Neuro Other Flashcards
Most common neuromuscular junction disorder
Myasthenia gravis
TIA definition
a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, WITHOUT ACUTE INFARCTION (ie no signs of infarction on imaging)
Driving rules for seizures and epilepsy
1st seizure: car license- no driving for 6 months, hgv license- no driving for 5 years
Epilepsy: no car driving for 1 yr since last event- iff eeg/mri abnormal. if eeg/mri normal- no driving for 6 months
, HGV- 10 years seizure free off all anticonvulsants b4 u drive
What pill should u not use with anti-convulsants
Progesterone only pill
Be careful with contraception in general as anti-convulsants can reduce efficacy of contraceptives
Status epilepsy mx (prehospital and hospital)
Stabilise patient
prehospital- PR diazepam/ buccal midazolam
hospital: IV lorazepam, repeat once after 5-10 minutes
if ongoing, start: leviratcetam/phenytoin/sodium valporate
when should a seizure be treated as status epilepticus
seizure lasting longer than 5 minutes
or
>=2 seizures within a 5-minute period without the patient returning to normal
What level does the spinal cord end
L1/L2
management of status epilepticus if no response within 45 minutes from onset
general anaesthesia or phenobarbital (acts on GABA A receptors and increase synaptic inhibition)
What is the dorsal column for and where does it cross the midline
where does the 1,2nd &3rd order neuron synapse
aka-fasiculous cutaneous and fasiculus gracilis
(ascending) Fine touch, vibration and propioception
Crosses midline at medulla
1st order- synapses at medulla and crosses to contralteral side
2nd order- synapses in thalamus
3rd order- travels to in somatosensory cortex (post central gyrus)
(3 neurons, 2 synapses)
What is the lateral spinothalamic tract for
When does it cross the midline
ascending, Temperature and pain
Crosses at the spinal cord segment
1st order neuron synapses at posterior horn then moves to contralteral side and up sinal cord
2nd order neuron synapses at the thalamus
3rd order neuron travels to post central gyrus
(3 cells, 2 synapses)
Descending pathways split into
Pyramidal: Cortiocspinal tract and corticobulbar spinal tract
Extrapyrimidal: rubrospinal, vestibulospinal, reticulospinal, tectospinal
what is the function of the ventral spinothalamic tract
(ascending) crude touch and deep pressure
(crude- non discriminative)
Cortico spinal tract
where is decussation
function
Voluntary movement of contralateral side of TRUNK and LIMBS
Splits into anterior (15%) and lateral (85%)
Lateral tract decussate at midline of pyramids
Anterior (aka ventral) decussate at the spinal level they innervate.
Where is the motor centre in brain
Pre-central gyrus
Where is the sensory centre in the brain
Post-central gyrus
brocas: where and function
frontal lobe on side of dominant hemisphere
speech production
wernickes: where and function
dominant hemisphere , superior temporal gyrus
comprehension, understanding of langauge
Give two examples of drugs that block N type calcium channels
pregabalin and gabapentin
give two examples of epilepsy drugs block sodium channels
lamotrigine and carbamezapine
give one example of a drug that enhances GABA synthesis
sodium valproate
give one example of a drug that targets gaba receptors
benzodiazepines
what is the basic function of the GABA system
reduces neuronal excitability
Focal seizures: frontal lobe seizure signs/symptoms
limb jerking
(frontal lobe contains motor cortex )
focal seizures: temporal lobe signs/symptoms
aura: epigastric sensation/ deja vu/ hallucinations (auditory, olfactory etc) and ORAL autoamtisms eg lip smacking
focal seizures: parietal lobe signs/symptoms
parasthesia
focal seizures: occipital lobe signs/symptoms
floaters/flashers
meningitis vs encephalitis symptoms
- note: meningitis affects meninge layers and encephalitis affects the acc brain therefore encephalitis has more brain related symptoms whilst meningitis is more general
meningitis : neck stiffness, seizure, skin rash
encephalitis: blurred vision, slurred speech, confusion, paralysis, SEIZURES
both: fever
hyperdense vs hypodense haematoma
hyper: bright in colour on scan: acute
hypo: dark n scan: chronic
common causes of injury for extradural, subdural and subarachnoid haemorrhage
extradural- head injury (often pterion), v acute and painful, ruptures middle meningeal artery
subdural- chronic or acute- RFs: anti-coagulants, OLD AGE + low impact trauma, alcoholism,
subarachnoid: most spontaneous cases caused by ruptured berry aneurysm in circle of willis, or severe trauma
subdural haemorrhage symptoms
subdural: tends to be more chronic. gradually increasing headache and confusion.
assoc.with alcoholics
subarachnoid haemorrhage sx
Sudden onset Thunderclap headache. Seizures, neurological deficits, loss of consciousness and death may rapidly ensue.
vomit soon after headache
meningism- neck stiffness, positive kernigs sign
mechanism of action of triptans
act on serotonin receptors (5HT) to induce vasocnstriction which eases the symptomes of migraines
headache symptoms: migraine
(8)
recurrent, severe, unilateral, throbbing pain
assoc.- nausea, aura, photosensitivity, periods
headache symptoms: tension headache
recurrent, non disabling, bilateral, ‘tight band’
headache symptoms:
cluster headache
(include time frame) (6)
duration 15 mins- 2 hrs, intense pain around 1 eye, restless during attack, eyes: redness, lacrimation, lid swelling
frontotemporal dementia vs huntingtons disease
both: personality change, disinhibition, impulsiveness
difference: huntingtons causes motor disturbance. f.t dementia does not
lewy bodies dementia symptoms
fluctuating consciousness, hallucinations & sleep disorders.
cerebrospinal fluid composition when there is a bacterial infection vs viral
glucose low in bacterial (bacteria eat glucose for energy)
glucose high in viral
3rd nerve palsy symptoms
down and out, dilated pupil
what is the most common form of brain tumour
metatastic cancer (most commonly from lung)
most common primary tumour in adults
- appearance on imaging?
gliobastoma multiforme- poor prognosis
- imaging: solid tumour w/ central necrosis & rim that enhances with contrast. assoc. vasogenic oedema
2nd most common primary brain tumour in adults
-histology
meningioma- benign
- histology- spindle cells in concentric whorls and calcified psammoma bodies
The most common primary brain tumour in children
- histology
- pilocytic astocytoma
- rosenthal fibres (corkscrew eosinphillic bundle)
pathophysiological hallmarks of alzheimers disease
loss of cortical neurons
Tau neurofibillary tangles-
senile plaques- amyloid b
what part of the brain affected in alzheimers disease
widespread cerebral atrophy, particularly involving the cerebral cortex (grey matter) and hippocampus
gyri narrow, sulci widen, ventricles appear larger
huntingtons disease genetics:
(5)
autosomal dominant
trinucleotide repeat expansion of CAG-increasesd glutamate
anticipation may be seen
results in degeneration of cholinergic and GABAnergic neurons in the striatum of basal ganglia
due to defect in huntingtin gene on chromosome 4
huntingtons symptoms
chorea - abnormal involuntary movement disorder
personality changes- irritability, apathy, depression and intellectual impairment
dystonia- abnormal muscle tone- muscle spasm/abnormal posture
saccadic eye movements-
multiple system atrophy vs supranuclear palsy vs parkinsons
all have parkinsonism
differentiating features:
MLA- autonomic disturbance. eg. postural hypotension, erectile dysfunction
SNP: impairment of vertical gaze
main exitatory neuron
glutamate
main inhibitory neruon
gaba
simultaneous inhibitory signal and excitatory signal result
redueced EPSP (reduced excitatory signal)
what do nocioreceptors sense
painful stimuli
what is adaptation regarding neurotransmission
the decrease in action potential frequency with sustained stimulius
most common cell in the nervous system
astrocyte
upper motor neurone lesion
1. muscle wasting?
2. fasiculations?
3. tone
4. weakness or paralysis
5. tendon jerk reflex
6. babinski response
- yes but to a lesser extent than LMN lesion
- no
- spastic
- yes- inefficient recruitment of alpha motor neuones
- hyperflexia
- positive (abnormal toe extension)
Lower motor neurone lesion
1. muscle wasting?
2. fasiculations?
3. tone
4. weakness or paralysis
5. tendon jerk reflex
6. babinski response
- yes
- yes
- flaccid
- yes- loss n muscle bulk
- reduced or absent
- negative- normal toe flexion
describe parkinsons tremor
reduced on action (resting tremor), unilateral
amytrophic lateral sclerosis vs primary lateral sclerosis
ALS has both UMN and LMN signs
ALS assoc with frontotemporal dementia and thenar atrophy
Primary lateral sclerosis- only UMN signs
pogressive bulbar palsy vs progressive pseudobulbar palsy
Progressive Bulbar and pseudobulbar palsy are caused by damage to cranial
nerves 9,10 and 12 and presents with dysphagia.
Bulbar palsy is due to LMN (to nerves 9,10,12) = reduced
jaw and gag reflexes and tongue fasciculations,
but pseudobulbar palsy is UMN lesion to CN 9,10,12=
causes slow speech and brisk jaw reflexes
what are the bulbar nerves
nerves exiting the medulla oblongata (bulb is the archaic term for medulla)
cranial nerves
IX- glosspharyngeal
X- vagus
XI- accessory
XII - hypoglossal
what are the symptoms of juvenile myoclonic epilepsy
infrequent generalized seizures, often in morning//following sleep deprivation
daytime absences
sudden, shock-like myoclonic seizure (these may develop before seizures)
what nerve innervates anterior 2 thirds of tongue
facial
what nerve innervates posterior third of tongue
glossopharyngeal nerve
TIA driving rules-
no driving until symptom free 1 month- no need to inform DVLA
myoclonic seizure vs tonic clonic
myoclonic is less severe- short jerky movements
tonic clonic- whole body involved. sometimes loww os urinary control etc.
where are post synaptic neurons found parasympathetic
within parasympathetic ganglia which lie near/within target organs
(pregnanglionic cells long/post ganglionic cells short)
what is an ataxic gait
A wide-based gait with loss of heel to toe walking
typically occurs following cerebral injury
finger nose ataxi- where is the lesion
cerebllar hemisphere
gait ataxia (without finger nose ataxia)- where is the lesion
cerbelllar vermis
