CASE 10 - temporal lobe, head trauma, anaesthesia etc Flashcards
where is the temporal lobe?
- middle cranial fossa, next to the temporal region/bone
- lies beneath the lateral fissure
what gyri are located on the lateral surface of the temporal lobe?
superior (area 22), middle (area 21) and inferior (area 20) temporal gyri
what gyri are located on the inferior surface of the temporal lobe?
inferior temporal gyrus and occipitotemporal (fusiform) gyrus
what sulci does the temporal lobe have on its lateral and inferior surfaces?
lateral surface: superior and inferior temporal sulci
inferior surface: collateral sulcus, midfusiform sulcus
what separates the superior and middle temproal gyri?
superior temporal sulcus
what separates the middle and inferior temporal gyri?
inferior temproal sulcus
where is the primary auditory area (A1)?
Brodmann area 41 — superior temporal gyrus
what area is the secondary auditory area (A2) in?
Brodmann area 42
where is the auditory association area?
brodmann area 22 (lateral to primary auditory area)
where is wernicke’s area?
posterior part of brodmann area 22 - superior temporal gyrus of dominant hemisphere
what mark the location of the primary auditory cortex on the superior surface of the superior temporal gyrus?
transverse temporal gyri (Heschl’s convolutions)
transverse temproal gyri (of Heschl) = found in the area of the primary auditory cortex buried within the ______ sulcus, occupying Brodmann areas ___ and _____
- lateral sulcus
- 41 and 42
where does the primary auditory cortex receive auditory information from?
medial geniculate nucleus of the thalamus
what is the auditory association area responsible for?
interpretation of auditory information and which, in the left hemisphere, constitutes Wernicke’s area (comprehension of the written and spoken language)
what does the temporal lobe work with in the formation of conscious memories?
amygdala (medial temproal lobe) and hippocampus (temporal lobe)
blood supply of the temporal lobe?
lateral surface supplied mainly by branches of the MCA
inferior surface supplied mainly by branches of PCA
which temporal lobe is typically dominant in most people and is associated with understanding language, learning, memorising, forming speech and remembering verbal information?
left
what is the non-dominant temporal lobe commonly associated with?
learning and memorising non-visual information (eg. drawings and music), recognising information, and determining facial expressions
how does blood reach the brain?
- anterior circulation = ICA + common carotid
- posterior circulation = vertebral arteries and subclavian artery
what vessel, if occluded, would affect both Broca’s and Wernicke’s area?
middle cerebral artery
what artery supplies blood to the occipital lobe?
posterior cerebral
what is the largest branch of the ICA?
MCA
what artery runs in midline on ventral surface of pons?
basilar artery
The scalp receives a rich arterial supply via the ________ and the _____________ (a branch of the internal carotid).There are three branches of the former involved:
- _________– supplies the frontal and temporal regions
- _________– supplies the area superiorly and posteriorly to the
auricle.
- __________– supplies the back of the scalp
Anteriorly and superiorly, the scalp receives additional supply from two branches of the ____________ – the ________ and _________ arteries. These vessels accompany the ___________ and ____________ nerves respectively.
The scalp receives a rich arterial supply via the external carotid artery and the ophthalmic artery (a branch of the internal carotid).There are three branches of the external carotid artery involved:
- Superficial temporal– supplies the frontal and temporal regions
- Posterior auricular– supplies the area superiorly and posteriorly to the auricle.
- Occipital– supplies the back of the scalp
Anteriorly and superiorly, the scalp receives additional supply from two branches of the ophthalmic artery – the supraorbital and supratrochlear arteries. These vessels accompany the supraorbital and supratrochlear nerves respectively.
photoreceptors absorb light using what?
11-cis retinaldehyde bound to opsin protein
what keeps opsin in the inactive state?
11-cis retinal
what is the G protein in photoreceptors?
transducin
what do photoreceptors respond to light with?
graded hyperpolarisation
what is the signal photoreceptors transmit in light?
reduction in Glu in response to absoprtion of light (lots of Glu released in dark as neurons release Glu when depolarised)
what provide an inhibitory link between bipolar cells and RGCs?
amacrine cells
axons from what layer project to the brain?
ganglion cell layer
what layer in the retina contains the cell bodies of rod cells?
outer nuclear layer
what layer in the retina contains the cell bodies of bipolar cells?
inner nuclear layer
what layer contains synapses between bipolar and amacrine cells?
inner plexiform layer
what layer contains synapses between photoreceptors (rod cells) and bipolar cells?
outer plexiform layer
is onset of anaesthesia faster with inhalation or iv?
iv
what is commonly used for induction of general anaesthesia?
propofol
when may inhalation be used over iv for induction?
where iv access is difficulty to obtain, where difficulty maintaining the airway is anticipated, or due to patient preference (eg. children)
maintenance of general anaesthesia is achieved by allowing the patient to breathe a carefully controlled mixture of what? how can it also be achieved?
oxygen, nitrous oxide and volatiles anaesthetic agent (isoflurane)
- can also be achieved by having a carefully controlled continuous infusion propofol through an intravenous catheter
what is the natural neurotransmitter at the NMJ which causes muscular contraction when it is released from nerve endings ?
ACh
muscle relaxants work by preventing…..
ACh from attaching to its receptor
since muscle relaxants paralyse the muscles of the larynx, how is the airway protected?
endotracheal tube
the effects of muscle relaxants are commonly reversed at the termination of a surgery by what type of drugs?
acetylcholinesterase drugs
in terms of airways, what is lost with the loss of consciousness?
- protective airway reflexes (eg. coughing)
- airway patency
- regular pattern due to the effect of of anaesthetics, opioids or muscle relaxants
what 2 things are used to reverse any muscle relaxants?
neostigmine and glycopyrrolate
what is monitored and assessed in reversal of anaesthesia?
oxygenation, pain control, fluid balance, post operative nausea and vomiting (PONV), cardiovascular stability, conscious level, urine output
- late management : wound infection, DVT, chest infection, surgical problems
what are some adverse effects of anaesthesia?
- PONV
- CV depression
- arrhythmogenesis
- hypotension : vasodilation
- loss of airway tone : airway obstruction
- malignant hyperthermia (uncontrolled temp —> if untreated, all the ATP stores are burned —> rhabdomyolysis, renal failure and cardiac arrest
- bronchial muscle relaxation and impaired cough reflex
- agitation and confusion (esp elderly)
- nephrotoxicity : RBF, GFR, UOP…. vs fluride induced nephrotoxicity
- hepatotoxicity : halothane hepatitis
- an iv anaesthetic for rapid induction = _______
- an inhalation anaesthetic to maintain anaesthesia during surgery = _______
- a perioperatie opiod analgesic = _________
- a muscarinic antagonist to prevent or treat bradycardia or to reduce bronchial and salivary secretions = _______/________
- anticholinesterase agent to reverse the neuromuscular blockade = ________
- propofol
- isoflurane
- fentanyl
- atropine/glycopyrrolate
- neostigmine
what are inhalation anaesthetics soluble in?
lipid — readily cross alveolar membranes
what are the main factors that determine the speed of induction and recovery? (properties of inhalation anaesthetics)
properties of the anaesthetic:
> blood:gas partition coefficient (solubility in blood) = speed of induction/recovery
oil:gas partition coefficient (solubility in fat) = potency
physiological factors:
> alveolar ventilation rate
cardiac output
anaesthetic potency is expressed as the what?
minimal alveolar concentration (MAC)
what is the MAC?
minimal alveolar conc
= the conc of vapour in the lungs that is needed to prevent movement (motor response) in 50% of patients in response to surgical (pain-incision) stimulus
what does the potency of a drug increase with?
increasing lipid solubility
link between lipid solubility and MAC?
the higher the lipid solubility, the lower the MAC
why does propofol have rapid recovery with a small hangover effect?
very rapidly metabolised to inactive metabolites
MOA of propofol
positive modulation of GABA through GABA-A receptor — cause an increased influx of Cl- ions into the post synaptic neuron
where do anaesthetics mainly work?
extrasynaptic GABA-A receptors
what type of receptors are GABA-A receptors?
ionotropic ligand-gated ion channels
what are common SEs of propofol?
SEs are less frequent for propofol than other iv anaesthetic agents. SEs include:
- hypotension and bradycardia
- resp depression
- pain with injection
- involuntary movement and adrenocortical suppression
- nausea and vomiting
what is the msot widely y used inhalation inducing agent and used for maintenance of general anaesthesia?
isoflurane
what is isoflurane always administered with?
air/pure O2 and nitric oxide
MOA of isoflurane
likely binds to GABA, NMDA (glutamates) and glycine receptors. NOT UNDERSTOOD
SEs of isoflurane
relatively free from SEs. major ones inc hypotension, coronary vasodilation (exacerbate cardiac ischaemia in patient with coronary disease), resp suppression
name a potent narcotic analgesic
fentanyl
MAO of fentanyl
strong agonist at the mu opioid receptor. upon binding, GTP —> GDP on the G-proteins which in turn down regulates adenylate cyclase, reducing cAMP concentrations —> reduced Ca++ influx in to cell —> hyperpolarisation of cell and inhibition of nerve activity
When fentanyl binds, downstream signaling leads to the inhibitory effects, such as decreased cAMP production, decreased calcium ion influx, and increased potassium efflux. This inhibits the ascending pathways in the central nervous system to increase pain threshold by changing the perception of pain; this is mediated by decreasing propagation of nociceptive signals, resulting in analgesic effects
adenylate cyclase inhibition —> deceased release of nociceptive substacens such as substance P, GABA, DA etc
name a non-depolarising NM blocking agent
atracurium
describe atracurium
- competitive antagonist at the ACH receptors of the motor endplate
- cause motor paralysis —> help facilitate endotracheal intubation
what are some major SEs of non-depolarising blockers?
hypotension, bronchospasm (due to histamine release), wheeze, tachycardia or bradycardia anaphylaxis, incomplete reversal
why is the short duration of action of atracurium a clinical advantage?
because of decreased CV effects and decreased dependency of good kidney function
how is atracurium excreted?
esterases and alkaline hydrolysis in plasma
—> Hoffman degradation
—> temperature and pH dependent
MOA of suxamethonium (succinylcholine)
persistent depolarisation of NMJ by mimicking the effect of ACh without being rapidly hydrolysed by acetylcholinesterase. constant depolarisation leads to desensitisation
what is suxamethonium hydrolysed by?
plasma cholinesterase (butyryrlcholinesterase)
what are some SEs of depolarising NM agents?
muscle pain, hyperkalaemia, malignant hyperthermia, anaphylaxis, suxamethonium apnoea, increased intracranial/ocular pressure (due to muscle twitching)
what is suxamethonium apnoea?
genetic inability to break it down
neostigmine MOA
- blocks acetylcholinesterase
- increases ACh in the NMJ (both nicotinic and muscarinic receptors)
- increases muscular contraction
—> acts to reverse the effects of non-depolarising muscle relaxants
how do atropine and glycopyrrolate work? why are they used?
- they antagonise the muscarinic receptor and thus inhibit cholinergic transmission
- used to limit the parasympathetic effects caused by neostigmine (prevents neostigmine’ symptoms muscarinic effects such as bradycardia)
what are the side effects of anti cholinesterase drugs?
autonomic:
- bradycardia
- hypotension
- bronchoconstriction
msucular:
- muscle fasciculations
- twitch tension
- depolarisation block
atropine vs glycopyrrolate
atropine can cross the BBB but glycopyrrolate cant
what else are anticholinesterase drugs used to treat?
myasthenia gravis (neostigmine)
what are the 2 main forms of cholinesterase?
describe mannitol
- osmotic diuretic
- used to treat raised intracranial pressure (eg. cerebral oedema)
MOA of mannitol
- pharmalogically inert substances that are filtered in the glomerulus but not reabospred by the nephron
- cause diuresis because they increase the solute content of the fluid in the proximal and collecting tubules
- this draws fluid from the body into the proximal tubule, thus decreasing the volume of fluid inside the body
- results in less water being reabsopred and less sodium
- decrease in extracellular fluid volume
what is NREM 1?
- light sleep
- lasts 1-5 minutes
- stage between wakefulness and sleep
what are skeletal muscles like in NREM sleep?
relax but maintain their tone
when in sleep is parasympathetic activity predominant?
NREM — promotes gastric motility and a decreased HR and BP
what EEG waves and waveforms are present in each of the sleep stages?
NREM 1 = 4-7 Hz waves, alpha and theta EEG waveforms
NREM 2 = 10-15 Hz waves, theta EEG waveforms + sleep spindles and K complexes
NREM 3 and 4 = <3.5 Hz waves, delta EEG waveform — “slow wave sleep” — lowest frequency, highest amplitude
awake = beta most common
in what type of sleep are BP, metabolism and blood flow to the brain increased?
REM sleep
when do most dreams occur?
REM
what act as “REM-on” cells that initiate REM sleep?
brainstem cholinergic neurons in the ascending arousal system
what are activated in REM sleep, causing skeletal muscles to become flaccid and muscel stretch reflexes to be absent?
inhibitory medullary reticulospinal neurons
only what muscles remain active in REM sleep?
ocular, respiration, and middle ear muscles
what act as “REM-off” cells, initiating transition from REM back to non-REM sleep?
noradrenergic and serotonergic neurons
what type of sleep do you need in order to survive?
NREM
what type of sleep decreases with age?
REM
in what sleep is sympathetic activity predominant?
REM
ASCEDNIG AROUSAL SYSTEM?
SEE NOTES
describe cytotoxic oedema
- initial mechanism
- fluid retained in cytoplasm
- loss of NaK ATPase
- Glu gated Ca channels open
- Ca draws water in
(BBB intact)
cerebral ischaemia - decreased blood flow and glucose supply — exhaustion of energy sources — failure of NaK pump
describe vasogenic oedema
- delayed mechanism (48 hours)
- breakdown of BBB
- fluid and protein extravasation into parenchyma
- esp important for patients with stroke or contusions
return of blood flow to these cells after an ischaemic stroke can cause excitotoxicity and oxidative stress — dysfunction of the endothelial cells and BBB disruption
what can an ACA occlusion cause?
paralysis and sensory loss in contralateral leg and perineum
what can a MCA occlusion cause?
contralateral paralysis (mostly in lower face and in arm), general somatosensory deficits, speech deficits (aphasia) if dominant hemisphere affected
what is the pterion?
where these meet:
- parietal bone, squamous part of temporal bone, frontal bone, greater wing of sphenoid
> skull is very thin at this point — structurally weak so more easily broken
what does the pterion overlie? clinical significance?
- overlies anterior division of MMA — fracture here can lead to an extradural haematoma
describe the typical symptoms of an extradural haematoma?
lose consciousness immediately, lucid interval, get drowsier and then lose consciousness again
why does the ICP rise rapidly in an extradural haematoma?
dura is attached tightly to sutures — blood doesn’t cross so is trapped with no where to go — ICP can rise rapidly
doesnt cross suture lines
symptoms of an extradural haemaotma
- headaches, nausea, vomiting, focal neurological symptoms (weakness, numbness, vision and auditory problems). cerebral oedema —> brain herniation —> loss of consciousness, coma, death
what is the usual bleeding source i a subdural haematoma?
bridging veins (connect superficial veins of skull and dural venous sinuses)
what are bridging veins susceptible to and when do they get stretched out?
- bridging veins are vulnerable to rapid acceleration and deceleration — commonly disrupted in car crashes
- these veins get stretched out in the elderly and in chronic alcohol abus
what type of haemotoma can shaking a child cause?
subdural
what are the typical symptoms of a subdural haematoma?
worsening headaches, nausea or vomiting, visual problems, slurred speech, dizziness, unsteady gait, confusion, cognitive impairment, seizures, hemiparesis
- venous therefore haematoma grows slower
- concave crescent shaped CT rhat does cross suture lines
why does ICP rise slower in subdural haematoma?
cross suture sites — disrupted over larger areas — pressure doesn’t build up as quickly — ICP rises gradually
how can density on CT help determine the age of a haematoma?
- acute : hyperdense (white)
- chronic : hypodense
what type of haematoma has a higher morbidity and mortality?
subdural — harder to detect in early stages
what disease/syndromes can predispose even young people to saccular aneurysms, leading to a subarachnoid haemorrhage?
autosomal dominant polycystic kidney disease, marfan syndrome, and ehlers-danlos syndrome
what is the first sign of a subarachnoid haemorrhage?
‘worst headache of life’ = thunderclap headache
symtpoms of subarachnoid haemorrhage
headache, nuchal rigidity (neck stiffness), seizures, and due to ICP : vomiting, vision changes and confusion
what does a subarachnoid haemorrhage look like on CT?
blood in ventricular cisterns, interhemispheric fissures, and within sulci
what can cause hydrocephalus and spit-traumatic vasospasm (leading to ischaemia)?
subarachnoid haemorrhage, subdural haematoma and cotunison, but not extra dural
what causes diffuse axonal injures?
- result from shearing forces on white matter axons in brain, causing the axons to stretch or tear apart
- can be caused by rapid acceleration or deceleration eg. car crash
what do diffuse axonal injures look like on MRI?
multiple small, hyperdense punctuate lesions along the gray-white matter junction
craniectomy vs craniotomy vs cranioplasty
A Craniectomy is similar to a craniotomy as both procedures involve removing a portion of the skull, the difference is that after a craniotomy the bone is replaced and after a craniectomy the bone is not immediately replaced.
cranioplasty : replacing the bone once the swelling is gone. if the bone piece has been preserved then it can be used. if not, options include titanium, acrylic or synthetic bone substitute. modern 3D printing are also used
what does fixed dilated pupils indicate?
- transtentorial herniation
- pressure on brainstem
- pressure on oculomotor nerve — pupils fixed and dilate, lose pupillary reflex
- poor prognostic marker
descirbe periorbital swelling as a symptom
- raccoon eyes — bilateral eye swelling
- base of skull fracture
- often accompanied by battle sign (bleeding behind ear), haemotymoanum, CSF leak
what connects broca’s and wernicke’s?
arcuate fasciculus
describe dysarthria
- difficulty speaking dude to muscle weakness
- swelling compressing arcuate fasciculus, broca’s
- damage to cranial nuclei
why do you get seizures after a head trauma?
- scarring in brain
- scars cant transmit electrical signals
- signals ‘jump over’
- chemical imbalance
- too much Glu:GABA
what lobe is frequently involved in seizures?
temproal
what is a seizure?
a sudden, uncontrolled electrical disturbance in the brain
what things are imbalanced in seizures?
excitatory (too much)
- excitatory psotsynaptic potential (EPSP)
- Na+ influx
- Ca++ currents
- paroxysmal depolarisation
inhibitory
- inhibitory postsynaptic potential (IPSP)
- K+ efflux
- Cl- influx
- pumps
- low pH
what is esteem support?
when other people increase one’s own self-esteem
what is informational support?
whereby other people are available to offer advice
what is companionship?
support throguh activities
what is instrumental support?
involves physical help
what are 4 types of social support?
- esteem support
- informational support
- companionship
- instrumental support
what does the main effect hypothesis suggest?
that social support itself is beneficial and that the absence of social support is itself stressful
what does the stress buffering hypothesis suggest?
that social support helps individuals to cope with stress
what waves are the slowest brain waves?
delta
what are the most common daytime brain waves, and are dominant in normal wakeful states and when you’re focuses on cognitive tasks?
beta
what are te fastest brain waves, which process info from various brain regions and are responsibel for conscious perception?
gamma
what brain waves are in REM sleep?
similar to when we are awake — beta
BATS DRINK BLOOD (waves)
from awake to deep sleep to REM
- beta = awake
N1 - alpha
- theta
N2 - spindles and K complexes
N3
- delta
REM
- beta
brain waves during anaesthesia resemble which stage of sleep?
- N1
- N2
- N3
- REM
- none of the above
none of the above
a decrease in which of the following neurotransmitters is most likely to result in post-traumatic epilepsy?
- serotonin
- dopamine
- GABA
- noradrenaline
- glutamate
GABA
which of the following is used to allow intubation during general anaesthesia?
- neostigmine
- suxamethonium
- isoflurane
- atracurium
- fentanyl
suxamethonium
which of the following is NOT assessed by the Glasgow Coma Scale?
- pupil response to light
- verbal response to questions
- eye opening with and without a stimulus
- motor response to trapezius pinch
- coherent communication
pupil response to light
action potentials from the eye are sent down the axons of what tract?
retinohypothalamic tract (RHT)
where does the AP in the retinohypothalamic tract go?
- to the suprachiasmic nucleus (SCN)
- releases specific chemicals (usually glutamate) which trigger the SCN
- the SCN secretes chemicals to stimulate different organs
what is the SCN and what does it regulate?
- suprachiasmic nucleus = biological clock
- regulates sleeping and walking
what is stimulated by the SCN? what does it do?
the paraventricular nucleus in hypothalamus — sends signals down through the lateral gray column of the spinal cord to the superior cervical ganglion (SCG)
where does the superior cervical ganglia send signals to?
the pineal gland via post ganglionic motor neurons — these secrete noradrenaline
describe the pineal gland
made of pinealocytes
- they have specific adrenergic receptors for noradrenaline
- these receptors stimulate every step of the intracellular pathway :
tryptophan —> 5-hydroxytryptamine —> serotonin —> melatonin
what sleep stage features hypnogogic hallucinations and hypnic jerks?
NREM 1
what is created over the course of the day, leading to sleepiness at night?
adenosine
when do melatonin concentrations peak? when does body temperature reach its lowest?
3am
what is the name of the area of the frontal lobe that takes up the majority of the lobe and cortex is crucial for the performance of almost all skills requiring intelligence?
prefrontal cortex
what is the name of the area of the frontal lobe that consciously monitors movement sequences, using sensory feedback and coordinates movement?
premotor cortex
what kind of fracture is it where the bone is broken but skin is intact?
simple/closed
what is a compound fracture?
involves a break in or loss of skin and splintering of the bone
what type of cerebral oedema is this describing : plasma dilution results in an abnormal pressure gradient and movement of water into the brain
osmotic
describe a tonic-clonic seizure
the person loses consciousness, muscles stiffen and jerking movements are seen
describe an atonic seizure
there is an abrupt loss of muscle tone, also known as a ‘drop attack’
which drug acts through the inhibition of ACh on structures with muscarinic ACh receptors?
glycopyrrolate
which drug may cause a dry mouth, constipation and ear congestion side effects?
glycopyrrolate
