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90 Cards in this Set
- Front
- Back
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What are the 5 main structures located in the brainstem?
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Sensory cells
Motor cells Pathways Reticular cells Cranial nuclei |
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The red nucleus, and superior colliculus are located in which part of the brain stem?
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Mid brain
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What is the brainstem reticular formation?
And what are its functions? |
Collection of nuclei
Medullary, pontine, midbrain RF 1) AROUSAL-MOOD SETTER - ascending -- receives inputs and tells brain to be awake/asleep + mood 2) AUTONOMIC POLICEMAN Controls autonomic reflexes (cardio, resp, GIT, urogenital) + reticulospinal tract |
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What is are the serotonin cells in the brainstem called?
Ie. What nuclei? |
Raphe nuclei
Has projections all over |
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What are the functions of the brainstem serotonin cells?
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Raphe nuclei and has projections all over
BEHAVIOUR - grip on reality (LSD reduces serotonin - hallucinations) MOOD - PFC - reduced 5HT = depression AGGRESSION - amygdala +hypothalamus PAIN - descending pathways - inhibit overactive pain signals BLOOD FLOW CONTROL - 5HT --> vasoconstriction -- HA |
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What are the nuclei associated with ACh in the brainstem?
And where to they project? |
BRF - ACh groups
Project all over |
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What functions do ACh cell groups in the BRF have?
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AROUSAL - ischemia = LOC
MEMORY - short term memory (1st cells lost in AD) DESCENDING PROJECTION - control of ANS (cardio + pain suppression) REM SLEEP - cells active only during REM sleep My also be involved in laying down of long term memories each day (hippocampal projections) - DREAMS |
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Which Brainstem nuclei contain dopaminergic cells?
Where do they project to? |
Substantia nigra and VTA (ventral tegmental area) -- both within the midbrain
PROJECTIONS Nigrostriatal/mesostriatal - basal ganglia Mesolimbic - amygdala, hippocampus Mesocortical - PFC |
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What are the functions of dopaminergic nuclei in the brainstem?
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BEHAVIOUR REGULATION - cortex - loss of pathway - negative symptoms of schizophrenia, limbic - positive schizophrenia symptoms (overactive pathway)
MOVEMENT - basal ganglia --- if pathway lost - Parkinson's (statue) ----If pathway over active -dyskinetic movements FOCUSING MOVEMENT - basal ganglia - suppress unwanted movements (tremor in parkinsons) PLEASURE/MOTIVATION PATHWAYS |
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What are the nuclei associated with noradrenaline in the brainstem?
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Locus coreleus
Projects everywhere. |
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What are the functions of the cells associated with the locus coreleus?
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noradrenaline cells
CONTROLS AUTONOMIC NS - cardio, CO2 levels, O2 levels, prepares for STRESS PLEASURE AND MOTIVATION BP CONTROL NEURAL PLASTICITY GLOBAL ATTENTION - focus all systems (touch, vision, hearing) |
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What brainstem structure/s may be involved the following symptoms?
Coma Cerebellar signs Nystagmus ANS control |
Coma --- BRF
Cerebellar signs --- cerebellar peduncles Nystagmus --- vestibular nuclei or medial longitudinal tract (combines info about head position (VIII) and eye movements ) ANS control --- BRF |
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What structure/s may be involved with the following S&S?
Gaze control Speech Vertigo/nausea/vomitting |
Gaze control --- BRF (midbrain, pons)
Speech - nucleus ambiguous/corticobulbar tract Vertigo/nausea/vomitting --- BRF (area postrema), vestibular nuclei |
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What brainstem structure/s may be involved the following symptoms?
Motor loss Sensory loss |
Motor loss - corticospinal, corticobulbar tracts, motor decussation, N. Ambiguous, III, IV, V, VI, VII, IX, X, XI, XII
Sensory loss --- trigeminal nuclei, spinothalamic tract, medial lemnisicus, dorsal column tract, internal arcuate fibres, Solitarius N, ,.. |
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What sign is specific to a brainstem lesion, with respect to sensory loss?
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Ipsilateral head
Contralateral body |
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What can cause a brainstem lesion?
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Ischemia
Tumor Trauma Degenerative disease Inflammatory/demyelinating infection |
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What are some cerebellar signs?
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Ataxic gait/stance
Intention tremor Nystagmus Speech disturbance |
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Where are the sensory nuclei/tracts usually found in the brainstem?
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Laterally
Motor medially |
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The cranial nuclei can be categorized into 7 categories. What are these?
And which belong to which? |
Somatic motor, somatic sensory, visceral motor, visceral sensory, autonomic, taste, special sense
Somatic motor - III, IV, VI, VII Somatic sensory - V (Vp, Vmes, Vsp), VII (Vp, Vsp) Visceral motor - Vm, VII, N. Ambiguus (IX, X, XI) Visceral sensory - solitary tract -caudal (.IX, X) Taste - solitary tract - rostral (VII, IX, X) Special Sense - vestibulocochlear (VIII) Autonomic - III (edinger-westphal), VII (sup. Salv), IX (inf. Salv), X (DMX) |
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From medial to lateral what are the cranial nuclei within the medulla?
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XII
DMX Solitary NAm Vsp |
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What tract contains motor fibers for the head?
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Corticobulbar --- cerebral peduncles
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What is special about motor supply to the the muscles of facial expression?
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Supplied by VII
But upper muscles have dual innervation from both sides of the brain stem Where as the lower facial muscles have only have contra feral innervation. Therefore LMN lesion = both upper and lower muscle function lost UMN - loss of only contralateral lower facial muscle function - as upper muscles have ipsilateral innervation as well (dual) |
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What are the main functions of the medulla?
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Ascending sensory inputs
Descending motor outputs BREATHING, BP, SWALLOWING, VOMITTING |
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What are the main functions of the pons?
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Ascending sensory
Descending motor RELAY CEREBELLUM to/from forebrain BREATHING |
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What is the main driving factor behind breathing?
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CO2 levels
Hypoxia can also stimulate breathing but not at strong Other inputs include lung street h receptors, arterial chemoreceptors, medullary chemoreceptors, exercise, stress, fear |
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Hw does phrenic nerve activity relate to breathing?
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Increased activity during inspiration
No activity during expiration (quiet breathing) |
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What is the respiratory center and where is it located?
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Neurons which set the basic respiratory rhythm
Integrate info from lungs, chemoreceptors and cortex ----> output DRIVES phrenic and intercostal nerves ---> diaphragm + intercostal muscles Located in the lower brainstem |
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The respiratory center can be split into several different nuclei. What are theses nuclei ?
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Pontine:
Pneumotaxic - inhibit inspiration Apneustic - promote inspiration Medullary: Dorsal respiratory group DRG - inspiratory neurons (fire during inspiration) Ventral respiratory group VRG - Inspiratory and expiratory Also - pre-Botzinger complex? |
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What are the 2 theories for respiratory rhythmogenesis?
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Pacemaker theory
Network theory |
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How does increased CO2 increase Respiratory drive?
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Increased arterial CO2 --> increased CO2 concentration in medulla --> increased H+ concentration in medulla --> medullary chemoreceptors stimulated --> increased breathing rate and depth
Chemoreceptors are located in the RTN - retrotrapezoid nucleus |
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What is the Hering-Breuer reflex?
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It is a respiratory reflex to prevent over inflation of the lungs
On inspiration pulmonary stretch receptors on the bronchi and bronchioles are excited --> nerves to respiratory center via vagus --> inhibit inspiration via PNEUMOTAXIC pontine respiratory center --> limits inspiration --> reduces depth and increases rate of breathing to compensate |
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Nucleus Solitarius is a sensory nucleus in the brainstem - what are some of it's sensory inputs?
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IX, X CNs
Taste Baroreceptors, carotid body receptors, aortic receptors, Lung stretch receptors... |
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RVLM - rostral ventrolateral medulla - is important in which reflex pathways?
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Cardiovascular reflexes -- ESP maintaining BP via baroreceptors and output via SNS
It is also important in tonic SNS activity - which maintains BP normally and also SNS to other organs - skin, kidney, skeletal m, GIT |
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What is gadolinium contrast used for in brain imaging?
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Demonstrate breakdown of the BBB - tumors, infection, vascular lesions
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What colour is fat and fluid in a T1 and T2 weighted MRI image?
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T1
Fat - white CSF - black T2 Fat - black CSF - white |
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What group of people cannot have a MRI scan?
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People with metal inside them - metal hip - newer metals are not magnetic
Also people with lead tattoos |
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What kind of substances may cause an artifact on a CT
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Metal
Glue from AVM repair |
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What is the most common vessel involved in strokes?
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MCA
75% |
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What is the Usefulness of CT in the clinical setting of a person presenting with a CVA?
What changes can be seen on a CT in a Pt who has had a CVA? |
CT can rule out hemorrhage to allow for thrombolysis Rx
CANNOT be used to Dx stroke within 1st 6hrs -- 60% will be clear Early changes - reflect the oedema -- loss of grey/white junction (definition of basal ganglia, internal capsule..) Clot in BV Cerebral edema Mass effect -- sulcal effacement + ventricular distortment (late sign) |
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What is the role of MRI in Dx of a Pt with possible CVA?
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More accurate than CT
Can be positive from 30min Cytotoxic oedema, swelling of grey matter --- increased signal on T2 & flair Thrombus within BV **** look at perfusion scan to see if any salvageable tissue**** Note: can only see recent infarcts on MRI (<3weeks) but on CT can see old infarcts |
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What is the most common cause of hemorrhagic stroke?
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Sudden reperfusion of damaged tissues
Also lamina necrosis, lacuna infarction, and venous infarction |
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What does a watershed infarction mean?
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A watershed area is an area that is usually supplied by 2 main vessels but contains end arteries.
Infarction of these areas may occur when BP is dropped too low (or if the arteries are diseased) |
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On brain imaging what are some differentiating features between low grade and high grade tumors?
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Low grade -
Well defined, enhance with contrast High grade Poorly defined, cross hemispheres, associated with oedema METASTASES - can be multiple lesions |
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What is a venous infarction?
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When there is a blockage in the venous drainage system -- the blood backs up but must go somewhere
Leads to INTRACEREBRAL HAEMORRHAGE |
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What is the most common cause of extradural haematoma/hemorrhage?
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Middle meningeal artery rupture - often due to trauma associated with skull fracture
Can lead to RAPID increase in ICP -- drill bur holes!! Looks like a D shape on CT |
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Where is a subdural hemorrhage located?
What does it look like on CT? |
Between the dural layers - potential space between periosteal and meningeal dura
Looks like a C shape - hugging 1 side of the brain |
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What is the most common cause of a subdural hemorrhage?
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Venous tears
Due to location between the dura - this is where the venous sinuses lie. Often due to cerebral atrophy (brain shrinks) and stretches the dura - tearing open the sinuses -- often slow developing (may be chronic) |
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What may cause a subarachnoid hemorrhage?
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Aneruysm rupture
Trauma Blood may enter the cisterns Blood present on lumbar puncture |
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A RCT is a way of testing what?
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Testing an intervention
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A cohort study can be used to investigate what?
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Aetiology, prognosis
(also therapy - but don't use!) |
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What can a "diagnostic test evaluation" be used for ?
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Assessing Dx measures/criteria/investigations
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What is a stroke?
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Rapidly developing S&S of focal or global loss of cerebral function with symptoms lasting > 24hrs or leading to death with no apparent cause other than vascular.
WHO |
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T/F
Stroke are most common in 50-60YO |
False
50% > 75yrs |
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What is the general prognosis for a stroke? (at 1 Yr)
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1/3 die
1/3 recover 1/3 have a persistent disability (outcome at 1 Yr) |
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What factors affect the prognosis associated with a stroke?
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Non-modifiable factors -
Age, gender, severity of illness, pre-existing disability/illness Modifiable factors Ue of medications, compliance, smoking, alcohol, exercise, nutrition, income, marital status |
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What are the main STROKE RF?
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cardiovascular disease/RF
HT Smoking Hypercholesterolaemia Diabetes ....Left ventricular hypertrophy, kidney dysfunction, AF, BMI, nutrition, exercise |
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What are some examples of primary, secondary and teritiary prevention - with regard to stroke.
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Primary - reduce RF in
Pt (before CVA) Secondary - reduce RF (post event) Tertiary - clinical guidelines for stroke management, treatment of HT, anti platelet therapy, statins |
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What does NNT (number needed to treat) mean?
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NNT - refers to the number of patients that must be treated to save 1 life
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What is a TIA?
And what is the importance of identifying a TIA? |
Like a mini stroke
Cerebrovascular event in which the S&S only last <24h Need to identify because it is an early warning sign for a stroke --> 5% will have a stroke within 1 week |
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What are the 2 main distinctions between the types of stroke?
How common is each? |
Infarction - 80%
Including VB blockage - (local hypoxia) or hypoperfusion injury (general hypoxia) Haemorrhagic -20% |
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What are the most common pathologies causing stroke ?
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Lrge artery artherothrombosis
Small penetrating artery occlusion Embolism Global ischemia - cerebral hypoperfusion Intracerebral hemorrhage Subarachnoid haemorrhage |
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What is the most common site of atheroma formation?
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Extra cranial vessels -- INTERNAL CAROTID ARTERY
Intracranial vessels - origin of MCA and BASILAR ARTERIES |
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What factors are produced by endothelial cells that have an anti-coagulant effect?
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PGI2 and NO - inhibit activated platelets from adhering to endothelial cells
tPA (tissue plasminogen activator) converts plasminogen to plasmin which clears fibrin from cell surface --> reduces adherence |
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If ICA is affected by atherosclerosis - which vessels and hence regions are likely to be affected?
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Embolic -- MCA
Complete reduction in flow - MCA + ACA These will depend on anastamosis (circle of Willis), BP, rate of occlusion ACA - Frontal lobe and medial parietal and temporal (strip down the middle and at the front) MCA - S1, M1, frontal, parietal, temporal |
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What may be the cause of vessel occlusion?
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Atheroma (not very common - more likely - In Small vessels)
Thrombosis Embolus |
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In a brain infarction - what are the acute pathological changes seen?
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ACUTE
Softening of tissue Swelling (raised ICP my lead to lead) Neutrophils present Ischemia "red cell" neuronal change |
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In a brain infarction - what are the post acute pathological changes seen?
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Post-ACUTE
Cavitation Foamy macrophages (day 3) - remove debris Reactive astrocytes (10 days) - form glial scar tissue |
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During acute ischemia in a CVA, what are the molecular events occurring?
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Glutamatergic exocitotoxicity
- raised intracellular calcium - stimulation of reactive intermediates - membrane damage and DNA damage - Decreased energy production (reduced oxygen and glucose supply) -- lack of Na/K ATPase pump --> membrane failure Mitochondrial injury produces free radicals |
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What is the ischemic penumbra?
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Is an area of tissue that may be still viable if blood flow is restored
- look at perfusion vs blood volume |
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What medications are used to prevent strokes (after stroke or TIA) ?
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Antiplatelet agents (aspirin, clopidergrel)
Statins Anti-hypertensives |
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Where are small penetrating artery occlusions most likely to occur?
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Deep structures of the brain
Basal ganglia, thalamus, internal capsule, brainstem Often associated with HT or atheroma |
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What is CADASIL?
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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
Inheritable strokes Due to Notch3 mutation |
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Are embolic strokes usually infarctions or haemorrhagic?
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Haemorrhagic due to reperfusion of blood into damaged tissue, following clot lysis
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What is the most common territory for embolic strokes?
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MCA
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What are some sources of thromboemboli?
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HEART
L. Atrium - mitral stenosis, AF L. Ventricle - Myocardial infarction Valves - infective or marantic endocarditis ARTERY - carotid, aortic arch VENOUS - DVT + cardiac septal defect (patent foramen ovale) |
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What are some sources of non-thrombus emboli?
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Atheroma, cholesterol, calcified debris (from arteries or cardiac valve)
Atrial myxoma Systemic emboli - fat, air, amniotic fluid Infective emboli - from infective endocarditis |
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Where will a global ischemia cause infarction to?
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Boundary zones between ACA and MCA territory and MCA and PCA territory
Caused by abrupt HYPOPERFUSION + rapid recovery |
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What may cause venous blockage leading to a venous infarct/haemorrhage ?
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Local - infection, trauma
Systemic - increased coagulation, dehydration |
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What is the main confounding RF/s for intracerebral hemorrhage?
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HT
Also old age, anticoagulants, anti-platelet drugs |
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What can cause intracerebral hemorrhage?
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Arterial HT -- small artery degenerative changes, microaneruysms
Vascular malformation - capillary telangiectasia, AVM Hemorrhage into brain tumour Vascular amyloid - same as in AD - beta amyloid Venous infarction Reperfusion hemorrhage Systemic hemorrhage disorder - leukemia, anticoagulants |
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What are the symptoms associated with a subarachnoid hemorrhage?
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Worst HA of life - (meningeal irritation)
Raised ICP -- LOC, vision disturbance |
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What can cause a subarachnoid haemorrhage?
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Ruptured berry aneruysm (congenital defects, collagen deficiency, acquired - haemodynamic stress, atherosclerosis, HT)
AVM Trauma |
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Is stroke the 1st, 2nd, 3rd or 4th most common cause of death?
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2nd
And most common cause of disability |
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What are some of the most common stroke symptoms?
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Monocular visual loss
Hemi/paresis (weakness) - facial, arm, leg Sudden speaking problem Hemianopia (visual field deficit) Diplopia Acute onset - neurological deficit, localizing signs |
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What are some DDx for CVA?
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Seizure
Toxic Metabolic Sepsis Syncope Confusion Vestibular dysfunction Peripheral nerve lesion Migraine |
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When looking at MRIs in Pt with suspects CVA - what is the difference in what you see on a diffusion weighted Vs perfusion weight MRI?
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Diffusion - lesions are INFARCTIONs
Perfusion - lesions are at RISK of becoming ischemic |
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What is tPA?
What is it used for? |
tPA - tissue plasminogen activator
Rx for non-haemorrhagic strokes - within first few hours To salvage penumbra |
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What group of people are at the highest risk for a stroke?
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People who have recently had a TIA or stroke and survived
NEED IMMEDIATE assessment to reduce risk |
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FAST is a educational tool used to teach the public about the main symptoms associated with stroke. What does FAST stand for ?
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Facial weakness
Arm weakness Speech difficulty Time to ACT FAST |
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What is the fatality rate for subarachnoid haemorrhage (not treated) ?
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80%
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