neurology Flashcards
Draw a nerve..
how are neurons classified?
in a number of ways..
by shape e.g. monopolor, bipolar, multipolar
or by size and myelination…
Aa- large myelinated fibres - 50-100m/s
Ab
Ag
Ad
B - smaller myelinated - 3-15m/s
C - v.small unmyelinated - 0.5 to 2 m/s
where are different types of neurons found?
bipolar - sense organs
monopolar - ANS
Aa - motor neurons, proprioception in muscle spindle
Ab - touch and pressure
Ag - motor to muscle spindle
Ad - spinothalamic , sharp pain and temp
B - Autonomic pre-ganglionic
C - dull pain and post ganglionic ANS
what is myelin and what is its purpose?
myelin is a form of insulation provided to neurons. it is formed from schwaan cells or oligodendrocytes wrapping around axons to create a fatty sheath.
this helps insulate neuronal transmission such that AP will travel further before needing to be propagated (at nodes of ranvier)
therefore results in faster transmission via saltatory conduction.
how does axon diameter affect speed of AP conduction?
the larger the diameter, the fast
this is because reduced S.A: V for ions to be lost during AP hence less need to propagate (which takes time)
what are glial cells?
these are specialised cells that support the nervous system in various ways.
e.g. oligodentrocytes (CNS) and schwaan cells (PNS) produce myelin and insulate neurons
e.g. microglial act as specialised macrophages in CNS
e.g. astrocytes - create BBB and provide structure support.
what is the resting membrane potential?
At rest cells have a charge difference inside and out. this is normally a negative charge inside with compared to outside. This resting membrane potential will vary on cell type but in neurons is -70mV, cardiac cells and skeletal cells is -90mV.
It is achieved through a number of mechanisms
* Na/K ATPase - 3Na out, 2K in
* negatively charged anions in the cell - donnan effect
* equilibrium potential for pottasium - as at rest the membrane is mostly permeable to pottasium.
how can the resting membrane potential be calculated?
The nersnt equation for pottasium can be calculated to estimate the membrane potential at rest. this is because the membrane is largely permeable to pottasium.
however this is just an estimation and for more accurate calculation the goldman Katz equation is needed that takes into account other ion permeabilities
state the nernst equation…
E = RT/zF ln [out]/[in]
R = 8.31j/k/mol - universal gas c.
T = temp in kelvin
z = ion valency
F = faradays constant
what is the relative ion conc of major ions intra and extra cellularly?
Na out 135-145
Na in 15
k out 3.5-5
k in 150
ca much smaller in than out.
what is the gibbs donnan effect?
describes the distribution of charged particles across the semi-permeable membrane.
It occurs when there are charged particles on one side that the membrane is impermeable to e.g. proteins.
leads to a driving force - electrochemical gradient for other ions that are permeable.
until and charge/conc balance is reached.
draw the neuronal action potential and describe the stages
An action potential is a rapid depolarisation, an all or nothing event seen when a threshold is reached after sitmulation. It is triggered and is regenerated for propagation down a neuron
resting membrane potential = -70mV
stimulus - causes depolarisation - e.g. ligand binding opens receptor ion channel.
threshold reached = -55mV
AP triggered - positive feedback of VG Na channels opening. all or nothing +30mV
VG K channels open - repolarisation
overshoot - hyperpolarisation
VG K channels close
resting membrane restored.
what is the refractory period? types?
refractory period describes a period of time following AP whereby it is impossible or difficult to produce another AP.
This is because of innactivation of VG Na channels immediately after they are activated.
Initially all of them will be innactive - impossible to stimulate - absolute
after some time, some will begin to recover - higher threshold needed to cause AP.
important to ensure unidirectional flow of AP
how does an action potential propagate?
depolarisation as ions spreads as current in cell.
causes further AP to be produced in next segment along.
behind in refractory.
in myelinated cells will travel to next node of ranvier where further VG Na channels found - saltatory conduction.
what affects the velocity of an action potential ?
diameter - wider, less SA:V for current to be lost
myelin - insulation from current being lost, promotes saltatory.
temperature - increases movement of ions
draw a compound action potential recorded over time…
within one nerve fibre are various axons each with different diameters/ degree of myelination so slightly different conduction velocities. hence different peaks seen as each depolarises at different speeds.
what determines the direction of the neuronal signal?
synape - receptors on one side , NT released from one side
Refractory period.
what is meant by orthodromic and antidromic conduction?
orthodromic - one direction
antidromic - if AP was stimulated in centre of a neuron it would travel in both directions.
what is axoplasmic flow?
NT are synthesised in cell bodies and transported to the synapse by axoplasmic flow.
can be anterograde - to the synapse
or retrograde - from synapse to cell body
describe the anatomy of the spinal cord..
From top to bottom:
Thin tubular structure that lies in the verebral canal. travels from foramen magnum and terminates at conus medularis (L1/2 in adults, L3 in paeds)
surrounded in meninges and CSF
tethered to coccyx by the filum terminale (strand of pia mater)
there is a dural sac containing spinal nerves (cauda equina that ends at S2
Transverse:
within the cord is grey and white matter - grey matter contains nuclei which are split into laminae and white matter contains ascending and descending myelinated tracts.
emerging:
along its length it emits pairs of spinal nerves that exit through intervertebral foramina. 8 Cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal.
describe the organisation of spinal nerves..
at each level of the spinal cord emerges a pair of spinal nerves - left side and right side.
7 cervical - above
C8 below
12 thoracic - below
5 lumbar - below
5 sacral
1 cocyx
these are mixed nerves and contain both sensory and motor components. the sensory fibres enter the dorsal horn, ventral fibres leave anterior horn and these come together to form a spinal nerve.
supplies each dermatome/ myotome.
describe the blood supply to the spinal cord…
3 arteries that run whole length vertically -
2 x posterior spinal artery - 1/3 posterior portion,
1 x anterior spinal artery - 2/3 anteiror portion.
anterior spinal artery arises from R+L vertebral arteries that are from basilar artery.
posterior spinal artery = arises from posterior inferior cerebellar artery (branch of vertebral artery)
plus there is blood supply form the anterior and posterior segmental arteries at each level.
Artery for adamkiewicz is largest of these in lower thoracic upper lumbar region.
(adam cer vit ch)
describe the venous drainage of the spinal cord?
3 anterior
3 posterior veins
then into systemic segmental veins
Describe the anatomy of spinothalamic tract
carries pain, temp and crude touch / pressure
pain and temp in lateral, others in anterior.
1st order = Ad and C fibres enter spinal cord via dorsal horn, synapse in dorsal horn substantia gelatinosa
2nd order = cross over to contralateral cord. travel up in spinothalamic tract to the thalamus where they synapse with 3rd order
3rd order = travel to cortex via internal capsule
describe the anatomy of dorsal columns medial leminiscus pathway
carries info on fine touch, proprioception and vibration sense
1st order = Abeta - into dorsal horn and ascend ipsilaterally to the medulla where they synapse with 2nd order
2nd order = from medulla cross to contralateral side and synapse to thalamus
3rd order = thal to cortex via internal capsule
Fasciculus gracilis: Carries information from the lower body (below T6).
Fasciculus cuneatus: Carries information from the upper body (above T6).
tell me about the descending spinal pathways..
the descending pathways carry motor information from brain and brainstem to peripheries.
The major one is the corticospinal tract which is responsible for conscious movement
- starts in pre-central gyrus of motor cortex
- UMN leave motor cortex and travel to medulla via the internal capsule
- at medulla some fibres cross over and 10% remains ipsilateral. The 90% that crossed are called the lateral corticospinal tract and responsible for limb movement, the other 10% are the anterior corticospinal tract, responsible for posture.
- at the ventral horn the UMN synapse with LMN
- the lLMN leave ventral root and join spinal nerves to innervate muscles.
other descending tracts includ corticobulbar e.g. responsible for head and neck. Also rubrospinal and others.
what areas of the brain do you that are involved in movement?
primary motor cortex = pre central gyrus
basal ganglia = fine tuning amplitude
cerebellum = coordination
pre-motor areas = planning
can you explain why in a stroke there is forehead sparring…
the motor supply for the face is by the corticobulbar tract.
this originates in cortex where UMN emerge and synapse with LMN at CN nuclei.
Most of these have b/l innervation i.e. right and left cortex both synapse with R and L CN nuclei except for hypoglossal nerve and the top part of facial nerve.
therefore the facial nerve - upper branches will show weakness if one side of brain is gone. the rest of the face will have innervation by other side.
draw a pic to help
what are the effects of acute spinal cord injury ?
In the acute phase spinal shock is seen. which includes
* hypotension
* flaccid paralysis
* hyporeflexia
* pripism
* urinary retention
depending on place of injury ..
if above C3 - diaphragm innervation effected - respiratory paralysis
if above T8 - loss of intercostals, poor cough, reduced FRC
at any level - loss of sensation/ motor control below that point.
later spastic paralysis, and hyperreflexia - UMN signs.
draw and label cross section of spinal cord showing major pathways…
what is brown sequard?
this is the syndrome presenation seen when there is a hemisection of the spinal cord. i.e. one half is injured.
it results in loss of contralateral spinothalamic pathways below the lesion. and loss of ipsilateral corticospinal and dorsal columns below the region.
what is anterior spinal artery syndrome?
stroke in the anterior spinal artery results in ischaemia to 2/3 anterior cord.
hence - pain, temp, motor
sparing of dorsal columns - proprioception and fine touch + vibration
describe central cord syndrome?
this is where there is injury to the cente of the cord extending outwards e.g. syringomyelia (cyst in central canal)
this will effect spinothalamic tracts crossin the cord at that level
**it will also affect motor nerves upper >lower ** = hallmark sign
it will also affect some dorsal columns
what is cauda equina syndrome?
the cauda equina is a collection of spinal nerves that continues on after the spinal cord has ended (L2/3).
Compression of these nerves results in a syndrome of back pain, saddle paraesthesia, loss of anal tone, b/l leg weakness and loss bladder / bowel control
can be caused most commonly by L5/S1 disc prolapse but also tumours, abscess, trauma.
what happens to spinal cord in B12 deficiency?
subacute degeneration of the cord
lack of B12 means it cant act as a co-factor for methionine synthase which is required to replenish myelin
hence dordal columns and lateral columns are most effected
- loss of prop, vibration, fine touch
- plus loss of lateral corticospinal - spasticity
describe the anatomy and function of the BBB
The BBB is a physical barrier created between the blood and brain to protect the brain for chemical injury.
It consists of endothelial cells with tight junctions, basement membrane and astrocytes.
This results in a physical barrier making it hard for free flow of molecules between blood and brain
hence
* maintains extracellular environment of brain
* protects from harmful chemicals
* maintain local high conc of NT and prevents spread to systemic
describe methods of transport across BBB?
simple diffusion - CO2, O2, inhalation agents (lipid soluble stuff)
active transport - small ions - allows regulation of CSF composition
fasciliated diffusion - GLUT1 and aquaporin
pinocytosis - vesicle transport e.g. insulin
can you tell me any areas of the brain that fall outside the BBB?
pituitary
pineal
choroid plexus
median eminence of hypothalamus - osmoreceptors
area postrema
can you name any substances that cant cross BBB?
bile and ammonia
drugs - L dopa, mannitol
what is the function of CSF?
CSF is fluid found between pia and arachnoid layers i.e. within the subarachnoid space. In total around 150ml of fluid at any one time and 500ml is produced per day by choroid plexus cells.
it has a number of roles including
1. acting as a shock absorber by increasing boyancy
2. regulates ICP - can act as a buffer for pressure changes
3. helps maintain a constant chemical environment inc removal of waste
4. part of the mechanisms for respiratory control based on PaCO2 by producing H+
describe the production and path for CSF…
produced in lateral ventricles by choroid plexus
travels via foramen monro into 3rd ventricle
then via aqueduct of sylvius into 4th ventricle and then via 2 further foramen into the subarachnoid space whereby it is absorbed by archnoid granulations.
foramen mag-en-die (medial foramen)
foramen lushk - lateral
(also produced by 3rd and 4th ventricles choroid plexus)
how does the composition of CSF compare to plasma?
slightly more acidic - 7.32
more chloride
less protein, less glucose, less bicarbonate
same K, same Na , same osmolality
what is the opening pressure of the CSF?
10-15mmHg lying down
20-30mmHg sitting up
what problems can occur with CSF circulation?
if too much/ too little CSF is produced it can result in problems in intracranial pressure
production - too much e.g. choroid tumour. too little e.g. choroid plexus are under perfused
flow / obstruction - tumours, bleeding - pressure can build up
removal - infection/ damage to arachnoid granulations - pressure builds up
if pressure builds up it can result in hydrocephalus
what is hydrocephalus?
increased volume of CSF
can be as a result of increased production, obstruction to flow or decreased resorption
pressure can build up and increase size of ventricles and compress the brain.
can be classified by onset e.g. congential vs acquired.
aquired causes include tumours, SAH, meningitis with adhesions.
managed by ventricular drains / shunts
how can CSF be used for diagnostication…
sampling of CSF is useful in diagnostics.
The biochemistry, cellular counts and gram stain can be analysed for example a low glucose may suggest bacterial infection, high white cells could suggest autoimmunity or infection, bleeding/ xanthachromia could suggest SAH.
Draw the circle of willis
the circle of wilis describes the organisation of blod supply to the brain. there is a posterior and anterior circulation which anastomose
anteriro = internal carotid
posterior = vertebral arteries feeding basilar artery.
basilar artery central one come down - not labelled on diagram.
which areas of brain are suplied by which arteries?
anterior cerebral artery = frontal and parietal
middle cerebral artery = lateral surfaces - temporal lobe
posterior cerebral artery = temporal and occipital
vertebral artery = brain stem and cerebellum
describe the venous drainage of the brain…
brain parenchyema is drain via cerebral veins which drain into sagital sinuses. eventually all meet into transverse sinus then sigmoid sinus then into IJV.
superior and inferior saggital sinus drain cerebral and cerebellar cortices
the superior sagital sinus drains into the transverse sinus
the inferior sagital sinus drains into the straight sinus and then the transverse sinus
what is the cerebral blood flow and resting O2 consumption?
50ml/100g of brain tissue / min
(around 750ml/min) - 15% of CO
50ml/min = 20% of total body consumption
define cerebral perfusion pressure, what is normal?
CPP is the pressure that drives blood to perfuse the brain
usually 60-80mmHg
defined by ..
CPP = MAP - ICP (or CVP if bigger)
ICP normally less than 20.
therefore MAP usually 80 -100.
A CPP less than 60 -results in reduced venous saturations from IJV
less than 30 results in critical ischaemia
Explain the factors that influence cerebral blood flow
cerebral blood flow = cerebral perfusion pressure / cerebral vascular resistance. hence anything affecting these will alter CBF
CPP in turn is affected by MAP and ICP
hence overall - MAP, ICP, radius vasculature, viscosity of blood all will effect blood flow
cerebral blood flow is autoregulated and under influence of a nother of physiological variables to ensure blood flow meets demand.
- autoregulation. CBF is autoregulated between a MAP of 50-150mmHg. therefore is MAP drops, there will be vasodilation to maintain blood flow (myogenic response)
- PaCO2 - linear relationship until CO2 is high e.g. more than 10kpa or very low less than 3kpa. this is because CO2 causes vasodilation
- PaO2 - minimal effect until less than 8kpa and then exponential rise with drop in PaO2. again due to vasodilation effect of hypoxia.
- temperature also affects CBF - reduced temp, reduces O2 consumption and thus CBF due to coupling.
how does CPP relate to CBF? explain autoregulation using this relationship
CPP = CBF x cerebral vasc resistance
i.e. V=IR
therefore in terms of autoregulation - if pressure drops, resistance also drops via vasodilation to maintain the CBF
draw a curve to show how autoregulation may be different in HTN ?
shifts to the right
auto reg occurs over higher range e.g. 70-170mmHg
therefore need to maintain a MAP about 70 in anaesthesia in those with HTN
what is meant by the metabolic theory of cerebral blood flow?
CBF and metabolism are coupled in health
i.e. regional blood flow varies with metabolic demadn
this is regulated by products of metabolism e.g. K, adenosine, NO, CO2 causing vasodilation and increasing blood flow to that local region
the overall blood flow is fairly constant however may be regional differences due to flow metabolism coupling.
why may CO2 be important to maintain constant in anaesthesia?
CO2 affects CBF
if high - increases - increased blood volume and ICP
if low - descreases - ischaemia
hence normocapnia important in brain injury, anaesthesia
how do anaesthetic drugs affect CBF ?
volatile - increase CBF and reduce O2 consumption - uncoupling of flow metabolism coupling
N20 - increases both CBF and O2 consumption
NMBA = no effect
ketamine = rise in ICP, O2 consumption and CBP
benzos and IV inductions agents = reduce CBF and reduce O2 consumption
what is meant by autoregulation?
the mechanism by which an organ maintains a constant blood flow despite changes in mean arterial pressure.
2 mechanisms = myogenic and metabolic.
e.g. demonstrated by kidneys and brain and others.
what affect does brain injury have on cerebral blood flow
- impaired autoregulation
- rise in ICP - monro keille doctrine - from haemorrhage, can lead to iscaemia in areas
- disruption of BBB
- vasospasm
- axonal injury
what is the monro kielle doctrine hypothesis?
brain is a closed box
composed of different compartments - brain tissue, blood, CSF.
for ICP to be maintained, these 3 compartments must be balanced, increase in one leads to compensation by decrease in another.
Eventually other compartments cant compensat and there is a sharp rise in pressure for small changes in volume.
once ICP increases CPP drops unless MAP is increased further. (CPP = MAP - ICP)
compensation occurs via - venous drainage and CSF drainage initially.
what can raise ICP
intracranial pressure is the pressure exerted by brain and CSF within the cranium.
In health it is below 20mmHg (usually 8-12mmHg)
this can be raised due to increase in any one of the compartments in the monro kielle doctrine hypothesis
e.g. increase CSF - blocked drainage/ absorption or increased production
e.g. increased brain tissue - tumour, abscess, bruising
e.g. increased blood volume - haemorrhage, venous obstruction (venous sinus thrombus)
other causes that are not explained with above include intracranial HTN and raised thoracic pressue e.g. coughing, PEEP.
what is the vasodilatory cascade?
this occurs following reduction in ICP which results in a viscious cycle…
reduced MAP leads to fall in CPP
this causes vasodilation (via autoreg)
increase in blood volume
further fall in ICP and so on.
draw an intracranial pressure waveform..
measured via an ICP transducer e.g. ventricular drain or subarchnoid bolt
3 components - 1. pulse wave (split into 3)
- P1 = arterial pressure
- P2 = tidal wave - reflection of pulse on brain tisue
- P3 - dicrotic wave - venous pressure.
baseline = respiratory wave = varies with respiration
some wave patterns can suggest pathology = slow wave = type A , B and C
what are the clinical features of raised ICP?
headache, N&V, papilloema, low GCS
bulging fontanelle in babies
worse in morning, bending over
cushings - HTN, bradycardia, irregular respirations
pre terminal signs = apnoea, hypotension, fixed dilated pupils = herniation
describe the management of a head injury patient…
ABC approach
if GCS - intubation
neuroprotective measures - principle is to maintain CPP and prevent secondary brain injury
maintain CPP: CPP = MAP - ICP/CVP
* ensure good venous drainage - head up 30degrees, loose ET ties, minimal PEEP
* MAP 90mmHg (since ICP >20mmHg and CPP needs to be 70-80mmHg).
* ideally would monitor ICP to target MAP correctly
* may need vasopressors
reduce ICP:
* PAO2 - above 10kpa (reduces risk of vasodilation and raised ICP)
* normocapnia - to reduce vasodilatory effects and too low results in vasoconstiction and poor O2 delivery.
* sedate and paralyse to avoid straining
* furosemide / mannitol / hypertonic saline
* decompressive crainectomy / burr holes
reduce cerebral metabolic O2 demand
* sedation - propofol/thio
* barbiturate coma
* treat pyrexia - normothermia (hypothermia not beneficial)
* normoglycaemia
how does mannitol work?
what is the dose of mannitol/ hypertonic saline ?
mannitol is an osmotic diuretic
causes diuresis and effectively this has a knock on osmotic effect in brain - causing fluid shift and reduction in oedema.
as long as BBB intact
also can scavenge free radicals and reduces CSF production.
0.25–2 g/kg, repeated if necessary, to be administered over 30-60 minutes, dose may be repeated 1–2 times after 4–8 hours.
(1ml/kg of 20%)
2-3 ml/kg of 5% NaCl
how is ICP measured?
by measuring ICP and MAP we can infer CPP and hence avoid secondary brain injury as best possible
- external ventricular drain
* gold standard
* transduces pressure and releases fluid
* increased risk of infection compared to others - subarchnoid bolt via burr hole
* most common
* continous measurement , slightly less accurate but less risk of infection (still risk)
* however local pressure, may not represent global ICP - subdural pressure transducer
* easy to place, less accurate - extradural fibreoptic probe via burr hole.
* sits between dura and skull
* easy and less infection risk. but doesnt drain fluid
how is cerebral blood flow measured?
A number of ways
* ficks principle using N20 - kety schmidt method. i.e. flow = amount of N2O removed by brain per unit time / Av difference in N20
radioactive techniques - xenon 133 - measure radioactiveness wil show regional differences in blood flow
transcranial doppler USS is most common method. USS is placed on temple and doppler principle used to determine blood flow via velocity and area of artery. this uses middle meningeal artery due to easy access. can also use basilar artery and anterior cerebral but not as easy.
jugular bulb catheterisation -CVC via seldinger. jugular bulb is a dilation of jugular vein - measure pO2, sats and pH to give indication of overall adequacy of flow. if sats fall, suggests poor flow or potentially increased demand. downfalls are it only looks globally. also confounded by O2 demand e.g. if both demand and flow fall, it would appear normal.
fucntional MRI and PET - rely on flow metabolism coupling. PET uses radioactive glucose. fMRI looks at areas of low and high O2
describe the structure and function of the meninges…
consists of 3 layers = pia, arachnoid, dura. subarchnoid space lies between pia and aracnoid and constains CSF.
functions to protect brain , support and involved in CSF circulation
what differnt types of nerve injury do you know?
ischaemia = transient - seconds to min
neuropraxia - local demyelination. axon intact. 1-3 weeks
axonetmesis - axon damage, nerve tube intact (perineureum etc) wallarian degen 1-3mm/day
neurotmesis - axon and nerve tube sethered. incomplete recovery.
what are reflexes?
neuronal pathways that produce rapid, automatic and predictable responses to stimuli
often only include spinal cord and have minimal neuronal connections
basic spinal reflex arc consists og
1. sensory neuron - myelinated A , to dorsal horn
2. interneuron - integrate signals within spinal cord
3. motor neuron - Aa from ventral horn
describe the physiology of the knee jerk reflex…
monosynaptic reflex arc that results in rapid contraction of quadricept in response to stretch of quadricep muscle.
at same time as monosynaptic reflex there is also inhibitory interneuron which inhibits biceps femoris = reciprical innervation.
similar stretch reflexes exist in many muscle groups and help to maintain posture and tone and prevent injury.
what is a polysynaptic reflex arc? or crossed extensor reflex
for example the withdrawal reflex in response to pain
Ad fibres carrying pain - synapse with motor neurons for withdawal and contralateral limb for stability. multiple motor neurons are involved to coordinate the whole withdrawal movement.
other inputs can over ride this.
what a golgi tendon organ?
sensory receptor
located in tendons of muscle
attached to the ends of muscle
recognise muscle tension
innervated by Ab fibres
when innervated lead to inhibition of motor neuron via interneuron and thus relaxation of muscle.
prevents excessive contraction.
what is the muscle spindle?
within a muscle are intrafusal and extrafusal cells - the extrafusal are normal myocytes making up the contractile unit and innervated by Aa motor neuron
the intrafusal fibres are the muscle spindle fibres.
muscle spindles are a stretch receptor containing both nuclear bag and nuclear chain fibres.
nuclear bag fibres = dynamic responses
nuclear chain fibres = static responses.
Send impulses via Aa (chain) and B (bag) fibres.
involved in knee jerk reflex, but also give info to brain on posture and position.
these are innervated by Ag motor neurons which alter their tension to match that of the overall muscle to maintain their sensitivity at detecting stretch.
what regulates muscle tone?
muscle tone is a continuous basal level of muscle contraction
controlled by descending extrapyramidal supraspinal neurons which innervate Ag motor neurons - these regulate the stretch of a muscle spinal which in turn will effect the overall tone of the muscle via the reflex arc.
what is the Jendrassik manoeuver?
patient clenches teeth/ pulls interlocked hands apart
knee jerk reflex is attenuated
this is because of descending modulation - increases Ag inputs to tighten the spindle and hence will seem more stretched.
what other reflexes do you know?
babinski = stroking outside of foot causes toes to point up in UMN damage
biceps = hit biceps tendon and contract of biceps (C5,6)
knee jerk = L3/4
ankle= S1,2
pupillary light reflex - optic nerve and occulomotor to contrict pupil.
gag/ corneal
state the functions of frontal lobe..
Sits in anterior cranial fossa
Primary motor cortex – precentral gyrus
Supplementary motor and pre-motor areas
Broca’s area – production of speech (left hemi)
Personality, behaviour, judgement
Dopamine reward pathways – behaviour and motivation
functions of parietal lobe..
Primary sensory cortex – post central gyrus
Calculation and writing
Parietal association cortex – spatial awareness – damage leads to neglect of one side of body/ world
functions of temporal lobe
Wernicke’s – understanding language
Auditory cortex
Smell, taste, emotion
Memory and visual recognition of faces
functions of cerebellum
Coordination of movements
Balance
Receives afferents from proprioceptors, eyes, vestibular apparatus .
what is the role of the internal capsule?
carries axons of sensory, motor and optical fibres in the posterior limb
It has a relatively weak blood supply – middle cerebral artery
Stroke results in contralateral hemiparesis (motor fibres decussate after internal capsule)
what is the function of the brainstem?
MIDBRAIN, PONS, MEDULLA
Midbrain
involved in innate responses to fear - sound and vision
Sleep wake and consciousness
Contains nuclei III and IV
Contains medial longitudinal bundle – to coordinate gaze
Pons
Some nuclei of respiration
Body equilibrium and posture
CN V, VI, VII and VIII
Medulla
Cardiac and respiratory centre, swallowing, digestion, vomiting
CN IX, X, XI and XII
whats the function of basal ganglia?
The basal ganglia are a set of structures that sit below the cortex and include
Putamen and caudate nucleus and globus pallidus
The basal ganglia are involved in fine tuning voluntary movements and procedural learning
Majority of GABA neurons
Direct and indirect pathways to control movement - involves dopamine .
what is the function of diencephalon?
consists of thalamus, pituitary and hypothalamus
Thalamus – collection of nuclei that process sensory info from body and relay to cerebral cortex and vice versa .
Hypothalamus – The hypothalamus contains neural centres for hunger, thirst and body temperature and thus is important in the regulation of homoeostasis.
Other functions include sleep, emotion, sexual arousal,. major neuroendocrine hormone system.
Pituitary gland – anterior and posterior - neuroendocrine secretion - linked closely to hypothalamus
what is the limbic system?
Limbic system:
Functional system including frontal lobe, thalamus, temporal lobe and amygdala, hypothalamus, hippocampus, cingulate gyrus
Involved in learning, emotion, behaviour and endocrine responses via hypothalamus
Hippocampus
Located in the inferior temporal lobe
Involved in new memory formation – damage leads to anterograde amnesia. also long term memory
Amygdala
Located in temporal lobe
Fear, anger, emotions.
result of SoL in frontal lobe?
Hemiparesis – contralateral
Brocas dysphasia
Personality/behavioural change
Incontinence
Reduced executive function e.g. planning
Anosmia
result of SoL in parietal lobe
Dominant:
Sensory inattention , reduced 2 point discrimination
Dyslexia, dyscalclia
Contralateral inferior homonymous quadrantanopia
Non-dominant = spatial neglect (one side of a clock, one half of face shaved)
result of SoL in temporal lobe and occipital lobe
Occipital lobe:
Homonymous hemianopia with macular sparing
Temporal lobe:
Dominant: contralateral upper quadrantanopia , Wernickes dysphagia, Poor memory, auditory agnosia, difficulty identifying faces
Non dominant – sounds, emotions
with any SoL can mention as lesion gets bigger - raised ICP (monro kielle doctrine) and brainstem herniation + cushings triad.
symptoms of cerebellar dysfunction
Cerebellum:
dysdiadokinesis, ataxia, nystagmus, intention tremor, slurred speech, hypotonia
Causes – tumour, stroke, toxins (alcohol), B12/thiamine deficiency
upper vs lower motor neuron signs
upper:
Wide spread i.e. not 1 myotome
Suppination is weaker than pronation: pronator drift (this is the first muscles to be affected
Hypertonia / spasticity
Hyperreflexia – positive Hoffman and Babinski sign
Clonus
Lower
Weakness in myotome
Hypotonia
Hyporeflexia
Muscle wasting and fasciculations
how does cerebral blood flow vary between grey and white matter?
overall cerbral blood flow = 50ml/100g/min
(around 750ml/min) (15% of CO)
grey matter = 70ml/100g/min
white matter = 30ml/100g/min
what is the cerebral metabolic rate
3ml/100g/min of O2 consumped (50ml/min for whole brain)
about 20% of total O2 consumption
what are the thresholds for cerebral ischaemia?
CPP is usually around 60-80mmHg
below 30mmHg - ischaemia develops
therefore if the MAP-ICP is less than 30mmHg this wil occur.
CPP and CBF are inversely related.
In terms of CBF
normal is 50ml/100g/min
acidosis will occur below this –> oedema
below 20ml/100g/min - neuronal functions caese
below 10ml/100g/min - cell death occurs
what is normal ICP?
normally around 8-12mmHg
slightly more when supine and less when standing
directly related to intrathoracic pressure and shows normal respiratory swing.
thus increases with straning, coughing and PEEP.
what are the effects of anaesthetic agents on ICP?
IV induction agents e.g. propofol and thio cause a dose dependant reduction in ICP, blood flow and metabolic rate. thus reduce risk of secondary brain injury.
ketamine can increase ICP and metabolic rate - however its advantage in CVS instability is favoured over this.
voltatiles cause vasodialtion and thus increase ICP - avoided in neurosurgery if possible.
N20 increases ICP and metabolic rate - again best avoided.
benzos reduce flow and metabolic consumption. but not ICP
NMBA do not alter ICP directly but prevent straining and coughing
sux may have transient rise in ICP
which anticonvulsants are used in seizures in TBI?
phenytoin
membrane stabiliser
reduces Na/Ca influx and hence depolarisation
how quickly should a mannitol infusion be given
rapid infusion to have effects
following brain injury what may happen to urine?
diabetes insipidus
lack of ADH
dilute urine, low urinary sodium
concentrated blood - high plasma sodium
why are dextrose solutions avoided in brain injury?
glucose metabolised and then effectively hypotonic solution
will diffuse across BBB and increase swelling
however if patient is hypoglycaemic, may need to be given.
what is a high level of urine output that may be seen in diabetes insipidus?
> 3L in 24 hours
125ml/hr
but usually much higher than this even
like 20L/day (800ml/hr)
what are important observations to look at in head injury patients
GCS
pupils
nuerological exam
MAP and ICP to work out CPP
trend in BP, HR and RR - cushings
urine output - diabetes insipidus
label the following structures of one of the cranial nerves shown in the picture
- Vagus nerve.
- Superior laryngeal nerve.
- Internal laryngeal nerve.
- External laryngeal nerve.
- Recurrent laryngeal nerve.
where does the vagus nerve originate from?
CN X
medulla oblongata
how many nuclei does the vagus nerve have?
dorsal nucleus
nucleus ambiguus
nucleus tractus solitarus
which foramen does the vagus nerve leave the cranium?
jugular foramen
what structures pass through jugular foramen?
CN IX, X, XII
internal jugular vein
describe the course of the vagus nerve in the neck
down within the carotid sheath
with the carotid artery and IJV
lies more deep to these and inbetween them.
describe the course of left and right vagus nerve within the thorax..
On the right side,
* passes across anterior to subclavian artery
* descends by the side of the trachea to root of lung to pulmonary plexus and oesophageal plexus
on left
* enters the thorax between the left carotid and subclavian arteries,.
* runs along the anterior surface of the oesophagus,
* it unites with the nerve of the right side in the oesophageal plexus
recurrent laryngeal nerve on the
left - hooks under the arch of the aorta, ascending to innervate the majority of the intrinsic muscles of the larynx. hence longer course.
right - hooks under subclavian
branches of vagus nerve?
superior laryngeal
recurrent laryngeal (inferior)
in thorax
cardiac branches
bronchial branches
oesophageal branches
gastric , coeliac and hepatic branches in abdomen
equilibrium potential for Na, K and cl
K = -90mV
Na +60mV
Cl = -70mV
what is the total CSF pressure normally? what factors affect this ?
5 -15mmHg
body position, hydration , pathology (hydrocephalus can increase it or brain tumours can reduce it ) or infection.
where are the arachnoid granulations?
within dural sinuses
how does pressure, protein, glucose and WCC change in CNS infections (bacteria, TB, viral)
which substances do you not want to get across BBB?
ammonium - astrocytes metabolise this (unless levels rise)
bile
some amino acids e.g histamine - acts as NT
