0.5 - UNSW Medical Society

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Transcript 0.5 - UNSW Medical Society

THE UNIVERSITY OF NEW SOUTH WALES
MEDICAL SOCIETY
Ageings and Endings B
End of Course Revision Tutorial
Henry Lin and Arty Selvanathan
www.medsoc.org.au
As promised!
“Chance to win a trip to Fiji”
http://www.hotelclub.com.au/getaway/competi
tionpage.asp
Pneumonics
•OOOTTAFVGVAH
•Cranial Nerves: OOO To Touch And Feel Virgin
Girl’s Vagina And Hymen
•Standing Room Only
•Where CNV leaves skull: Superior Orbital Fissure
(V1), Foramen Rotundum (V2) & Foramen Ovale
(V3)
•The Zoo Bought Monkey Clothes
•Branches of CNVII: Temporal, Zygomatic, Buccal,
Marginal Mandibular and Cervical Branch
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Helpful Resources
• 3D Brain App
• Youtube videos on tracts
• Neuroanatomy made easy
Functional Neuroanatomy
Important areas
• Primary Auditory Cortex: Superior Temporal
Gyrus
• Broca’s Area: Posterior Inferior Frontal Gyrus
of the dominant hemisphere (usually left)
• Wernicke’s Area: Posterior Superior Temporal
Gyrus of dominant hemisphere
Somatotopy
Somatosensory
Motor
General Rule
Tracts in Cord Cross Section
Corticospinal Tract
• Origin: 40% Primary Motor Cortex, 30%
Secondary Motor Cortex, 30% Somatosensory
Cortex
• 90% Lateral Corticospinal for limb muscle
control i.e. voluntary movement
• 10% Anterior Corticospinal for axial muscle
control i.e. posture
• Lateral decussates at Medulla Oblongata
• Anterior decussates at Anterior White
Commissure
Dorsal Column-Medial Lemniscus
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Fine touch
Proprioception
Vibration
Discriminative touch (i.e. 2 point
discrimination)
• Decussate at Medulla Oblongata through the
Internal Arcuate Fibre (NOT FASICULUS)
Spinothalamic Tract
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Pain (lateral)
Temperature (lateral)
Crude touch (anterior)
Decussate within the spinal cord within 2
segments through the anterior white
commissure
Sample Question
Cee-Lo was driving ‘round town, and whilst he was
gesturing at a girl he recognised, he crashed into
a pole and hemi-transected his spinal cord on
the left side at T4 (Just below T3 Nerve Root
level).
1. Compare and contrast Upper and Lower motor
Neuron disease (6 marks)
2. Discuss what clinical features would be elicited
on exam and explain the underlying mechanism.
(10 marks)
Question
1. Model Answer
Upper Motor Neuron
Lower Motor Neuron
Disease
Disease
Neurons originating at the
motor cortex and synapse
at the ventral horn (0.5)
Neurons that synapse
below the ventral horn
(0.5)
Mechanism
Lack of inhibition from
cortex (0.5)
Lack of conduction to
skeletal muscle (0.5)
Wasting
Can have disuse atrophy if
chronic (0.5)
Neurogenic atrophy (0.5)
Fasiculations
None (0.5)
Present (0.5)
Fibrillations on EMG
(bonus)
None (0.5)
Present (0.5)
Power (MUST)
Decreased (Spastic
Paralysis) (0.5)
Decreased (0.5)
Tone (MUST)
Spastic (0.5)
Flaccid (0.5)
Reflex (MUST)
Hyperreflexic (0.5)
Hyporeflexic/Areflexic (0.5)
Babinski reflex
Up-going (0.5)
Down-going (0.5)
Clonus
Can be present (0.5)
None (0.5)
Definition (MUST)
Diagram!
Question 2: Model Answer
• All Neurological function and physical exam
findings will be normal above T4 level (0.5
mark).
• In the areas at and below T4, Upper motor
neuron signs will be elicited as descending
inhibition from the cortex will be lost (0.5
mark).
• Labelled Diagram for Corticospinal tract (0.5
mark)
• Pathway of Corticospinal tract (1.5 mark)
-Mention Anterior and Lateral Corticospinal Tract
• Therefore if you transect at T4, you will have
Hypertonia, Decreased/absent Power and
Hyporeflexia/Areflexia on the ipsilateral Left Limb
and Trunk, below and at the T4 Level of muscular
innervation (1 mark)
– Must mention Babinski Reflex upgoing
• Labelled Diagram for DCML (0.5 mark)
• Explain Pathway of DCML (1.5 mark)
– MUST mention Fasiculus Gracilus and Fasiculus
Cuneatus
• Therefore if you transect at T4, you will lose
Fine touch, Vibration, Proprioception and
Discriminative Touch sensation on the
Ipsilateral Left side below and at the T4
dermatomaI Level (1 mark)
• Labelled Diagram for Spinothalamic Tract (0.5 mark)
• Explain Pathway of Spinothalamic Tract(1.5 mark)
– MUST mention usually ascends 1-2 spinal segments and
sensation transmitted via Anterior and Lateral Tracts
• Therefore if you transect at T4, you will lose Crude
Touch (ant), Pain (lat) & Temperature (lat) sensation on
the:
– Ipsilateral Left side at T4 & T5 dermatomes (0.5 mark)
– Contralateral Right side at T6 dermatome and below (0.5
mark)
Bonus marks
• 1 mark for discussion of rubrospinal,
vestibulospinal, tectospinal & reticulospinal
which adds to loss of balance, orienting and
posture
• 0.5 for identifying condition as Brown Sequard
Syndrome
• 0.5 for mentioning loss of anal tone,
incontinence, etc.
Neuroplasticity & Repair: summary
•
Moral of the first 100 cool stories: Grey matter can get redistributed according to need
Good stuff
After stroke, recovery and compensation occurs via axonal sprouting and neurogenesis:
1.
Axonal sprouting occurs when the periinfarct cortex upregulates production of growth factors e.g.
GAP43, down-regulates growth inhibitory factors like NogoA and activates growth genes in
successive waves
2.
Neurogenesis occurs post-stroke when the cytokine EPO is released near the infarct to signal
neuroblasts to move from the subventricular zone to the infracted site.
3 phases of brain reorganization during language recovery:
1.
Strongly reduced activation of language areas in left hemisphere in acute stage
2.
Up-regulation of recruitment of homologue language zones to help with language improvement
3.
Normalised activation of left language areas, showing consolidation of language
Cerebral Blood Supply
• Rote Learning
– Internal Carotid Arteries (Anterior Circulation)
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Ophthalmic Artery
Anterior Choroidal Artery
Anterior Cerebral Artery
Anterior Communicating Artery
Middle Cerebral Artery (terminal branch)
– Vertebral Arteries
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Anterior Spinal Artery
Posterior Spinal Artery
Posterior Inferior Cerebellar Artery
Combine to form the Basilar Artery
– Basilar Artery
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Pontine Arteries
Internal Acoustic Artery
Anterior Inferior Cerebellar Artery
Superior Cerebellar Artery
Posterior Cerebral Artery (terminal branch)
Cerebral Blood Supply
• Functional Understanding!
In Answering a Sample Question
• Which artery is affected?
• What are the branches of this artery that I
know?
• Including branches, which areas of the brain
are supplied by this artery (and therefore
affected)?
• What are the functional manifestations of
affecting those areas of the brain?
Sample Question
• Mr X is a 50-year-old Collingwood supporter
who has a stroke affecting his middle cerebral
artery while standing in his local Centrelink
cue.
– Detail some of the deficits that one might see in
Mr X if a neurological examination was performed.
• Artery Affected: Middle Cerebral Artery
• Branches: ?
• Areas supplied by these branches
– lateral surfaces of the brain (including the sensory
and motor homunculi except for “leg and foot”)
– Broca’s and Wernicke’s area (of dominant
hemisphere)
– Basal ganglia and internal capsule
Use Neurological Phrases to Describe
Neurological Deficits!
– Contralateral hemiparesis/hemiplegia, mostly in
muscles of the arm and face)
– Loss of sensation on the contralateral side of the face
and arm
– Aphasia (expressive and/or receptive) if dominant
hemisphere involved
– Sensory neglect syndrome (if non-dominant
hemisphere involved)
– Contralateral hemiparesis in the legs as well if the
internal capsule is involved
– Hyperreflexia and hypertonia (upper motor neuron
lesion)
Pathophysiology of Stroke
• Stroke = “an abnormality of the brain of acute onset
caused by a pathological process affecting blood
vessels”
• 85% due to infarction, 15% due to haemorrhage
• Infarction risk factors: atherosclerosis, hypertension,
heart disease, diabetes
• Causes: thrombosis, embolism, vasospasm, herniation,
local vasculitis, poor perfusion without acute
obstruction.
• TIAs: episodes of non-traumatic focal loss of cerebral
function (eg. vision) lasting no more than 24 hours
Thrombotic Stroke
• Pale infarcts
• Superimposed on atheromatous plaques
• Key locations: internal carotid artery (carotid
bifurcation), middle cerebral artery
bifurcation, vertebrobasilar system
Embolic Stroke
• Haemorrhagic infarcts (≠ haemorrhagic
stroke!)
• Could be from thrombus in carotid arteries
• BUT heart is the most common source of
emboli
– Mural thrombus overlying myocardial infarct
– Valvular vegetations
– Thrombus in left atrium (atrial fibrillation)
• Often end up in MCA territory
Sample Question
• Mr Y is a 65-year-old man who has presented
to you for rehabilitation following a stroke 3
months ago. His past history includes a
myocardial infarct 10 years ago.
– What are some of the key risk factors that you
would ask for to determine likelihood of stroke?
– Is Mr Y’s stroke likely to have been thrombotic or
embolic? Contrast the different pathophysiologies
of these two subcategories.
Parkinson’s Disease
and Its Treatment
Parkinson’s Disease
• Disorder of the basal ganglia (death of
dopaminergic neurons in the substantia nigra)
• Characterized by:
– Tremor
– Hypokinesia (bradykinesia, akinesia)
– Rigidity
– Postural instability
• Often, eventually develop cognitive and
behavioural problems
For each drug learn:
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•
•
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Name
Class (‘tag phrase’)
Mechanism of Action
Side Effects/Contraindications
Other Points
• Pharmacology questions are where you can
make up time!
• AND don’t forget non-pharmacological
methods for treating disease (stretching and
strengthening, training in transfer techniques)
List of Drugs
• Synthetic L-DOPA (Levodopa)
• (Peripheral) Dopamine Decarboxylase
Inhibitors (Carbidopa)
• Monoamine Oxidase B (MOAB) Inhibitors
(Selegiline)
• Catechol-O-MethylTransferase (COMT)
Inhibitors (Entacapone, Tolcapone)
• Dopamine Agonists (Bromocriptine,
Cabergoline, Pramipexole)
The class of drug should give an
indication of the mechanism of action!
Side Effects
• Learn side effects that are common, but also
ones that you won’t forget
• All dopaminergic drugs: nausea, vomiting,
hallucinations
• DYSKINESIAS (end-of-dose, but also at peak
plasma levels)
• Dopamine Agonists: Hypersexuality, gambling
addiction, punding
Sample Question
• Mr Z is a 65-year-old man who has come to
see you for a review of his Parkinson’s
medications. His current regimen of L-DOPA is
causing significant morbidity due to
dyskinesias.
– List two other drugs used to treat Parkinson’s
Disease
– For each, state its mechanism of action, and list
two side effects of the drug.
Sample Answer (One Drug)
• Class: Dopamine Agonists
• Names: Ropinirole, Pramipexole
• Mechanism of Action: Increases stimulation of
dopaminergic neurons in the substantia nigra
• Side Effects: Punding, gambling addiction,
hypersexuality
Slide Title
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