Laz neuro Flashcards
What four lobes is the brain composed of? Draw diagram and label
Frontal lobe (anteriorly)
Parietal lobe (between frontal and occip)
Occipital lobe (posteriorly)
Temporal lobe ( lateral)
Where is the primary motor cortex?
in the posterior aspect of the frontal lobe
Where is the primary somatosensory cortex=
In the anterior aspect of the parietal lobe (so right behind the primary motor cortex)
Where is the primary visual cortex?
right at the BACK = posterior aspect of occipital lobe
How are visual signals transmitted to the primary visual cortex
from retinal to LGN
LGN to primary visual cortex
where is the LGN located
in the temporal lobe
Where is Broca’s area located and what is it responsible for?
Located in Frontal lobe (anterior to 1’ motor cortex)
PRODUCTION of speech (b-b-broca)
Where is Wernicke’s area located and what is it responsible for?
Located in Temporal Lobe
responsible for understanding of speech
What are the three key arteries to the brain
anterior cerebral
middle cerebral
posterior cerebraL
What artery supplies the anterior and miiddle cerebral arteries?
the internal carotid
what artery supplies the posterior cerebral?
the vertebral artery
What area does the anterior cerebral artery vascularise in the brain?
Frontal lobe (medially region)
Parietal lobe (anterior)
What sx does a ischaemia in anterior cerebral artery territory cause?
change in behaviour
weakness in LEGS > ARMS (remember homunculus is upside down)
mild sensory defect
What region does the Middle CA supply
some frontal, parietal and temporal lobe
What sx does ischaemia in middle cerebral artery territory cause?
Weakness in FACE > ARMS > LEGS
Hemisensory defect
Homonymous hemianopia (as it includes LGN / some of the optic tract in the temporal lobe
What sx does ischaemia in posterior cerebral artery territory cause?
VISUAL (as it affects the visual cortex)
- homonymous hemianopiaa
- visual agnosia
- prosopagnosia
what is the difference between ascending and descendiing pathways in the spinal cord?
ascending pathways: carry SENSORY inputs from skin etc to brain
descending pathway: carry MOTOR inputs from brain to muscle
How is white and grey matter distributed in SC, and how does this compare to the brain?
grey matter = centre of SC = bodies of neurons
white matter = periphery of SC = neuronal tracts
what are the sensory pathways in the SC
dorsal column (posterior)
spinocerebellar tract (lateral)
spinothalamic tract (anterior)
what sensory function does the dorsal column carry?
FINE TOUCH, PROPRIOCEPTION, VIBRATION (ascending, aka transmits to the brain)
what is the pathway of the dorsal column?
first order neuron: sensory receptor to medulla
second order: medulla to thalamus
third order: thalamus to priumary somatosensory cortex
where does the dorsal column decussate?=
at the level of the MEDULLA
what sensory function does the SPINOTHALAMIC TRACT carry?
pain and temperature
what s the pathway of the spinothalamic tract=
first order neuron: nociceptor to substantia gelatiinosa (in SC grey matter)
second order: substantia gelatinosa to thalamus)
third order: thalamus to primary somatosensory cortex
where does the spinothalamic tract decussate
at the substantia gelatinosa, at the LEVEL OF ENTRY INTO SC
what does the corticospinal tract carry?
MOTOR info from brain to muscle
outline the corticospinal tract pathway
primary motor cortex > (UMN) > anterior horn > (LMN) >muscle
where does UMN and LMN cross ovr
at the anterior horn
what else must you do for ischaemiic stroke management once pt has recieved CT head, aspirin +/- thrombolysis?
Investigate for CAUSE of STROKE
- AF: ECG
- structural heart disease: echo
- carotid atherosclerosis: carotid doppler
why must you always suspend anticoagulants once you start stroke pt on aspirin?
because of high risk of haemorrhagic transformation (i.e. bleeding into the space where ischaemia had occurred)
risk is highest in the first 2 weeks after stroke
after which you may consider restarting or starting the anticoags
What are the three meningeal layers in the brain?
dura
arachnoid
pia
where does an extradural haemorrhage occur
between the skull and the dura
what is the most common cause of an extradural haemorrhage
rupture of the Middle meningeal artery (which is superficial)
usually due to trauma > skull fracture
what are sx of an extradural haemorrhage
transient LOC > lucid interval> gradual headache, eventual reduction in consciousness
how does an extradural haemorrhage appear on CT
pear shaped (biconvex, lens shaped), does NOT cross suture lines (which connect dura to skull)
where does a subdural haemorrhage occur
between dura and arachnoid
what is cause of subdural haemorrhage
tearing of the bridging VEINS
(occasionally precipitated by mild trauma)
most common in elderly and alcoholics, who have brain atrophy > greater tension on the bridging veins
what are the two different types of subdural haemorrhage, what are the differences in their causes and what do they look like on CT
acute vs chronic
acute: often precipitated by mild trauma, white crescent (banana) shaped blood
chronic: black bleed on CT very extensive
CROSS SUTURE LINES
What are the two key causes of a subarachnoid haemorrhage
aneurysm rupture
severe trauma
symptoms of subaarachnoid
sudden onset worse headache ever
may have meningeal irritation (photophobia, neck stiffness)
how does a subarachnoid appear on CT
white blood along sulci and fissures
what is parkinson’s disease
neurodegenerative disease of dopaminergic neurons in the substantia nigra
What are the two tract categories in the motor system (from thhe primary motor cortex) and what are their function
PYRAMIDS > corticobulbar / corticospinal (VOLUNTARY MOVEMENT)
EXTRAPYRAMIDAL > basal ganglia, cereellum, vestibulart nucleus and substantia nigrqa (INVOLUNTARY; regulates movement and SMOOTHNESS)
what are the four core symptoms of PD
Bradykinesia
Rigidity
Resting tremor (4-6hz, usually asymmetrical)
Postural instability
what are the core symptoms of PD due to
malfunction of the extrapyramidal tract
what is the aim of PD medication
to increase dopamine within the substantia nigra
what is the mainstay of PD treatment and why is it DUAL
L-DOPA + peripheral DOPA-decarboxylase inhibitor
e.g. co-careldopa, co-demeldopa
needed because L-DOPA alone is converted by peripheral dopa-decarboxylase into dopamine, which cannot cross the BBB and instead triggers the CTZ to cause N&V
by giving an inhibitor you stop this enzyme’s function
so L-DOPA crosses into the brain
And in the brain is coverted to dopamine by dopa-decarboxylase
what is another type of treatment for PD and how does it work
Dopamine agonist e.g. ropinirole, pramipexole
stimulates dopamine receptors and can cross the BBB
what characterises progression of alzheimers
PROGRESSIVE decline in cognitive function
give all the types of dementia
alzheimers (most common)
vascular
lewy body
frontotemporal
depressive pseudodementia
explain key fts of vascular dementia
STEPWISE DECLINE in cognitive function
background of vascular disease
explain key fts of lewy body dementia
TRIAD of
- dementia
- hallucinations
- parkinsonism
explain key fts of frontotemporal dementia
personality change, early onset
what is epilepsy
recurrent unprovoked seizures (2 or more, or 1 + epileptogenic markers)
what management is used for epliepsy
valproate for all types
except:
- absence seizures = valproate or ethosuximide
- focal seizures: lamotrigine
DO NOT give valproate in women of childbearing age. Give:
- lamotrigine (tonic clonic/absence)
- levetiracetam (tonic, atonic, myoclonic)
UMN signs
spasticity
hyperreflexia
upgoing plantars
LMN signs
hypotonia
hyporeflexia
fasciculations
muscle wasting
What does a brainstem lesion present as in terms of MOTOR deficit?
Weakness in limbs CONTRALATERALLY
Weakness in face IPSILATERAL
How do you differentiate between motor lesion in brain vs spinal cord?
SC: likely bilateral
Brain: likely unilat
which types of dementia have parkinsonism
Lewy body
Frontotemporal
explain frontotemporal dementia
Parkinsonism
Behavioural change s
Self neglect and abandonment of habits
what is hydrocephalus
accumulation of CSF within ventricular system
types of hydrocephalys
OBSTRUCTIVE (non communicating)
COmmunicating (normal pressure hydrocheph)
causes of obstructive hydroceph
tumour
aqueduct stenosis
causes of non-obstructive hydroceph / Normal presssure hydrocephalus
impaired CSF reabsorption in subarachnoid villi
e.g. meningitis
triad NPH
DUG
dementia
urinary incontinence
gait disturbance
ix hydroceph
CT head
LP (also curative in NPH)
what are bulbar signs
LMN signs of CN 9-12
impaired speech and swlalowing!!
what is the progression of ALS
bulba rsigns > spastic weakness, paralysis > resp failure
which functions are spared in ALS
oculomotor, sensory, autonomic functions! think hawking
whhat is the mode of inheritance of neurofibromatosis
AUTOSSOMAL DOMINANT
