control term two (2) Flashcards
what would dementia affecting the frontal lobe present as?
abnormality in behaviour
- impaired judgement
- abstract reasoning
- strategic planning
- emotional restraint
- control of appetite + continence
what do dementias affecting the medial temporal lobe, hippocampus, amygdala + limbic systems present with?
disorders of memory + hallucination
what do dementias affecting the parietal lobe present as?
impairment of visuospatial skills + integration of sensory inputs
leading to:
- sensory agnosias
- apraxias
what do dementias affecting the temporal lobe present with?
- receptive dysphasia (can’t understand what they’re being told)
- automatisms (actions performed involuntarily or unconsciously)
name 8 differential diagnoses for dementia?
- depression
- hypothyroidism
- B12 deficiency
- iatrogenic (drugs)
- normal pressure hydrocephalus
- subdural haematoma
- encephalitis
- neurosyphilis (rare but do see it)
what types of drugs could have side effects which look like dementia? 4
- anti cholinergics
- sedatives
- narcotics
- H2 blockers (reduce stomach acid)
multiple meds
name 10 types of dementias
- alzeihmers
- lewy body dementia
- parkinsons disease
- frontotemporal dementia (a syndrome, lots of causes)
- huntingtons
- vascular dementia (treatment may slow down progression but won’t cure)
- progressive supranuclear palsy (PSP)
- corticobasal degeneration (CBD)
- normal pressure hydrocephalus (NPH)
- prion disease (eg CJD)
which lobes of the brain are normally most affected by alzeihmers?
parietal + temporal lobes
what is the drug valproate used for?
mainly used for the prevention of seizures
- epilepsy
- bipolar disorder
- to prevent migraine headaches
what three classic symptoms does normal pressure hydrocephalus present with?
- dementia (cognitive problems)
- gait disturbance (ataxia)
- urinary incontinence
what are the causes of normal pressure hydrocephalus?
50% are idiopathic
50% have a preceding cause, eg:
- subarachnoid haemorrhage
- meningitis
- trauma
- radiation-induced
symptoms are caused by expansion of the lateral ventricles
what is levitiracetam?
anti-epileptic drug
histilogically, what does CJD look like?
a sponge
- hence name: transmissable spongiform encephalopathy
describe the 4 general stages of dementia
stage 1 mild:
- changes in memory
- changes in personality
- changes in visuo-spatial abilities
stage 2 moderate:
- aphasia
- apraxia
- confusion
- agitation
- insomnia
stage 3 severe:
- resistiveness
- incontinence
- eating difficulties
- motor impairment
stage 4 terminal:
- bedfast
- mute
- dysphagia
- intercurrent infection
what macroscopic findings are seen in the brains of patients with alzheimers? 3
reduced brain weight: 900-1200 (norm:1200 - 1400)
atrophy of gyri + widening of sulci:
- frontal
- temporal
- parietal
- hippocampus
ventricular dilatation
what microscopic findings are seen in dementia with lewy bodies?
underlying mechanism involves the buildup of Lewy bodies, clumps of alpha-synuclein protein in neurons
what is vascular dementia?
what is it also known as?
a dementia caused by problems in the supply of blood to the brain, typically a series of minor strokes, leading to worsening cognitive decline that occurs step by step
multi-infarct dementia
name a type of frontal temporal dementia?
what microscopic changes are seen in the brain?
pick’s disease
accumulation of tau proteins in the neurons
these accumulate into silver-staining spherical aggregations known as pick bodies
what is a febrile seizure?
who normally gets them?
seizure associated with a high body temperature (fever) but without any serious underlying health issue.
They most commonly occur in children between the ages of 6 months and 5 years
what is the definition of epilepsy?
2 or more unprovoked non-febrile seizures
types of epilepsy:
- generalised?
- focal?
- idiopathic?
- symptomatic?
- cryptogenic?
generalised:
- whole brain affected from onset
focal:
- seizures begin in part of brain (normally temporal or frontal)
idiopathic: - cause unknown (but assume genetic) symptomatic: - cause identified (ie can see tumour/lesion on scan) cryptogenic - pathology suspected but not identified
what is a tonic clonic seizure?
tonic part:
- lasts only a few seconds
- all muscles get tense (if standing fall over)
- may make a load groan or similar
clonic part:
- muscles contract + relax very fast -> jerking movements, biting tongue, hypoxia, can get urinary or faecal incontinence etc
when come round:
- very confused + can get angry/irrational
- often get headaches + need to sleep
what are some causes of symptomatic epilepsy? 8
- birth injury (eg hypoxic brain injury)
- disorder of neural development
- brain infection (eg meningitis)
- brain trauma
- brain tumour
- cavernoma
- cerebovascular disease (eg stroke)
- brain degeneration (eg dementia)
what is a cavernoma?
cavernoma is a cluster of abnormal blood vessels, usually found in the brain and spinal cord
excised ones look like raspberries
can cause haemorrhage as well as seizures
what is periventricular node dysplasia?
grey matter gets ‘stuck’ around the ventricles during brain development = high chance of seizures
what are the three types of focal epilepsy seizures?
simple partial
- patient retains awareness
complex partial
- patient looses awareness
secondary generalised tonic-clonic
- ie spreads to whole brain
what are the 4 types of generalised epilepsy seizures?
absence
- brief, patient looses awareness + stops talking etc
myoclonic
- tend to happen in morning - ‘clumsy episodes’
primary generalised tonic-clonic
atonic or tonic drop attacks
what are the four main groups of differential diagnoses for epilepsy?
syncope
psychiatric illness
hypoglycaemia
- particularly if happens at night (as this is when blood sugar is lowest)
rare disorders
- cataplexy
- sudden raised intracranial pressure
what are the three types of syncope which can be mistaken for epileptic seizures?
- vasovagal syncope
- postural syncope
- cardiac syncope
vasovagal syncope:
- prodrome? 4
- convulsions?
- recovery?
- investigations if lots? 7
prodrome:
- feel warm
- light-headedness
- visual disturbances (blurring)
- hearing disturbances (muffled hearing)
convulsions:
- can get ‘reflex seizure’ due to slight brain hypoxia, esp if propped up after faint
- slight jerking
recovery:
- fast
- may be weepy or sweaty
investigations: - blood glucose - anaemia - cardiac exam (look for murmur) - neurological exam - ECG - tilt test (- holter monitor - 24hr ECG) - rarely!
what is the treatment for repeated vasovagal syncope? 4
- recognition of prodrome
- avoid dehydration
- salt loading
- exercise
cardiac syncope:
- age affected?
- risk factors?
- posture?
- prodrome?
- recovery?
usually over 50 years
often vascular risk factors (eg hypertension etc)
posture:
- can occur at ANY posture (incl lying flat)
doesn’t tend to be a prodrome
rapid full recovery
cardiac syncope:
- investigations? 6
- treatment? 1
investigations:
- cardiac exam
- neuro exam
- ECG
- holter monitor (24hr ECG) - particularly if normal ECG is normal
- exercise test
- reveal device (inserted like a pacemaker, monitors ECG, can detect things like intermittent heart block)
treatment:
- pacemaker
what are dissociative seizures?
another name for them?
describe the seizures.
seizures which are caused by psychological stimuli (either immediate or chronic)
- often a history of physical/sexual abuse and/or mental illness
psychogenic seizures
(about 20-30% of people who turn up at epilepsy clinics)
sezures start and stop gradually (often waxing and waning for half an hour)
- prolonged attacks
nb can get epilepsy AND dissociative seizures
nb 75% are women (often presents in young adults/late teens)
dissociative/psychogenic seizures:
- investigations? 5
- treatment? 2
investigations: - cardiac exam - neuro exam - thorough social history - EEG (- get relatives to film attacks on their phones)
nb EEGs + imaging etc should all be normal
treatment:
- stop anti-epileptic drugs (have no or negative effect!)
- psychological support/family therapy/CBT
after first epileptic tonic-clonic seizure:
- investigations? 4
- risk of 2nd seizure within 5 years?
- treatment?
- driving?
investigations:
- ECG
- EEG
- MRI brain
- blood tests (to rule out other causes)
risk of 2nd seizure within 5 years:
- if tests normal = 20-30%
- tests abnormal = 50-60%
treatment:
- if tests normal = none (just conselling re what to do if another)
- if tests abnormal = anti-epileptic drugs
driving:
- if tests normal: 6 month ban
- if test abnormal: 1 year ban
what sort of things can provoke epileptic seizures in people who are prone to them? 6
- lack of sleep
- stress
- alcohol
- lots of caffiene
- recreational drugs
- flashing lights`
juvenile myoclonic epilepsy:
- how presents?
- EEG appearance?
- cause?
- triggers? 2
- treatment?
lots of myoclonic jerks
- esp in morning
- mainly affects arms, drops objects
occoasionally get generalised tonic-clonic seizures
EEG = polyspike + wave
(affects all leads as generalised over whole brain)
idiopathic (genetic + familial link)
- sleep deprivation
- alcohol
treatment:
- anti-epileptic drugs
- – first line levetiracetam
nb AEDs are effective but are life-long, if you come off them, seizures will return
which anti-epileptic drug (AED) should be avoided in women before/during child-bearing age/in pregnancy?
sodium valproate
- is a teratogen
30-40% risk of developmental abnormalities
10% risk of major congenital malformaitons
temporal lobe focal epilepsy:
- type of seizures?
- risk factor?
- investigaitons + findings? 5
- treatment? 2
- normally absent seizures, loose awareness
- can stare and/or lick lips etc
- takes a while to come back around
- trouble finding words (expressive dysphasia) for few minutes afterwards
- febrile seizures in infancy can lead to this (though majority don’t)
investigations:
- MRI brain
- – eg high signal + atrophy in left hippocampus
- interictal EEG
- – left temporal spikes
- ictal EEG
- – left temporal rhythmic activity
- neuropsychology
- – low average IQ + poor verbal memory
- video EEG
treatment:
- anti-epileptic drugs
- possibility of surgery if can see causative lesion (try two AEDs first)
nb 5% of patients are allergic to AEDs - may get rash
nb same treatment for frontal lobe focal epilepsy
what is:
- interictal EEG?
- ictal EEG?
interictal = taken between seizures (ie when a seizure is not currently occuring)
ictal = taken DURING seizure
what typical sign is seen on EEGs of people with temporal lobe epilepsy?
phase reversal
when might EEGs look normal when they are actually not? why?
if frontal lobe epilepsy
as frontal bone is quite thick so not all eletrical impulses are conducted through it
Lennox Gastaut syndrome:
- what is it?
- typical presentation?
- age of onset?
- treatment? 2
seizure syndrome
get lots of different types of seizures: - infantile spasms (9-40%) - tonic seizures - atonic drop attacks - prolonged trances - myo-clonic jerks - absent seizures - tonic-clonic seizures basically combination of any type!
have learning difficulties/developmental delay (also autism)
EEG is abnormal (slow spike wave pattern), MRI + genetics normal
age of onset: 1-7 years
treatment:
- AEDs
- vagus nerve stimulator
(rarely surgery)
what is the most important thing in making a epilepsy diagnosis?
history from a seizure witness
what are the two broad types of changes in neuronal activity that can cause seizures?
give details of ions/neurotransmitters involved
too much neuronal excitation:
- ions: too much Na+, Ca+ influx
- neurotransmitters: too much glutamate, aspartate release
too little neuronal inhibition
- ions: too little Cl-, K+ efflux
- neurotransmitters: too little GABA release
basically any abnormal increase in neuronal activity -> seizure
GABA:
- what cells release it?
- what is it?
- what two receptors does it act on?
- which receptor is relevant for epilepsy?
inhibitory interneurones
- these allow activity to spread in one direction, but not to spread out sideways
(make up 10-20% of neurones)
inhibitory neurotransmitter
- GABAa (ligand gated chloride channel)
- GABAb receptors (G protein coupled recptor)
GABAa receptor mutations can result in epilepsy
name 5 epilepsies which are currently known to be caused by GABAa receptor mutations
what type of mutation is seen in these conditions?
- childhood absence epilepsy (CAE)
- pure febrile seizures (FS)
- generalised epilepsy with febrile seizures plus (GEFS+)
- juvenile myoclonic epilepsy (JME)
- Dravet syndrome (DS) (aka SMEI - severe myoclonic epilepsy in infancy)
non-sense mutations
- production of truncated proteins instead of norm receptors
nb these are rare, but severe, forms of epilepsy
nb can be inherited or de novo muta
why are infants a lot more prone to febrile seizures?
ie seizures due to high temp/fever
- due to difference balance between excitation and inhibition in infant brain (more excitation than inhibition)
Means they are prone to seizures when they get fevers
nb most infant febrile seizures don’t develop to epilepsy
what type of seizures are seen in Dravet syndrome?
what’s another name for this?
basically any and all types of seizures
nb early onset (infant/child)
severe myoclonic epilepsy in infancy (SMEI)
what is status epilepticus (SE)?
treatment?
what are the risks associated with it?
life-threatening condition in which brain is in a state of persistant seizure:
- more than 30 mins
- 2 or more sequential seizures spanning this period (without full recovery between seizures)
treatment:
- GABA receptor agonist
- – eg diazepam
- – sedative effect
SE confers a greater risk of future unprovoked seizures
nb the longer a seizure lasts, the less likely it will stop on its own
nb diazepam is only used acutely as:
- it’s addictive
- body can become resistant
what are the three commonest modes of action of anti-epileptic drugs?
suppress action potential
- Na+ channel blocker/modulator
- K+ channel opener
enhance GABA transmission
- GABA uptake inhibitor
- GABA mimetics
suppression of excitatory transmission
- glutamate receptor antagonist
what are the 3 drugs of choice in partial simplex, partial complex + generalised tonic-clonic seizures?
- carbamazepine
- phenytoin
- valproate
“big seizures are exhausting, needs CARBS from CARBamazepine”
nb valproate = valproic acid = sodium valproate
what are the 2 drugs of choice in absence seizures?
- ethosuximide
- valproate
“ethoSUXimide SUCKS the life out of you - you are absent”
what is the drug of choice in atypical absence, atonic + myotonic seizures?
valproate
2nd line: clonazepam
what is the treatment for febrile seizures?
diazepam
nb given rectally or IV as infants struggle to take tablets
benzodiazepines (class of drugs)
- mechanism of action?
- effects/common uses? 4
- examples? 2
GABA receptor agonist
- increase Cl- inflow
- raises action potential threshold
- sedatives
- anti-anxiety
- anti-epileptic
- muscle-relaxants
and others.. - diazepam (aka valium)
- clonazepam
nb the body can become resitant to these and they are addictive so are only used in acute settings!
nb if used with other CNS depressants (eg alcohol) then can be fatal (due to resp depression)
which anti-epileptic drugs work by inhibiting Na+ channels? 3
- phenytoin
- carbamazepine
- lamotrigine
valproate:
- mechanism?
- types of seizures can be used against
unknown mechanism
- lots of different actions
tonic-clonic + absense
what is the first and second line treatment for mania in bipolar disorder?
first line: lithium
second line: valproate
which two anti-epileptic drugs are absolutely contraindicated in pregnancy?
for which other do you use a similar drug instead?
- phenytoin
- valproate
oxocarbamazepine is used instead of carbamazepine
what is foetal hydantoin syndrome?
symptoms?
occurs in 30% of children whose mothers are taking phenytoin during pregnancy
- intrauterine growth restriction + microcephaly
- minor dysmorphic craniofacial features + limb defects
- possible developmental delay`
nb also more rarely caused by carbamazepine
what does FVS stand for?
what is it?
foetal valproate syndrome
increased risk of congenital malformations in infants exposed to valproate prenatally
what is refractory epilepsy?
what is it also known as?
when epileptic seizures cannot be brought under control with anti-epileptic medications
uncontrolled, intractable, or drug-resistant epilepsy
what is epilepsia partialis continua?
A rare type of brain disorder
Patient experiences recurrent motor epileptic seizures that are focal (hands and face)
Recur every few seconds or minutes for extended periods (days or years)
Usually due to large, acute brain lesions resulting from strokes in adults and focal cortical inflammatory processes in children
They are very medication and therapy-resistant, and the primary therapeutic goal is to stop secondary generalization
what is proprioreception?
ability to know where different parts of your body are in space
the sense of the relative position of neighbouring parts of the body
what are the two main ascending sensory pathways in the spinal cord?
what types of sensation do they transmit?
what type of fibres are used?
how fast is conduction?
spinothalamic pathway = pain = temp = some touch - thin, poorly myelinated fibres - slow conduction
dorsal column pathway = discriminitive touch = vibration = proprioreception - thick, heavily myelinated fibres - fast conductioon
generally, in ascending sensory pathways, how many neurones are involved?
what is the job of each one?
three
primary neurone
- from sensory receptor to CNS
- cell body is in dorsal root ganglion
- synapse location depends on pathway
secondary neurone
- synapse with primary neurone depends on pathway
- CROSSES over the MIDLINE
- synapses in the thalamus
tertiary neurone:
- thalamus to the primary sensory cortex
where is the primary somatosensory cortex?
post-central gyrus
in parietal lobe
where, in the thalamus, does the secondary neurone synapse with the tertiary neurone? (in ascending sensory pathways)
venteroposterolateral nucleus
in the primary somatosensory cortex, which parts of the cortex corresponds to which body part? (generally, not specific)
(from most lateral to most medial)
- face
- hand
- arm
- trunk
- leg
- genitals
nb cortex of each hemisphere is for contralateral side of body
spinothalamic pathway:
- where does the primary neurone synapse?
- where does secondary neurone cross midline?
- contralateral or ipsilateral in spinal cord?
- becomes in the medulla?
1° synapse:
- dorsal grey horn (after ascending 1-2 segments)
2° neurone crosses midline
- after ascending 1-2 segments
- in ventral white commissure (anterior to central canal)
contralateral (in spinal cord)
in medulla: lateral (or spinal) lemniscus
nb lemniscus = ribbon
what are the 4 parts of the dorsal column? (nb 2 parts mirrored)
- how far up the spinal cord does each go?
- what part of the body do they receive sensation from?
gracile fascicle
- most medially
- run whole length of spinal cord
- sensation from anything below T6 (legs + trunk)
- “GRACILis muscle is in leg”
cuneate fascicle
- most laterally
- above T6 only
- sensation from anything above T6 (arms) - NOT head
dorsal column pathway:
- where does the primary neurone synapse?
- where does secondary neurone cross midline?
- contralateral or ipsilateral in spinal cord?
- becomes in the medulla?
1° synapse:
- gracile (below T6) or cuneate (above T6) nucleus in the closed medulla
2° neurone crosses midline
- in closed medulla
- in internal arcuate fibres
ipsilateral (in spinal cord)
in medulla: once crossed over midline, ascend in contralateral medial lemniscus to thalamus
where are the gracile and cuneate nucleis found?
- deep to the cuneate and gracile tubercles (found on dorsal side of medulla)
what is the syndrome you get when the spinal cord is hemisected?
what does hemisected spinal cord mean?
what is the typical neurological sensory presentation?
why?
brown-sequard syndrome
damage to one half of the spinal cord
on ipsilateral side of lesion, loss of:
- proprioreception
- discriminatory touch
on contralateral side of lesion, loss of:
- pain sensation
- temp sensation
as dorsal column pathway is ipsilateral in spinal cord, whereas spinalthalamic pathway is contralateral
nb neurological deficits occur in body parts whose innervation is BELOW the level of the lesion
inflammation of the optic nerve:
- what is it called?
- symptoms? 3
- treatment?
- % who develop MS within 10 years?
optic neuritis
- pain
- partial or complete loss of vision
- reduced pupillary light responses
can give steroids which speeds recovery but doesn’t improve overall vision so tend not to give now
50%
nb is often retrobulbar (behind eyeball) sooften cannot see on fundoscopy or brain scan
transverse myelitis:
- what is it?
- symptoms? 4
- causes? 2
- treatment?
inflammation inside the spinal cord
- sensory loss (ascending, starting in toes) - sometimes motor too
- fatigue
- Lhermittes phenomenon
- may affect bladder
- 50% go on to develop MS
- shingles virus can also cause!
nb hard to differntiate cause clinically
- high dose steroids
what is the diagnostic definition of MS?
what tests can you do to support the diagnosis?
MS if inflammation, demyelination + axon loss of the CNS (NOT PNS!)
have at least 2 attacks (eg optic neuritis + transcerse myelitis) in 2 different times in 2 different places (in the body)
- oval white matter lesions on brain scans
- having antibodies in CSF that aren’t in serum indicates inflammation in CNS
nb there is no diagnostic test! - lots of false positives + negatives if you go by these tests alone
Multiple sclerosis:
- who gets it?
- types?
- treatment? 3
- women twice as likely as men
- caucasians (vikings)
- any age (norm between 25 + 40)
relapsing-remitting
- often proggresses to secondary progressive
- can also have primary progressive
immuno-suppressants (efficacy is correlated to -ve side effects)
- eg interferon
- for relapsing remitting
steroids
- for acute attacks
physiotherapy
- for everyone
nb MS is an autoimmune condition
what is Lhermittes phenomenon?
what causes it?
electric shock down spine when bend neck forwards
- often considered a classic sign of MS but can be caused by other things too
Natalizumab/Tysabri:
- used to treat?
- how it works?
- major adverse event it can cause?
MS
The drug is antibodies against the adhesion molecules which normally allow leucocytes to cross blood-brain barrier
- So they can’t cause inflammation in CNS but can still fight infection in the rest of the body
Progressive Multifocal Leukoencephalopathy (PML)
- caused by JC virus in the brain
- a lot of people have it normally but no problem as easily fought of but if immune cells can’t get to CNS (as with this treatment) then it causes PML
- AIDs patients also tend to get this
what is clonus?
what is it a sign of?
is a series of involuntary, rhythmic, muscular contractions and relaxations
upper motor neurone lesions (ie in CNS)
- eg MS
what does paresis mean?
what does para- mean?
what does hemi- mean?
partial paralysis
- ie sensory and motor functions impaired
para- = two legs hemi- = half body (ie one arm and one leg)
what sort of problems do patients with proggressive MS tend to get? 7
- fatigue
- mood problems
- pain
- sensory problems
- tremor
- spasticity
- genitosphincteral problems
nb these are normally treated symptomatically
what are the 3 divisions of the trigeminal nerve?
which foramen do they enter the skull via
opthalmic (V1)
- superior orbital fissure
maxillary (V2)
- foramen rotunda
mandibular (V3)
- foramen ovale
essentially form the 3 dermatomes of the face
which four cranial nerves carry sensation from the head?
what area do they recieve sensation from?
what pathway does all the sensory information from these nerves travel in?
5) trigeminal (major one):
- face
- nose
- scalp
- dura
7) facial:
- external ear
9) glossopharyngeal:
- posterior 1/3rd tongue
- pharynx
- middle ear
10) vagus:
- auditory canal
- larynx
- pharynx
- oesophagus
trigeminothalamic tract
where are all the cell bodies of the sensory neurons of the cranial nerves found?
what’s the one exception?
trigeminal ganglion
the cell bodies of sensory neurones concerened with PROPRIORECEPTION are locateed in the mesencephalic nucleus
where do the primary sensory neurons from the cranial nerves synapse?
4 different modalities
trigeminal nucleus (3 parts):
- mesencephalic nucleus (in midbrain)
- pontine nucleus (in pons)
- spinal nucleus (in medulla)
pain/temp:
- caudal (inferior) spinal nucleus
simple touch/pressure:
- rostral (superior) spinal nucleus
discriminitive touch:
- pontine nucleus
propriorecption:
- mesencephalic nucleus
what is the pathway of the ‘jaw jerk’ reflex arc?
afferent limb:
- V3 of trigeminal
- propriorecption fibres
- cell body in mesencephalic nucleus
- synapse in motor nucleus (more medial than trigeminal nucleus)
efferent limb:
- V3 of trigeminal
- > muscles of mastication
what would be the clinical signs of a lesion on the RIGHT side of the closed medulla? why?
what might cause this?
sensation from face:
- loss of pain, temp, touch + pressure on RIGHT (ipsilateral) side
- due to modalities in spinal nucleus (lateral in medulla), before they cross midline
sensation from body:
- loss of pain, temp, touch + pressure from LEFT (contralateral) side
- due to modalities in spinothalamic tract (ascends laterally in spinal/lateral lemniscus in medulla on contralateral side)
aneurysm on junction of posterior inferior cerebellar artery (PICA) and vertebral artery
- pushing on lateral aspect of closed medulla
what are the 5 main functions of the skin?
- thermoregulation
- metabolic function
- sensory organ
- rapid repair of injuries
- protective barrier
what 3 things does skin protect against?
- UV light
- pathogens
- water loss
what are the 3 main layers of skin? describe them
epidermis
- continuosly proliferating keratinised stratified squamous epithelium
- no blood vessels
dermis
- fibrous + fibroadipose tissue supports the epidermis
- contains small blood vessels, nerves + sensory receptors
subcutis
- adipose tissue with supporting fibrous bands (septa)
- larger blood vessels
what are the 5 layers of epidermis in thick skin?
which layer is not present in thin skin?
stratum basale - single layer of basal cells
stratum spinosum - prickle cell layer “spiney cells + also the spine is quite deep in the body”
stratum granulosum - cells start to loose nuclei + organelles, get more keratinised - “granulation happens with injury, so cells here start to get injured and die”
stratum lucidum - thin layer of dead cells containing keratohyalin - “lucid, like dreams, sometimes there, somtimes not - only present in thick skin”
stratum corneum - dead cells w hard protein envelope, cells contain a lot of keratin - “cornea is in eye which is organ on outside of body, so this is outermost layer”
what are the 4 types of cell found in the epidermis?
- keratinocytes (ie the epithelial cells)
- melanocytes
- langerhans cells
- merkel cells
what do melanocytes look like histiologcally?
round nuclei with a white ‘halo’ around them
- cells are surrounded by brown pigment (melanin)
what are langerhans cells?
intra-epidermal antigen-presenting cells
- dendritic cells
mainly in epidermis but can get them in dermis too
what 3 things make up a pilosebaceous unit?
- hair follicle (with hair bulb inside)
- sebaceous gland
- arrector pilli muscle
nb hair follicles are downgrowths of epidermis into the dermis
what is the definition, new nomenclature + pain level of:
- 1st degree burns
- 2nd degree burns
- 3rd degree burns
1st degree burn:
- superficial burn
- only affects epidermis
- painful
2nd degree burn:
- superficial partial thickness burn
- affects epidermis + dermis
- painful
3rd degree burn:
- full thickness burn
- affects epidermis, dermis + subcutis (+ possible deeper)
- only painful round edges as, in middle, pain receptors are destroyed
what are the 4 types of encapsulated nerve endings in the skin?
what’s the one type of free nerve ending?
what does each MAINLY detect? where are they in the skin? and are they slow or rapid acting?
meissners corpuscles
- low freq vibration
- epidermal/dermal border
- rapid acting
pacinian corpuscles
- high freq vibration
- deep dermis (onion-looking)
- rapid acting
merkel’s corpuscles
- pressure/touch
- epidermal/dermal border
- slow acting
ruffini endings
- stretch/shearing/pressure
- deep dermis
- slow acting
nocicecptors
- noxious/harmful/pain/temp
- (free nerve endings)
what are the 2 types of proprioceptors in muscles + joints?
how do they differ?
muscle spindles
- provide sensory feedback from muscle fibres on body position + movement
- wrap around muscle fibres
golgi tendon organs
- regulate muscle tension or force of contraction + prevent muscle overloading
what is the correlation between diameter of axon and conduction velocity?
what type of receptors are associated with thick + thin nerve axons?
higher the diameter of axon, the faster the conduction
thick:
- proprioreceptors of skeletal muscle
- mechanorecptors of skin
thin:
- pain
- temp
boundaries of dermatomes are not absolute and overlap over each other. What is the main advantage and disadvantage of this?
advantage:
- if you loose sensation from one spinal nerve, you don’t loose all sensation from area
disadvantage:
- due to overlap, harder to localise where pain/touch is exactly on body
where is the secondary sensory cortex/association areas?
what is its function?
what 2 neurological disorders can result from damage to this area?
posterior parietal cortex
sensory integration
- ie allows us to combine different modalities + submodalities
- eg identify an object by touch alone (coin in pocket)
- or touch + vision (stroking a cat)
asteroagnosia
- inability to identify objects on basis of touch alone (describe coin in pocket as list of traits: cold, hard etc but unable to put together to realise it’s a coin)
neglect syndrome
- body part or visual field is disregarded
- most common after damage to right hemisphere (so left side body etc affected)
- usually improves or disappears with time
are fibres faster conducting in the dorsal column or spinal thalamic pathways?
dorsal column
what is myelitis?
2 normal causes?
infection/inflammation of the spinal cord
(aka transverse myelitis)
- viral
- presentation of MS
35 year old rugby player presented with pain in neck after a rugby match
Rapidly developed: - vertigo/unsteadiness - hoarse voice - difficulty swallowing On examination: - Left Horners syndrome - loss of pain + temp on the left side of the face - loss of pain + temp on the right side of the body
what is the diagnosis?
- what is the explanation of the symptoms?
lateral medullary syndrome (aka wallenbergs syndrome) - this example lesion is on left side
damage to vertebral artery at the neck leading to a stroke -> infarct of vertebral artery branch or PICA
-> lesion on lateral side of medulla
cranial nerves nuclei affected:
- vestibulocochlear (8): vertigo/unsteadiness
- glossopharyngeal (9): dysphagia
- vagus (10): hoarse voice
spinothalamic pathway affected on side of lesion as lies laterally (crossed in spinal cord so contralateral side of body affected)
- facial primitive sensation is on ipsilateral side
nb dorsal column pathway not affected as lies more medial in medulla
56 year old smoker underwent repair of an abdominal aortic aneuysm
Afterwards, he realised he had lost all strength in both legs (paraplegia).
On examination:
- lost pain and temperature sensation below the umbilicus
- but vibration and proprioception was preserved.
diagnosis? why?
anterior spinal syndrome
caused by occlusion of the anterior spinal artery -> infarction of anterior spinal cord
- (in this case, secondary to clamping the aorta during surgery)
posterior spinal arteries supply basically supply the dorsal columns whilst anterior spinal arteries supply everything else (ie spinothalamic sensory pathway and all motor pathway)
hence in anterior spinal syndrome:
- loss of muscle power
- loss of pain/temp sensation
- NO LOSS of fine touch/proprioreception
nb no imaging for this condition, can’t see it! use history/examination to diagnose!
58 year old smoker
Suffers sudden onset loss of sensation of the left side of the whole body including the face.
Loss of sensation to all modalities
Accompanied later by deep aching pain in the left-sided limbs
what is the diagnosis + where is the lesion?
what are the normal risk factors for this condition? 3
pure sensory stroke
right thalamus
thalamus is only place where ALL sensory modalities run together
- all are contralateral
nb even a tiny stroke in thalamus does a lot of damage
- smoking
- hypertension
- diabetes
what is a lacunar stroke?
type of ischemic stroke that occurs when blood flow to one of the small arteries deep within the brain becomes blocked
what sort of sensory disturbances does a lesion in the partietal cortex cause? 3
- dysgraphaesthesia (unable to identify numbers when they are traced onto patients hand)
- hemisensory neglect
- right/left confusion
what is agnosia?
inability to interpret sensations, and thus to recognise things
24 year old lecturer
Gradually developed loss of pain and temperature sensation in both hands and across her body in a cape like distribution.
Also complained of wasting in small muscles of the hands and weakness in the legs.
what is the diagnosis?
syringomyelia
expansion of spinal canal, due to problems with csf drainage
- pushes against medial spinal cord
- > affects crossing fibres of spinothalamic tract first (pain/temp)
- later can cause paraparesis (partial paralysis of lower limbs) + root lesions
can be treated surgically by creating space for csf to drain but can’t reverse damage
clasically shows a ‘cape-shaped’ distribution
name 7 causes of peripheral neuropathy
- diabetes mellitus
- autoimmune (guillian-barre, CIDP, vasculitis)
- inherited (charcot-marie-tooth disease)
- toxic (including medical drugs)
- vitamin deficiency (thymine, B12)
- paraneoplastic
- chronic kidney/liver disease
nb there are lots more causes too!
what is the normal presentation of peripheral neuropathy?
what results are found on investigation?
gradual onset of tingling + burning in hands and feet
numbness to pain, fine touch + vibration with a ‘stocking + gloves ditribution’
absent peripheral reflexes
- normal MRI scan
- abnormal nerve conduction studies
what is vitaligo?
cause?
white patches on skin (depigmentation) due to lack of melanocytes
autoimmune
what serious condition of the spinal cord can B12 deficiency (eg caused by pernicious anaemia) cause?
symptoms?
2 other neurological conditions caused by b12 deficiency?
subacute combined degeneration of the spinal cord
- loss of vibration sense up to waist
- loss of propriorecption in feet
- normal strength
- walked with ‘sensory ataxia’ (fall over if you turn out lights, as compensate for lack of proprioreception by using sight)
- peripheral neuropathy
- dementia
(nb 3 things can occur in combination)
nb often occurs alongside other autoimmune conditions
what is Ronberg’s sign?
positive/negative mean?
patient is asked to stand and close their eyes
positive: patient falls over (CATCH THEM!)
negative: patient stays standing
used to assess whether ataxia is sensory (ie due to damage to dorsal column, thus lack of proprioreception) or motor (due to cerebellar damage)
positive = sensory cause negative = motor cause
nociceptors:
- what sensory modality do they detect?
- what nerve endings do they have?
- in what layer of the skin?
- what type of nerve fibres are they? 2 (incl speed)
pain:
- mechanical: react to strong pressure
- thermal: react to burning heat/extreme cold
- chemical: respond to histamine/chemicals
some ncioreceptors respond to just one but most are polymodal and respond to all 3 types of stimuli
free, unmyelinated nerve endings in dermis
thermal + mechanical nociceptors
= A(delta) fibres (slightly myelinated, but thin)
- slow
polymodal nociceptors
= C fibres (unmyelinated, very thin)
- even slower
hyperalgesia:
- mechanism?
- why have it?
tissue damage + inflammation trigger release of prostaglandins
- these sensitise peripheral nociceptors + so reduce threshold for activation -> hyperalgesia
can be:
- reduced threshold for pain
- increased intensity of painful stimuli
- spontaneous pain
protective mechanism to prevent further damage to a part of the body which is already damaged
what are the differences between first + second pain:
- type of fibre?
- sensation?
- localised easily?
- onset?
- duration?
- type of nociceptor modality?
first pain:
- FAST A(delta) fibres
- sharp or prickling
- easily localised
- occurs rapidly
- short duration
- mechanical + thermal nociceptors
second pain:
- SLOW C fibres
- dull ache, burning
- poorly localised
- slow onset
- persistent
- polymodal nociceptors
referred pain:
- what is it?
- where is oesophagus pain referred to?
- where is heart pain referred to?
- where is right prostate pain referred to?
visceral pain is percieved to have a cutaneous source by the sufferer
oesophagus = chest wall
heart = upper chest wall + left arm
right prostate = right lower trunk + leg
what neurotransmitter + neuropeptide are the main ones used in nociceptor fibres?
neurotransmitter = glutamate
neuropeptide = substance P
“child P who got abused = painful for him”
acute pain:
- beneficial consequences? 3
- adverse consequences? 4
beneficial:
- part of trauma response
- protective (avoid further damage)
- learning experience
adverse:
- humanitarian issues
- cardiovascular stress
- respiratory compromise
- hypercoagulation
broad mechanisms of action in acute pain:
- non-opiod analgesics?
- opiod analgesics?
non-opiod:
- NSAIDs/COX-2 inhibitors act mainly peripherally
- paracetamol has central activity
- efficacy in acute pain management + control of nociceptive pain
opiod:
- presynaptic pain signal transmission is reduced
- post synaptic membrane is hyperpolarised, decreasing the probability of AP generation
- main efficacy in nociceptive pain
what are the side effects of opiod analgesics? 7
- nausea
- vomiting
- constipation
- dizziness/vertigo
- fatigue
- dry skin
- pruritis
what two opiod analgesics should you not use in patients with renal failure?
why?
which 2 can you use?
un-safe:
- morphine
- codeine
as sedative metabolites accumulate (can cause resp depression)
safe:
- fentanyl
- oxycodone
what broad types of drug therapy is used for neuropathic pain? 4
- tricyclic antidepressants
- anticonvulsants
- opiods
- membrane stabilising drugs
nb NSAIDs are not useful
anti-cholinergic side effects? 6
- constipation
- dry mouth
- fatigue
- abnormalities in HR or rhythm
- insomnia
- increased appetite
name 3 anticonvulsant drugs used to treat neuropathic pain.
what are the side effects? 6
- gabapentin
- pregabalin
- carbamazepine
- sedation
- dizziness
- nausea
- ataxia
- peripheral oedema
- weight gain
what type of haemorrhage can be caused by a lateral blow to the head?
which artery is likely to be ruptured?
what shape will it produce on CTs/MRIs?
epidural
middle meningeal
biconvex (lense) shape
- ie won’t follow the shape ofthe skull!
what are the 3 bones in the middle ear called as a group and individually?
the ossicles
malleus (hammer)
- “like a mallet”
incus (anvil)
- “incas built with stone”
stapes (stirrup)
- “horses live in stables”
what are the two regions inside the cochlea?
what is the name + composition of the fluid inside each?
cochlea
- split into SCALA VESTIBULI (superior to cochlear duct) + SCALA TYMPANI (inferior to cochlear duct)
- filled with PERIlymph
- high in Na, low in K (like extracellular)
cochlea duct
- closed membranous tube within cochlea
- filled with ENDOlymph
- high in K, low in Na (like intracellular)
what is the apex of the cohlea called?
what is the part of the cochlea which the stapes articulates with called?
what is the part of the cochlea where vibrations ‘leave’ the cochlea called?
helicotrema
- where scala vestibuli + scala tympani meet
oval window
- start of scala vestibuli
round window
- end of scala tympani
what occurs in the inner ear when sounds are heard?
how are high + low frequency sound differentiated between?
stapes vibrates against oval window, sending vibrations through perilymph in scala vestibuli, these push against and deform the endolymph in the cochlea duct.
This pushes on the BASILAR MEMBRANE (between the cochlea duct + scala tympani)
HAIR CELLS, which are imbedded in the BASILAR MEMBRANE brush up against the TECTORIAL MEMBRANE and thus tilt (due to the hydrostatic pressure changes)
as they tilt, they open + close various ion channels
-> action potential which goes down the cochlear nerve
cochlea nerve are in the SPINAL GANGLION (close by) then nerve travels to pontomedullary junction, via the INTERNAL ACOUSTIC MIATUS (out of the PETROUS part of the temporal bone)
the basillar membrane is flexible insome areas and stiff in other parts
- the stiff parts are only distorted at higher frequencies of sound
- > different hair cells will be moved by different frequencies-> different signals to brain
The closer to the oval/round window, the stiffer the cochlear duct, thus the higher freq sounds heard
The closer to the apex/helicotrema, the ‘floppier’ the cochler duct, thus ‘hear’ the lower freq sounds
what is the path of the auditory fibres once they have left the petrous part of the temporal bone?
the vestibulocochlear nerve (CN8) enters brain stem at pontomedullary junction (aka cerebellopontine angle)
then synapses with secondary neurons in DORSAL and VENTRAL COCHLEAR NUCLEI
then may (or may not) DESICATE at the TRAPEZOID BODY
then go through SUPERIOR OLIVARY NUCLEUS in the pons
then the INFERIOR COLLICULUS in the midbrain
then go to MEDIAL GENICULATE NUCLEUS of thalamus
where they are projected up to HESCHL’S GYRUS (primary auditory cortex) on the cerebral cortex in the temporal lobe
nb is more complex than this and is polysynaptic but don’t need to know more detail
which areas of the cochlear pick up low and high pitch sound?
which areas of the cortex process high and low pitch sound?
apex (helicotrema) responds to Low pitch
sound information of Low pitch projects to anteroLateral part of hescl’s gyrus
therefore high pitch sounds are picked up in areas away from apex in cochlear and travel to POSTEROMEDIAL area of heschl’s gyrus
which hemisphere of the brain is the secondary auditory cortex present on? (in most people)
what + where are broca’s + wernicke’s area? what type of aphasia do they cause if damaged?
left hemisphere (broca’s + wernickes are here)
Broca’s area
- anterior to precentral gyrus in frontal lobe
- motor/production of words
- expressive/non-fluent aphasia
- – understand what they here but only communicate in single words
Wernicke’s area
- posterolateral to post central gyrus at border of temporal + parietal lobes
- sensory/understanding
- receptive/fluent aphasia
- – speak in sentences but don’t really understand what they are hearing, so what they’re saying doesn’t make much sense
occlusion of which artery causes damage to:
- broca’s area?
- wernicke’s area?
broca’s area
- ANTERIOR distribution of left MIDDLE cerebral artery
wernicke’s area
- POSTERIOR ditribution of left MIDDLE cerebral artery
what are the 2 mechanisms by which sound amplification is reduced (thus preventing damage due to loud noise) using descending auditory pathways?
how do they work?
stapedius muscle
- when contracted, pulls on neck of stapes, reducing vibrations of it -> reducing amplkification of sound waves
- innervated by facial nerve (CN7)
tensor tympani
- when contracted, pulls on malleus, this tenses tympanic membrane, reducing amplification of vibrations of tympanic membrane
- innervated by mandibular division (V3) of trigeminal nerve (CN5)
what is the visual pathway from the entry of photons into the eye to the optic nerve?
photorecpetors (rod + cone cells)
- > bipolar cells
- > ganglion cells (which then, together, form the optic nerve
nb horizontal/amacrine cells act as modulators etc between different bipolar cells
why, when you get raised intracranial pressure, do you get papilloedema?
because optic nerve is an outgrowth of the diencephalon and so takes the 3 layers of meninges with it.
As the optic nerve is surrounded by the meninges
increases in CSF pressure can swell the optic nerve.
Increases in CSF pressure are associated with head-
aches, drowsiness, blurred vision and vomiting
This increase in pressure compresses the central
retinal vein preventing venous drainage from the eye = papilloedema , a swelling of the optic disk
(vessels on retina look thicker)
between which layers of meninges is csf found?
sub arachnoid space
between arachnoid and pia
where do neurones from the ..
- auditory pathway synapse?
- visual pathway synapse?
auditory:
- medial geniculate nucleus
visual:
- lateral geniculate nucleus
both in thalamus
describe the visual pathway from the retina to the lateral geniculate nucleus
information from the left temporal field hits the left nasal retina
- travels up the left optic nerve
- desicates at the optic chiasma
- travels up the right optic tract
- synapses at the RIGHT lateral geniculate nucleus
information from the left nasal field hits the left temporal retina
- travels up the left optic nerve
- does NOT desicate at the optic chiasma
- travels up the left optic tract
- synapses at the LEFT geniculate nucleus
(same all happens with the right eye)
basically:
- nasal field of view goes to temporal retina and vice versa
- info from nasal retinas cross at chiasma, info from temporal retinas do not
- right visual cortex recieves left visual field from each eye and vice versa
what is the visual pathway after synapsing in the lateral geniculate nucleus (thalamus)?
optic radiationto the primary visual cortex
= striate cortex
(this is the gyri superior and inferior to the CALCARINE SULCUS)
nb the calcarine sulcus runs inferior from the parietooccipital sulcus (perpendicular to it)
what is the other name for the primary visual cortex?
where, in this cortex, does the:
- upper visual field go?
- lower visual field go?
- central visual field go?
striate cortex
upper visual field:
- lower bank of the calcarine sulcus
lower visual field:
- upper bank of the calcarine sulcus
central visual field:
- occipital pole (most distal/posterior part of striate cortex)
- nb this is most detailed part of the visual field
nb right visual field goes to left striate cortex + vice versa
what is the area of the retina which recieves the centre of the visual field (the most detailed part)?
the macula
what is the term used to describe a localised patch of blindness?
scotoma
the term that refers to the loss of one or more quadrants of the visual field?
anopia
terms for when:
- half of the visual field is lost?
- a quarter of the visual field is lost?
half lost = hemianopia
quarter lost = quadrantanopia
terms for when:
- visual field losses are similar for both sides?
- visual field losses are on different sides?
visual field losses are similar for both sides:
= homonymous
- (eg loss of L nasal + R temporal field)
visual field losses are on different sides:
= heteronymous
- (eg loss of L temporal field + R temporal field)
what visual field defect would a lesion in the left optic nerve results in?
monocular blindness in the left eye
what visual field defect would a lesion in the midline of the optic chiasma result in?
what is most likely to cause this?
heteronymous hemianopia
- specifically loss of L + R temporal visual fields
- get ‘tunnel vision’
enlarged pituatory gland
what visual field defect would an aneurysm in the right internal carotid artery result in?
why?
loss of the right nasal visual field
because these fibres run laterally in the optic chiasma and the internal carotid artery is lateral to the chiasma
what visual field defect would a lesion in the left optic tract result in?
homonymous hemianopia
- specifically loss of the R temporal visual field + L nasal visual field
- so basically loss of right hand visual field in each eye
90% of visual nerve fibres go via (and synapse in) the lateral geniculate nucleus of the thalamus, where do the other 10% go?
the pre-tectal area (the midbrain)
pupillary light reflex:
- afferent limb?
- efferent limb?
- two components?
afferent limb:
- optic nerve + tract
efferent limb:
- occulomotor nerve
two components:
- direct component: light in one eye, same pupil constricts
- consensual component: light in one eye, other pupil constricts
decribe the pathway of the pupillary light reflex, including where the neurones synapse
optic nerve recieves light
(90% of fibres go to LGN -> primary visual cortex)
10% of fibres go to midbrain and then to interneurons + synapse in pre-tectal area (specifically in the Edniger-Westphal nucleus) with the occulomotor nerve
- > then interneurons and then the fibres synapse in the ciliary ganglion
- > motor fibres to sphinter pupillae muscle which contracts, constricting the pupil
nb this happens to both eyes due to interneurons in the midbrain making sure the signal is transfered to both occulomotor nerves
is the pupillary light reflex a sympathetic or parasympathetic response?
what is the opposite response and what muscle does it cause to constrict
pupillary light reflex
= parasympathetic
parasympathetic
- constrict pupil
- sphincter pupilae muscle (circular fibres)
sympathetic
- dilate pupil
- dilator pupilae muscle (straight fibres)
if you do the pupillary light reflex in the left eye and only get the consensual response, where is the lesion?
left occulomotor nerve
if you do the pupillary light reflex in the right eye and don’t get a direct or consensual response but then do the reflex in the left eye and do get both a direct and consensual response, where is the lesion?
right optic nerve
accommodation reflex:
- what is it?
- afferent limb?
- efferent limb?
- what 3 things happen?
series of changes that occur when gaze is transferred from a distant to near object,allowing the eye to refocus on the near object
afferent:
- optic nerve
efferent:
- occulomotor nerve
1) accomodation
- lens becomes rounded
- due to contraction of CILIARY MUSCLES
2) pupil constricts
- due to contraction of sphincter pupillae
3) occular convergence
- eyes adduct
- due to contraction of medial rectus
where is the vision problem most likely to be for each of these main symptoms:
- blurred vision/out of focus? 2
- glare/difficulty seeing in bright light? 1
- distortion of vision? 1
- things look pale/darker/less colour? 2
- ‘floater’ in view? 1
blurred vision/out of focus:
- refractive problem (cornea/lens/shape of eye)
- macular problem
glare/difficulty seeing in bright light:
- corneal/lens problem (norm cataracts)
distortion of vision (eg kinks in straightlines)
- problem with retina (eg wet macular degeneration, macular hole, retinal detachment)
things look pale/darker/less colour:
- optic nerve disease (optic neuritis or compression)
- problem with retina (eg wet macular degeneration, central serous retinopathy)
‘floater’ in view
- opacity in vitreous fluid (eg vitreous syneresis, posterior vitreous detachment, vitreous haemorrhage)
cataracts:
- what is it?
- risk factors? 2
- symptoms? 5
clouding of the lense
- sun exposure
- increased age
- harder to see in dim or very bright light
- colours may be faded
- get glare +/or halos around bright lights
- blurred vision
- may have double vision
dry age-related macular degeneration (ARMD)
- pathophysiology?
- symptoms? 3
- onset of symptoms?
- signs? 3
breakdown of retinal pigment epithelial cells (RPE)
- they normally function to remove waste products from cones + rods
- so, if not functioning, build up of waste products -> drusen -> symptoms
- blurred central vision (peripheral vision unaffected)
- colours appear less vibrant
- trouble reading etc
slow onset (wet = fast)
on fundosopy:
- drusen present
- RPE pigmentation
- RPE atrophy
what is the fovea?
what is its function?
‘pit’ in the centre of the macula of the retina
is the point of highest visual acuity in the retina, where light can reach photoreceptors directly
when rays of light enter the eye what happens to them? why?
what happens if the light is coming from an object which is far away?
they are refracted by the cornea and then refracted further by the lense
so that the image can be focused on the back of the retina, to provide a clear, non blurry image
if the image is closer to the eyes then more refraction is needed in order to focus it on the retina, therefore the ciliary muscles contract -> lens becoming rounder -> more refraction, this = accomodation
what is long sightedness and short sightedness?
where does the image focus? (with respect to the retina)
who tends to be affected by each?
long-sightedness:
- things close are blurry
- things far away are clear
- image focuses BEHIND retina (lense is unable to accomodate)
- progressive as you get older, most people get this as they age to varying degrees
- “hence why grannys need reading glasses”
short-sightedness:
- things close are clear
- things far away are blurry
- image focuses IN FRONT of retina (lense is too round)
- often inherited and get at younger age
what are the medical terms for:
- normal-sightedness?
- long-sightedness?
- short-sightedness?
which needs concave glasses to correct and which needs convex?
normal-sightedness
= emmetropic
long-sightedness
= hyperopia
- convex lense needed
short-sightedness
= myopia
- concave lense needed
is the optic disc in the nasal retina or the temporal retina?
what marks the difference between the two halves of the retina?
optic disc (‘blind spot’) is in nasal retina
the fovea of the macula
- anything medial = nasal retina
- anything lateral = temporal retina
rods vs cones:
- sensitivity to light?
- night/day vision?
- colour?
- speed of reaction?
- visual acuity?
- where in retina?
rods:
- high sensitivity
- best for night vision
- black + white
- slower response
- low visual acuity (3 rods per neuron)
- all over retina, none in fovea
cones:
- low sensitivity
- best for day vision
- trichromatic
- faster response
- high visual acuity (1 rod per neuron)
- high conc in fovea/macula
what are the technical terms for these levels of light? and are rods +/or cones being used?
- night time
- twilight
- daytime
night time
- scotopic (“SCared in the dark”
- rods only
twilight
- mesotopic (“meso = middle”)
- rods AND cones
day time
- photopic (“needs lots of light to take phots”)
- cones only
general suffix of a photorecpetor pigment/protein?
name of the photoreceptor in rods?
what 3 colours can cones detect?
-opsin
RHODopsin (in rods)
- blue
- green
- red
in motor pathways: does the upper motor neuron or lower motor neuron cross the midline?
upper motor neurone dessicates (crosses the midline)
what are two causes of peripheral nerve lesions?
symptoms? 5
- crush or cut injuries
- poliomyelitis (due to polio virus)
- muscle wasting
- muscle weakness/reduced power
- hypotonia
- absent tendon reflexes
- fasciculation/fibrillation (visible spontaneous contractions)
what is the pathway of upper motor neurons from cortex to brain stem/spinal cord?
what are the two main motor pathways? what does each supply?
cerebral cortex
- > precentral gyrus
- > internal capsule
- > brainstem/spinal cord, pyramid section (via cerbral peduncles)
corticospinal
- cortex to spine
- spinal nerves
corticobulbar
- cortex to brain stem
- cranial nerves
where is the internal capsule situated?
what type of fibres?
where in internal capsule are motor fibres that supply:
- face?
- trunk?
- arm?
- leg?
medial to the lentiform nucleus (putamen + globus pallidus) and lateral to the caudate nucleus and the thalamus
projection fibres (cut end on in a horizontal section of brain)
all in posterior limb of internal capsule
from anterior to posterior:
- face (corticobulbar)
- arm
- trunk
- leg
in the spinal cord, where do 85% of upper motor neuron corticospinal fibres pass? what about the other 15%?
85% of UMNs descend cord contralaterally in LATERAL corticospinal tract
15% of UMNs descend cord ipsilaterally in ANTERIOR/VENTRAL corticospinal tract
- and then dessicate at level of spinal cord which it supplies fibres to that spinal nerve
where do ALL upper motor neurons synapse with lower motor neurons?
and how do the lower motor neurons then leave the spinal cord?
nb this is just corticospinal, not corticobulbar
synapse in contralateral ventral grey horn
lower motor neurons leave spinal cord via ventral root to combine with dorsal roots to form mixed spinal nerve
nb somatotopic representation is retained through cord
describe the corticobulbar pathway.
including where UMNs synapse with LMNs
fibres originate LATERALLY within pre-central gyrus (see motor homunculus)
UMNs synapse with LMNs at cranial nerve nuclei
innervation of LMNs is largely BILATERAL (unlike corticospinal pathway, with one exception!)
- eg the right cortex will command both the left and right occulomotor nerves
which cranial nerve is the exception to the rule? (ie is not controlled completely bilaterally)
how is it controlled?
facial nerve (CN7)
face is split into 4 quarters (upper right etc)
the two upper face regions are served bilaterally (by both cortex hemispheres)
the two lower face regions are served only by CONTRALATERAL motor cortex
what would be the facial signs of LEFT sided corticobulbar (ie UMN) damage?
what would be the facial signs of lesion in left facial nerve (LMN)?
corticobulbar (UMN):
- RIGHT lower face would be paralysed (droopy mouth)
facial nerve (LMN): - LEFT upper AND lower face would be paralysed (droopy mouth + eyes/eyebrows)
nb UMNs are contra/bilateral whereas LMNs ipsilateral
what is the technical name of a lesion which affects the corticobulbar (UMN) fibres?
supranuclear
as it is a lesion which is proximal to synapsing at the cranial nerve nuclei
nb opposite (ie lesion on LMN fibre) = infranuclear
common causes of lesions to facial nerve:
- supranuclear? 1
- infranuclear? 4
supranuclear:
- vascular stroke
infranuclear:
- tumours of cerebellopontine angle
- middle ear disease
- parotid tumour
- bell’s palsy (idiopathic)
facial nerve (CN7):
- intracranial branches? 3
- foramen it exits skull via?
- extracranial accessory branches? 3 (NOT 5 terminal branches)
intracranial branches:
- greater petrosal nerve (supplies lacrimal duct)
- nerve to stapedius
- chorda tympani
then it exits via stylomastoid foramen
extracranial accessory branches:
- posterior auricular nerve (motor to muscles around ear)
- nerve to digastric muscle
- nerve to stylohyoid muscle
what does the chorda tympani branch of the facial nerve supply? 3
- submandibular gland
- sublingual gland
- taste to anterior 2/3 of tongue
what are the 5 TERMINAL branches of the facial nerve (CN7)?
“Two Zebras Bit My Coccyx”
- Temporal branch
- Zygomatic branch
- Buccal branch
- Marginal mandibular branch
- Cervical branch
what would be the clinical signs of lesions affecting the:
- chorda tympani?
- nerve to stapedius?
- greater petrosal nerve?
chorda tympani:
- reduced salivation
- loss of taste on ipsilateral 2/3 of tongue
nerve to stapedius:
- ipsilateral hyperacusis (hypersensitivity to sound)
greater petrosal nerve:
- ipsilateral reduced lacrimal fluid production
definition of a local anaesthetic?
a drug which REVERSIBLY prevents transmission of the nerve impulse in the region to which it is applied, without affecting conciousness
where do you inject local anaesthetics? (relative to the nerve you want to anethatise)
in the muscle/tissue AROUND the nerve
ie not directly IN to nerve, as risk of permanently damaging it
what is the general mechanism of action of local anaesthetics?
they block SODIUM channels in the nerve cells
- block them from the INSIDE of the cell (so have to get into cell first)
what was the first local anaesthetic?
cocaine
what is the general structure of local anaesthetics?
what are the two main types?
how can you tell the difference between them?
esters/amides with an aromatic ring on one end and an amino group on the other end
- amides
- esters
amides have an ‘i’ in the first part of their name (nb all LAs end in -caine)
- eg lidocaine or bupivacaine
what does pKa mean? (in reference to local anaesthetics)
why is this important?
pKa = the pH at which 50% of local anaesthetic is ionised and 50% is non-ionised
only NON-ionised form can get inside cell (as has to be lipid-soluble to get through membrane) but then only the ionised form can block the Na channel, once inside the nerve
so optimum is 50% of each
so basically the pKa is the optimum pH that any given local anaesthetic works at
- so the closest the pKa of the LA is to the pH of the environment in which it needs to work (eg body = 7.4), the faster the onset
nb not an absiolute science though: clinical onset is not the same for all LAs with the same pKa, but good for a general rule!
why don’t local anesthetics work very well on infected tissue?
because pus (often found in infected tissue) has a lower pH (about 6.8) than normal body tissue and so is further away from the pKa than most LAs (which are made to be close to normal body pH)
what determines the duration of action of local anaesthetics?
protein binding
the more protein binding, the longer the duration
(eg procaine is 6% protein bound and lasts for about 45mins, bupivacaine is 95% protein bound and lasts for about 12 hours)
what does drug potency mean?
what determines the level of potency of a local anaesthetic?
dose required to produce the desired effect (high potency = lowe dose needed)
depends on ‘lipid solubility’
- the more lipid soluble, the higher the potency
what modalities do these nerve fibres conduct:
- A-alpha?
- A-beta?
- A-gamma?
- A-delta?
- B?
- C?
which have the largest diameter?
which have the highest conduction velocity?
A-alpha
- proprioreception
- somatomotor
A-beta
- touch
- pressure
A-gamma
- motor to muscle spindle
A-delta
- pain (esp cold, touch)
B
- preganglionic autonomic
C
- thermal pain
- mechanoreceptor
- post-ganglionic autonomic
A-alpha is fastest and fattest! C is slowest and thinest
- “A is first thing you have to do on ABCDE emergency thing, so thats the fastest”
which nerve fibres are most sensitive to local anaesthetics?
in what order are modalities lost when given local anaesthetics?
the thinest, slowest fibres loose conduction first! - ie C fibres
- cold/warmth
- pain
- touch/deep pressure
- motor function
what drugs are frequently given with local anaesthetics?
why? 4
when are they NOT used together?
vasoconstrictors
- prolong action + early detection of toxicity
- reduce plasma levels (less risk of toxicity)
- ‘greater anaesthesia’ or reduced dose
- reduced post-operative haemmorhage
not used for extremities
- eg fingers, toes, penises, nose, ear
- because risk of body parts falling off!
what vasoconstrictor is commonly used alongside local anesthetics?
- how does it work?
when is this not used?
what is used instead?
adrenaline
- stimulation of alpha adrenoreceptors -> constriction of blood vessels
- however also stimulates cardiac Beta1 receptors
therefore can be contraindicated in people with severe anxiety or certain heart problems
felypressin
- an analogue of vasopressin (aka ADH)
- vasoconstriction, but less effective than adrenaline
- no effect on heart conduction/contraction
describe the two main possible adverse effects of local anaesthetics (not incl LA toxicity)
what LAs do they normally occur with?
hypersensitivity (allergic response)
- skin rash to full anaphylactic shock
- normally to esters (very very rare with amides)
methaemoglobinaemia
- cyanosis, lethargy + resp distress (which does not respond to oxygen)
- prilocaine (an amide)
what are the clinical signs symptoms of local anesthetic toxicity, as it progresses?
- light-headedness
- tinnitus
- lips/tongue numbness
- metallic taste
- visual disturbances
- muscular twitching
- convulsions
- drowsiness
- arrythmias + heart attack
what do you do if you start noticing signs of local anaesthetic toxicity?
when would you give IV lipid emulsion?
- stop injecting the LA
- call for help
- A: maintain airway, secure with tracheal tube if necessary
- B: give 100% oxygen + ensure adequate ventilation
- C: give IV fluids
- D: control seizures (using anti-convulsants)
nb start resus is go into cardiac arrest
give IV lipid emulsion when they start seizing
does adrenaline increase or decrease the safe dose of local anesthetics?
increase
