two main actions of oxytocin?

A

Oxytocin is a CONTRACTOR molecule. Main actions: Contraction of the myometrial cells during CHILDBIRTH MILK EJECTION - contraction of myoepithelial cells in the breast during lactation

188
Q

Explain these two actions of oxytocin.

A

Oxytocin is release in massive amounts during delivery It acts on the myometrial cells to cause contraction Prolactin stimulates milk PRODUCTION but NOT milk ejection Oxytocin stimulates the contractile myoepithelial cells around the ducts and alveoli to cause MILK EJECTION

189
Q

What is a stimulus for oxytocin release when breastfeeding?

A

Stimulation of tactile receptors around the nipple passes message via a neuroendocrine reflex arc to the neurohypophysis and stimulates oxytocinergic neurons, resulting in oxytocin release. NOTE: this is a different neuroendocrine arc to the one that stimulates release of prolactin from the adenohypophysis

190
Q

State two conditions associated with vasopressin.

A

SIADH - too much ADH produced, decreases plasma osmolality, increases urine concentration Diabetes Insipidus - characterised by polydypsia and polyuria, in central diabetes insipidus - NO VASOPRESSIN produced

191
Q

Describe the arrangement of the adrenal veins.

A

The right adrenal vein drains directly into the IVC The left adrenal vein drains to the left renal vein and then to the IVC

192
Q

Describe the passage of blood through the adrenal gland.

A

The blood flows through the adrenal arteries and arterioles in the cortex where it picks up all the adrenal hormones and then it drains into a single CENTRAL VEIN.

193
Q

What are the three layers of the adrenal gland from the outside to the inside?

A

Zona Glomerulosa (aldosterone) Zona Fasciculata (cortisol) Zona Reticularis (doesn’t do much - evolutionary remnant) Adrenal Medulla (catecholamines)

194
Q

What is the precursor for ACTH?

A

Proopiomelanocortin – POMC

195
Q

Why does an increase in ACTH cause hyperpigementation of the skin?

A

POMC is broken down to ACTH and Melanocyte Stimulating Hormone (MCH) which stimulates the pigmentation of the skin.

196
Q

What is Addison’s Disease?

A

Primary adrenal failure

197
Q

What can Addison’s Disease be caused by? State the most common cause in the UK and the most common cause worldwide.

A

UK - autoimmune disease - the immune system wipes out the adrenal cortex Worldwide - tuberculosis

198
Q

Describe the arrangement of the adrenal veins.

A

The right adrenal vein drains directly into the IVC The left adrenal vein drains to the left renal vein and then to the IVC

199
Q

Describe the passage of blood through the adrenal gland.

A

The blood flows through the adrenal arteries and arterioles in the cortex where it picks up all the adrenal hormones and then it drains into a single CENTRAL VEIN.

200
Q

What are the three layers of the adrenal gland from the outside to the inside?

A

Zona Glomerulosa (aldosterone) Zona Fasciculata (cortisol) Zona Reticularis (doesn’t do much - evolutionary remnant) Adrenal Medulla (catecholamines)

201
Q

What is the precursor for ACTH?

A

Proopiomelanocortin – POMC

202
Q

Why does an increase in ACTH cause hyperpigementation of the skin?

A

POMC is broken down to ACTH and Melanocyte Stimulating Hormone (MCH) which stimulates the pigmentation of the skin.

203
Q

What is Addison’s Disease?

A

Primary adrenal failure

204
Q

What can Addison’s Disease be caused by? State the most common cause in the UK and the most common cause worldwide.

A

UK - autoimmune disease - the immune system wipes out the adrenal cortex Worldwide - tuberculosis

205
Q

State some clinical features of Addison’s Disease.

A

Pigmentation of the skin Weight loss Hypotension Muscular weakness Autoimmune vitiligo

206
Q

What are the steps that need to be taken if a patient is experiencing an Addisonian Crisis?

A

Rehydrate with saline Dextrose tablets to counteract the hypoglycaemia due to lack of cortisol Hydrocortisone or another glucocorticoid medication

207
Q

What are the consequences of excess cortisol?

A

Impaired glucose tolerance (due to chronic elevation of blood glucose) Interscapular fat pad Moon face Hypertension Striae Thin skin and easy bruising Proximal myopathy

208
Q

State four causes of Cushing’s Syndrome.

A

Oral steroid drugs Pituitary tumour causing overproduction of ACTH Ectopic ACTH (some lung cancer cells can produce ACTH) Adrenal adenoma or carcinoma

209
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A

Cushing’s Syndrome is a constellation of symptoms Cushing’s Disease = when the cause of Cushing’s Syndrome is known as being a pituitary adenoma

210
Q

What is Conn’s Syndrome?

A

Aldosterone producing adenoma Leads to hypertension, oedema and hypokalaemia

211
Q

State some clinical features of Addison’s Disease.

A

Pigmentation of the skin Weight loss Hypotension Muscular weakness Autoimmune vitiligo

212
Q

What is Conn’s Syndrome?

A

Aldosterone producing adenoma Leads to hypertension, oedema and hypokalaemia

213
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A

Cushing’s Syndrome is a constellation of symptoms Cushing’s Disease = when the cause of Cushing’s Syndrome is known as being a pituitary adenoma

214
Q

State four causes of Cushing’s Syndrome.

A

Oral steroid drugs Pituitary tumour causing overproduction of ACTH Ectopic ACTH (some lung cancer cells can produce ACTH) Adrenal adenoma or carcinoma

215
Q

What are the consequences of excess cortisol?

A

Impaired glucose tolerance (due to chronic elevation of blood glucose) Interscapular fat pad Moon face Hypertension Striae Thin skin and easy bruising Proximal myopathy

216
Q

What are the steps that need to be taken if a patient is experiencing an Addisonian Crisis?

A

Rehydrate with saline Dextrose tablets to counteract the hypoglycaemia due to lack of cortisol Hydrocortisone or another glucocorticoid medication