Neuro Flashcards
Frontal lobe function (5)
- regulate and initiate motor function
- language
- cognitive functions
- attention
- memory
Parietal lobe function (3)
- sensation – touch, pain
- sensory aspects of language
- spatial orientation and self perception
Occipital lobe function (1)
process visual info
Temporal lobe function (3)
- process auditory info
- emotions
- memories
limbic lobe parts (4)
amygdala, hippocampus, cingulate gyrus, mamillary body
limbic lobe functions (5)
- learning
- memories
- reward
- emotion
- motivation
Which are white matter tracts (3)
- Association fibres
- Commissural fibres
- Projection fibres
which association fibres connect which lobes (4 pairs)
- superior longitudinal fasciculus (frontal nad occipital)
- arcuate fasciculus (frontal and temporal)
- Inferior longitudinal fasciculus (temporal and occipital)
- Uncinate fasciculus (anterior frontal and temporal)
characteristics of localisation of function in primary cortices
- function predictable
- organised topographically
- left right symmetry
function of primary motor cortex
- controls fine, discrete precise voluntary movements
- provide descending signals to execute movements
function of premotor area
planning movements (externally cued)
function of supplementary area
planning complex movements (internally cued)
function of primary somatosensory area
process somatic sensations from receptors in body (eg fine touch, vibration, proprioception, 2-point discrimination, pain, temp)
function of somatosensory assocation
interpret significance of sensory info
difference between broca’s area and wernicke’s area
Broca: speak, production of language
wernicke’s understanding of language
what happens to frontal lobe lesions
change in personality and inappropriate behavior
what happens to parietal lobe lesions (eg right hemisphere lesion)
contralateral neglect
lack of awareness of self on left side
lack of awareness of left side of extrapersonal space
what happens to temporal lobe lesions
agnosia (inability to recognise), anterogade amnesia (cannot form new memories)
what happens to broca’s and wernicke’s area lesions
broca: expressive aphasia (poor production of speech)
wernicke’s: comprehensive aphasia (poor comprehension of speech, production is fine)
what happens to primary visual cortex lesion
blindness in corresponding part of visual field
what happens to visual association lesion
deficits in interpretation of visual info
prosopagnosia (inability to recognise familiar or learn new faces
what are some scans to assess cortical function
PET (positron emission tomography)
fMRI
EEG (electroencephalography)
MEG (magnetoencephalography)
TMS (transcranial magnetic stimulation)
tDCS (transcrania direct current stimulation)
what are some scans to assess structures
DTI (Diffusion tensor imaging) –> based on diffusion of water molecules
what is MS
autoimmune
loss of myelin from neurons of CNS
main symptoms of MS (5)
blurred vision
fatigue
difficulty walking
numbness and tingling
muscle stiffness
what are the blood supplies to brain
carotid artery and vertebral
artery
what are types of haemorrhage (4)
epidural, subdural, subarachnoid, intracerebral
what is extradural haemorrhage
trauma caused
immediate clinical effects (arterial, high pressure)
what is subdural haemorrhage
trauma caused
delayed presentation of clinical effects (venous, low pressure)
what is subarachnoid haemorrhage
ruptured anneurysm
what is intracererbral haemorrhage
spontaneous hypertensive
risk factors of stroke
age
hypertension
DM
smoking
cardiac disease
what are the cerebral artery perfusion for cerebrum
anterior, middle, posterior cerebral artery
what are anterior cerebral artery symptoms lesion
paralysis of contralateral structures (leg > arm) , loss of appropriate social behavior, disturbance of intellect, executive function &w judgement
what is middle cerebral artery symptoms lesion
classic stroke
contralateral hemiplegia (arm > leg)
contralateral hemisensory deficits
hemianopia
aphasia
what is posterior cerebral artery symptoms lesion
visual deficits (homonymous hemianopia, visual agnosia)
what are the 2 major descending tracts
pyramidal(pass thru pyramids of medulla) and extrapyramidal (dont pass thru pyramids of medulla)
what are the 2 pyramidal tract pathway
corticospinal
corticobulbar
what are the 4 extrapyramidal tract pathway
tectospinal
vestibulospinal
rubrospinal
reticulospinal
function of pyramidal tracts
voluntary movements of body and face
where nerve pass from in pyramidal tracts
motor cortex to spinal cord or cranial nerve nuclei in brainstem
function of extrapyramidal tracts
involuntary movements for balance and posture and locomotion
where nerve pass from in extrapyramidal tracts
brainstem nuclei to spinal cord
function of primary motor cortex
controls fine, discrete voluntary movements
provide descending signals to execute movements
function of premotor area
plan movements
regulate externally cued movements
function of supplementary area
plan complex movements (internally cued, speech)
function of vestibulospinal
stabilise head during body &head movements
coordinate head movements with eye movemetns
mediate postural adjustments
function of tectospinal
orientation of head and neck during eye movements
from superior colliculus of midbrain
function of reticulospinal
from medulla n pons
change in muscle tone asociated with voluntary ovement
postural ability
upper motor neuron lesion negative signs (3)
loss of voluntary motor function
paresis (graded weakness of movements)
paralysis (complete loss of voluntary muscle activity)
upper motor neuron lesion positive signs (5)
increased abnormal motor function due to loss of inhibitory descending inputs
spasticity (increase muscle tone)
hyper-reflexia (exaggerated reflexes)
clonus (abnormal oscillatory muscle contraction)
babinski’s sign (abrnomal response in foot)
lower motor neuron lesion signs (6)
weakness
hypotonia
hyporeflexia
muscle atrophy
fasciculations (visible twitch)
fibrillations (twitching of individual muslce fibres, recorded in needle EMG)
what is motor neuron disease (MND)
neurodegenerative disorder of motor system
MND Upper Motor Neuron signs
spasticity (increased tone of limbs and tongue)
babinski’s sign
brisk limbs and jaw reflexes
loss of dexterity
dysarthria(difficulty speaking)
dysphagia (difficulty swallowing)`
MND lower motor neuron signs
weakness
muscle wasting
tongue fasciulations and wasting
nasal speech
dysphagias
structure of basal ganglia
caudate nucleus
lentiform nucleus (lentiform +caudate = putamen)
caudate +putamen = striatum
substantia nigra (midbrain)
function of basal ganglia
decision to move
perform associated movements (change facial expression)
perform movements in order
suppress unwanted movements
signs of parkinson’s disease
bradykinesia
hypomimic face
akinesia
rigidity
tremor at rest
what is parkinson’s disease
degeneration of dopaminergic neurons that originate in substantia nigra and project to striatum
what is huntington’s disease
degeneration of GABAergic neuron in striatium, caudate and then putamens
signs of huntington’s
choreic movements
rapid jerky involuntary mvoements (hand–> face –> legs –> rest of body)
speech impairment
difficulty swallowig
dementia
cognitive decline
unsteady gait
what is ballism
from stroke affecting subthalamic nucelus
uncontrolled flinging
contralaterally
what is cerebellum separated from cerebrum by
tentorium cerebelli
signs of cerebella dysfunction
ataxia (impairment in movement coordination and accuracy)
dysmetria (inappropriate force and distance for target directed movement)
intention tremor
dysdiadochokinesian (inability to preform rapidly alternating movements)
scanning speech (staccato)
what is alpha motor neuron
LMN of brainstem and spinal cord
innervate extrafusal muscle fibres of skeletal muscles
activate muscle contraction
what are the 3 types of motor unit
S, type l
FR, type llA
FF, type llB
how do we regulate muscle force
recruitment and rate coding
motor unit type switching
llB to llA after training
l to ll in severe deconditioning or spinal cord injury
loss of l and ll but preferentially ll in ageing
what stimulates involuntary coordinated pattern
peripheral stimuli
example of descending control of reflexes
jendrassik manoeuvre
which dominates normal condition, inhibitory or excitatory control
inhibitory
which dominates decrebration condition, inhibitory or excitatory control
excitatory from suprasinal areas
what is order of descending control of reflexes
activate alpha motor neurons
activate inhibitory interneurons
activate propriospinal neurons
activate gamma motor neurons
activate terminals of afferent fibres
what motor neuron is hyper reflexia associated with
UMN lesion
what is clonus (abnormal, hyper reflexia) associated with
UMN lesion
involuntary and rhythmic muscle contractions
loss of descending inhibition
what is babinski’s sign associated with
UMN lesion
big toe curl upwards in adults when sole stimulated with blunt instrument (normally curl downwards) –> positive babinski’s sign
what is hypo-reflexia associated with
LMN disease
examples of primary headache
migraine
tension-type headache
cluster headache
what are secondary headache
spercipitated by other condition (eg tumor)
which is more long lasting – tension type or cluster headache
tension type , migraine
they can last long but usualy shorter (30mins-1hr)
which is more short lasting – tension type or cluster headache
cluster headche
but usually longer (45mins -3hrs)
key red flags of secondary headache
age, onset, systemic symptoms, neurological signs
migraine characteristics
unilateral
pulsating quality
moderate or severe pain intensity
aggravation by routine physical activity
last hrs or some days
does migraine associate with aura
can be with or without aura
symptoms associated with migraine
nausea and / or vomiting
photophobia and or phonophobia
what is visual aura in migraine
complex array of symptoms reflecting focal cortical or brainstem dysfunction
how long is the graded evolution of visual aura
5-20 mins (< 1hr)
describe aura in migraine
expanding C
elemental visual disturbance
4 phases of migraine
premonitory
aura
headache
recovery
acute treatment for migraine
paracetamol
NSAIDS
prokinetics
triptans
long term preventives of migraine
TCA (tricyclic antidepressants)
B-blockers
serotonin antagonists
ACEi
calcium channel blockers
anticonvulsants
is tension type headache episodic
yes
how will patients describe tension type headache
tight muscles ard head and neck
characteristics of tension type headache
bilateral
mild or moderate pain
not aggravated by any movements
no added features (eg N+V, photophobia phonophobia)
treatments for tension type headache
simple analgesics (paracetamol, aspirin)
characteristics of cluster type headache
unilateral pain
at least one of the following ipsilateraly (conjnctival redness, lacrimation, nasal congestion and/or hinorrhoea, forehead and facial sweating, miosis, ptosis, restlessness or agitation, not associated with brain lesion on MRI)
acute treatment for cluster headache
triptan (nasal or subcutaneous)
high flow O2
preventive management for cluster headache
verapamil (calcium channel blcokers)
what is the difference between vestibular and hearing organ
vestibular: capture low frequency (movement)
hearing: capture high frequency (sound)
what is the function of outer ear
capture sound and focus it to tympanic membrane
amplify upper range of speech frequencies by resonance in canal
protect ear from external threats
function of middle ear
mechanical amplification
what is the hearing part of inner ear
cochlea
function of cochlea
transduce vibration into nerve impulses
captures the frequency and intensity of sound
cochlea contain which 3 compartments
- scala vestibuli
- scala media
- scala tympanic
function of scala vestibuli and scala tympanic
bone structure
contain perilymph
high in sodium
function of scala media
membranous structure
contains endolymph
high in potassium
location of Organ of Corti
where does organ of corti lie on
basilar membrane
how is basilar membrane arranged
tonotopically, same principle of xylophone
which 2 hair cells do organ of corti contain
inner hair cells (IHC)
outer hair cells (OHC)
what is above the hair cells
tectorial membrane
function of inner hair cells
carry 95% of affernet info of auditory nerve
transduction of sound into nerve impulse
function of outer hair cells
carry 95% of efferent info of auditory nerve
modulate sensitivity of response
name of hairs of hair cell
stereocilia
longest cilia name
kinocilium
what happens when deflection of stereocilia towards kinocilium
opens K+ channels
depolarise the cell releasing NT to afferent nerve which then depolarises
how does stereocilia deflection change according to amplitudes
higher amptitudes, cause greater deflection of stereocilia and K+channel opening
describe the auditory pathway
- spinal ganglions via CN8 (vestibulo-cochlear nerve) travels to ipsilateral cochlear nuclei in brainstem (pons)
- auditory info crosses at superior olivary complex , after that all connections are bilateral
- signals then travel to lateral lemnisicus, then to the inferior colliculus, then to the medial geniculate body at thalamus
- lastly to the auditory cortex
what are the types of hearing loss (3)
- conductive hearing loss: problem in outer or middle ear
- sensorineural hearing loss: problem at cochlear (hearing organ) or auditory nerve (nerve) (90% of hearing loss)
- central hearing loss: problem at brain and brainstem (v. rare)
conductive hearing loss causes
outer ear: wax, foreign body
middle ear: otitis (inflammation, build up of fluid behind eardrum)
sensorineural hearing loss causes
cochlear: noise, presbycusis (age related), ototoxicity (drugs, chemotherapy)
auditory nerve: acoustic neuroma
clinical assessments for hearing loss
weber test, rinne test, tuning fork
what are otoacoustic emissions (OAEs)
normal cochlea produces low intensity sounds called (OAEs), these sound are produced by OHCs as they expand and contract
performed in newborn hearing screening and hearing loss monitoring
where is the vestibular organ
in inner ear, contain hair cells for hearing and balance
what are vestibular organs (4)
utricule, saccule, semicircular canals, cochlea
what joims the utricule and saccule
conduit, saccule also joined to cochlea
what are otolith organs
utricle and saccule
where are utricle and saccule
on maculae, placed horizontally in utricle and vertically in saccule
what are maculae
contain hair cells, a gelatinous matrix , with otoliths on top
which otolith for which movement
utricule –> horizontal
saccule–> vertical
what are functions of otholiths
they are carbonate crystals, help with deflection of hairs
where are hair cells in canals located in
crista on ampulla
what do the rest of the canal has
endolymph (high in potassium)
what are hair cells surrounded by
cupula, which helps hair cell movement
describe hair cells potentials
resting potential: basal discharge to nerve
depolarisation: move towards kinocilium
hyperpolarization: move away kinocilium , reduction in nerve discharge
what are vestibular reflexes(2)
vestibulo-ocular reflex (VOR)
vestibulo-spinal reflec (VSR)
what is vestibulo ocular reflex
keep images fixed in retina
connection between vestibular nuceli and oculomotor nuclei
eye movement in opposite direction to head movement but same velocity and amplitude
how do we categorise vestibular disorders
timing
laterality
in vestibular disorder, what complaints are in acute and unilateral
imbalance, dizziness, vertigo, nausea
in vestibular disorder, what complaints are in slow, unilateral or any bilateral loss
imbalance and nausea, BUT no vertigo
where are the problems for peripheral vestibular disorders
vestibular organ or CN VIII
BPPV (bnenign paroxysmal positional vertigo)
vestibular neuritis
where are the problems for central vestibular disorders
CNS (brainstem or cerebellum)
stroke, MS, tumors
core exams for vestibular disorders
eyes, ears, legs
red flags for vestibular disorders
headache, gait problems, hearing loss, prolonged symptoms,hyper-acute onset
timings for balance disorders:
vestibular neuritis and stroke?
acute
timings for balance disorders:
BPPV
intermittent
timings for balance disorders:
migraine, meniere’s disease
recurrent
timings for balance disorders:
schwannoma vestibular, degenerative conditions (MS)
progressive
what is HINTS exams for acute dizziness
Head Impulse test Nystagmus Test of Skew deviation
what is BPPV
peripheral disorder
otoliths (crystals) from utricle detach from maculae and float around semi-circular canals
induce bigger endolymph flow when head moves
what happens in alzheimers MRI
slightly large ventricle
narrowed gyri
widened sulci
atrophy
hippocampal atrophy (shrinkagemof hippocampus with space taken by CSF)
what is lewy bodies dementia
caused by aggregation of alpha synuclein
lead to lewy bodies deposition and internal symptoms
presentation of lew bodies dementia
preserved hippocampus volume
medial temporal lobe lower volume
reduced availability of dopamine transporter in caudate and putamen
presentation of AD
hippocampus atrophy
medial temporal lobe atrophy
what is meningitis and cause of it
inflammation of meninges caused by viral or bacterial infection
what is encephalitis and cause of it
inflammation of brain caused by infection or autoimmune mechanisms
what is cerebral vasculitis
inflammation of blood vessel walls
functions of BBB
solutes that can exchange across peripheral capillaries cannot cross BBB
allows BBB to control the exchange of these substances using specific membrane transporters in and out of CNS
reduce entry of infectious agents into CNS tissue
what happens in BBB disruption (4steps)
- endothelial layer disruption, BBB gets compromised (eg stroke / physical trauma)
- blood component leas into brain including fibrinogen
- astrocytes react to fibrinogen leakage, withdraw astrocyte end feet from vessel walls, compromising BBB
- compromising BB leads to build up of collagen in basement membrane which narrows vessel walls leading to small vessel diseases
symptoms of encephalitis
- initially flu like symptoms (eg high temp and headache)
- then, confusion, disorientation, seizures, change in personality and behavior, weakness, loss of movement, speaking difficulty, loss of consciousness
encephalitis causes
viral infection (Herpes Simplex, Measles, varicella, rubella)
mosquito, tick, insect bites, bacterial and fungi infection, trauma, autoimmune
encephalitis treatment
antivirals (acyclovir)
steroids
antibiotics/antifungi
ventilation
analgesics
anti-convulsants
what is the cellular pathology of MS (4 steps)
inflammation
demyelination
axonal loss
neurodegeneration
what are some bacterial causes of meningitis
meningococcal
pneumococcal
haemophilus influenzae type B (Hib)
Streptococcal (esp in new borns)
what is myelitis
infection of spinal cord
what is encephalomyelitis
when both brain and spinal cord are involved in infection
hallmarks of encephalitis
fever
seizures
behvaioural changes
confusion and disorientation
hallmarks of meningitis
sudden fever
severe headache
n+v
double vision
drowsiness
sensitivity to bright light
stiff neck
rash
what are tests to diagnose meningitis / encephalitis
neurological exam
CT, MRI
lumbar puncture (CSF usually clear & colorless, low glucose in bacterial meningitis, increase WBC =infection)
blood and urine tests
what are common treatments for meningitis and encephalitis
AB, antivirals, corticosteroids, immune suppressors
what are the 3 layers of coat of eye
sclera – hard and opaque
choroid – pigmented and vascular
retina – neurosensory tissue
what is characteristic of sclera
white of eye
high water content
protective outer coat layer
what is uvea
vascular coat of eyeball
where is uvea located
between sclera and retina
what does uvea consist of (3 parts from front to bk)
iris
ciliary body
choroid
(intimately connected and a disease of one part can affect the other portions but not necessarily the same degree)
function of retina
capture light rays that enter eyes
these light impulses are then sent to brain for processing via optic nerve
what does optic nerve connect to
connects to back of eye near the macula
what is the visible portion of optic nerve
optic disc
where is macula located
centre of retina, temporal to optic nerve
what is macula responsible for
detailed central vision eg reading
where is fovea
centre of macula (for detail central vision, contains only cones) so for sharper visions
what is blind spot
where the optic nerve meets retina and no light sensitive cells
which part has the highest cone photoreceptors
fovea
what is central vision responsible for
detail day vision
color vision
reading
facial regonsition
how to assess central vision
visual acuity assessment
what is peripheral vision responsible for
shape
movement
night vision
navigation vision
how to assess peripheral vision
visual field assessment
what happens when there is loss of visual field
unable to navigate in environment
pt need white stick
how many layers for retina
3
outer, middle, inner
function of retina outer layer
contains photoreceptors (1st order neuron)
for light detection
function of retina middle layer
bpolar cells (2nd order neuron)
for local signal processing to improve contrast sensitivity
function of retina inner layer
retinal ganglion cells (3rd order neuron)
for transmission of signal from eye to brain
2 main classes of photoreceptors
rods and cones
compare rods and cone photoreceptors
rod: x100 more sensitive to light , slow response to light , responsible for night vision , more rods than cones
cone: less sensitive to light, faster response, resposnsible for day light, fine vision and color vision
what lens in convex lens
converging lens
what lens in concave lens
diverging lens
what is emmetropia
perfect vision, parallel light rays fall on retina
what is ametropia
msimatch between axial length anad refractive power
parallel light rays don’t fall on retina
what is near sightedness
myopia
what is far sightedness
hyperopia
what is myopia
parallel rays converge at a focal point anterior to retina
vision: not clear, genetic factor
need concave lens
causes of myopia
excessive long globe (long eye)
lens thinner in middle and thicker at edges
excessive refractive power
symptoms of myopia
blurred distance vision
headache
squint to try to improve vision
what is hyperopia
parallel rays converge at a focal point posterior to retina
need convex lens
causes of hyperopia
excessive short globe
insufficient refractive power
symptoms of hyperopia
visual acuity at near tends to blur relatively early
eyepain
headache in frontal region
burning sensation in eye
what is presbyopia
loss of accommodation for near objects naturally
start at 40yo
corrected b reading glasses to increase refractive power
what is near response triad
adaptations for near vision
steps for near response triad
pupillary miosis (reduce size of pupil) to increase depth of field (done by sphincter pupillae) thickening of lens
convergence to align both eyes towards near object (medial recti from both eyes)
accommodation to increase refractive power of lens for near vision (contraction of circular ciliary muscle)
visual pathway from eye to visual cortex
eye
optic nerve
optic chiasm
optic tract
lateral geniculate nucelus
optic radiation
primary visual cortex / Striate cortex
visual pathway of retina
first order neurons (rod and cone)
second order neurons( retinal bipolar cells)
third order neurons (retinal ganglion cells)
optic nerve (CN ll)
partial decussation at optic chiasm
optic tract
lateral geniculate nucleus in thalamus
how many ganglion fibres cross at optic chiasm
53%
what happens to crossed fibres at optic chiasm and where do they originate
originate from nasal retina
responsible for temporal visual field
what happens to uncrossed fibres at optic chiasm and where do they originate
originate from temporal retina
responsible nasal visual field
what happens to lesions anterior to optic chiasm
affect visual field in one eye only
what happens to lesions posterior to optic chiasm
affect visual field in both eyes
what happens to lesions at optic chiasm
damages crossed ganglion fibres from nasal retina in both eyes
bitemporal hemianopia (temporal field deficit in both eyes)
what happens to lesions posterior to optic chiasm
right side lesion– left homonymous hemianopia in both eyes
left side lesion – right homonymous hemianopia in both eyes
main cause of bitemporal hemianopia
pituitary gland tumor enlargemen
main cause of homonymous hemianopia
stroke
what is homonymous hemianopia with macular sparing
damage to primary visual cortex
often due to stroke
what happens to pupil in light
pupil constriction
increase depth of field
mediated by PNS in CN lll
cause circular muscle to contract
what happens to pupil in dark
pupil dilation
mediated by SNS
cause radial muscle contract
what is direct pupillary reflex
constriction of pupil of light stimulated eye
what is consensual pupillary reflex
constrcition of pupil of other eye
what is neurological basis of pupillary reflex
afferent pathway on either side alone will stimulate efferent pathway on both sides
what are afferent pathway of eye
sends messages from the pupil to the brain along the optic nerve to the optic tracts
what are efferent pathway of eye
sends the message back from the brain to the pupil via nerves, resulting in pupil constriction and dilation
what happens to right afferent defect
no pupil constriction in both eyes when right eye stimulated with light
normal constriction in both eyes when left eye stimulated with light
what happens to right efferent defect
pupil constriction
no right pupil constriction when right or left eye stimulated with light
left pupil constricts whether right or left eye stimulated with light
function of superior rectus
move eye up
CN lll
function of inferior rectus
move eye down
CN lll
function of lateral rectus
move eye towards outside (abduct)
CN Vl
function of medial rectus
move eye towards nose (adduction)
CN lll
function of superior oblique
move eye down and out in a diagonal pattern
CN lV
function of inferior oblique
move eye up and out in diagonal pattern
CN lll