Revision course Flashcards
UMN vs LMN
UMN- to anterior horn cell—Tone up, Power down, Reflex brisk/up
LMN-from anterior horn cell onwards-Power down, decreased tone, reflex down, fasciculation, wasting
Sensory pathways
Spinothatlamic tract-pain and temp-crosses at points it exits
Other tract- cross at the medulla higher up- vibration and proprioception, pin prick
Spinal cord stops at L1/2—after that its all LMN
Stroke, tia and blood supply
TIA- sx of stroke <24h-can be 15mins
Stroke -rapid onset of local neurology- due to ischemia or heamorrgahe
Blood-ACA, MCA, PCA, and posterior- Basilar, communicating,
Anterior- ACA/MCA- hemiparesis, cortical signs (aphasia, apaxia, visual field)-face arm and leg
Posterior-diplopia, dizziness, nausea, dysphagia — CROSSED findings (face vs limbs)
Neuro homonculus- Foot->legs-> arms-> hand-> face->tongue
Tongue on the side- and more MCA
Feet in central-more of a ACA
Neuro homonculus
Neuro homonculus- Foot->legs-> arms-> hand-> face->tongue
Tongue on the side- and more MCA
Feet in central-more of a ACA
Homonymous hemianopia pathways
Contralateral damage of the occipital region- as it crosses over at the chiasm-
STROKE SIGN
occipital stroke eye changes
If you have an occipital stroke– lose CONTRALATERAL homonymous hemianopia-can see one side (same side in both eyes)
unlike- before chiasm- eye issue
chiasm- bitemporal hemianopia
issues in the tracts to the occipital lobe-quadrianopia (TEMPORAL- SUperior, Parietal->inferior
in PACES- just want to tell- nerve, chiasm or after
Best management of stroke
acute-
CT HEAD AND CONTACT STROKE team
thrombolysis (4.5h) and throbectomy (6h)+ Aspirin 300mg
long term
Clopidogrel is the best anticoagulant to use–
but it depends on causes (if AF-DOAC/APIXABAN, carotid stenosis (>70% w/ SX), etc)
also need to image the carotids-doppler or CT- and consider removing w/ endartrectomy
COnsider other RF- HTN, Diabetes-and treat
causes are important- cause thats how you treat (CHAD-VASC2 is important to know clopido vs DOAC)
dissections, GCA, Heamatological disorders (Sickle Cell, LPS)
Cerebellar stoke
Ataxia, nystagmus (fast phasing beat towards issue)
intetion tremor on same side
Unsteady gait
Dysdidokinesia
Speech changes
Hypotonia
DANISH
IPSILATERAL
Brainstem stroke
Crossed findings-posterior circulation
Cranial nerves and Limb nerves dont cross in same area-
Contralateral limbs, ipsilateral face (fully)
+ dizzyness, nausea,
Brainstem stroke
Crossed findings-posterior circulation
Cranial nerves and Limb nerves dont cross in same area-
Contralateral limbs, ipsilateral face (fully)
with crossed signs- usually numbness this time (face ipsi, limbs contralateral)
Vertebral artery dissections
important cause of young people stroke–
its lateral medullary syndrome/PICA-vertebral arteries issues-
crossed SENSORY signs- face and limbs paresthesia
+ vertigo+ataxia (very posterior)
Horners syndrome can present
What is horners, causes
Ptosis, meisosis, anhidrosis, enopthalmos
blockage of sympathetic chain-
starts in brainstem- why can happen in PICA
Pass via carotid-carotid dissection
Pass via lung- pancost tumour, 1st rib
SAH ix
Can present with only headache and no neuro
CT head is the start- but not always as it can not show up 98% if done within 12h– see bright areas (bleeding).but after a week 50% sensitive
2nd- LUMBAR puncture for blood degradation products-xanthochromia-best within 12h-2w is very reliable
need to cover from light!
also do other LP measurments as usual
SAH ix
Can present with only headache and no neuro
CT head is the start- but not always as it can not show up 9– see bright areas (bleeding)
2nd- LUMBAR puncture for blood degradation products-best within 12h-1w
Status epilepticus
5mins seize or 2 without recovery
O2, ressus, protect airway, glucose, bloods, pabrinex if alcohol
IV acesss-> IV lorazepam 2 doses
PR diazepam/buccal midazolam also
-> phenytoin/levitaceram/sodium valporate if not recovering
-> if not ITU and General anesthetic
Seizure definition and presentations
discharge of electrical activity-
generalised or focal
epilepsy is just the tendency to have seizures- 2> with 24h different
children–
absence/atonic- childhood seizures (need specific EEG changes)
Juvenile - Myoclonic- Jerks
Generalised-
Tonic clonic
Focal- one limb, area-jacksonian march
either simple (no loss of awareness)
or complex (with loss of awareness)
usually last a few seconds, and has a drowsy period afterwards (post ictal), and pre-ictal + period they dont remeber
eyewitness is most crucial
biting tongue, pee, smacking limb
Epilepsy Ix and Mx
Eye witness always
MRI, EEG, ECG
mx-
safety- no baths, no driving (Contact DVLA->2 seizures=cant drive until 1y seizure free. Only 1 seizure- 6m no drive. Provoked seizure- case by case)
start management if no visible cause
generalised- sodium valp male, Lamotrigine female
Focal- lamotrigine
Chord compression sx, ix and mx
Bilateral leg weakness and pain
upgoing plantars, brisk reflex
Numbness in legs up (progressess up as compression is left)
Urinary incontinence, bowel
-> UMN signs tell you the block is higher and need MRI whole spine-crucial
assox with cancer,
NO CAUDA EQUINA— thats LMN (and would be lumbar MRI-probs MRI whole spine)
Ix- MRI WHOLE SPINE -usually above the sensory level
Mx- immediate neurosurgery refer and
Spinal hemicord syndrome sx
Brown sequard sequence
Half the cord is lost-so lose only some tracts
Paralysis (motor) and Loss of vibration/proprioception (dorsal tract) on one side
loss of pain and temp on other side (spinothalamic)
Motor Neuron disease sx and ix, mx
PURE motor weakness-anterior horn cell issue
with UMN and LMN signs (usually UMN but with fasciculations)
usually 60y/o
ALS is most common (70%)-month to years
Bulbar Palsy (20%)-dysarthria/phagia-limbs later
ix- muscle conduction is usually best
can do MRI brain for ddx (Spondylitic neck, Syringomeglia)
mx-v little
rulazole maybe helps a few months
and supportive- like NG/Peg tube, NIVentilation
GBS sx, ix, mx
GBS- post viral illness-fully LMN
Weakness and paresthesia, Distal>proximal, usually legs>arms
Gloves n stock distribution
down reflexes, down plantars,
fasciculation and wasting
can get ANS issues
rare millerfischer variant-eye, ataxia, no limbs
ix-other neuropathy causes-
Bloods
LP– high protein is GBS. WCC raised-> not GBS
Mx-IVIG/Plasma exchange are usually reserved for later/motor sx- will resolve on their own
support- cardiac monitor for dysarrythmia
DVT prophylaxis
Spirometry measure
rarely MRI- if not clear
Neuropathies
Pure sensory- diabetes, alcohol, b12/folate, cancer medication, cancer
Pure Motor- GBS, lead, Porypheria
also mono vs poly
mono- carpal tunnel
Poly-acute or chronic
acute- axonal, demyelinating
Chronic-axonal, demyelinating
axonal- decreased amplitude but speed fine
demyelinating- speed slower but amplitude fine
Myasthenia gravis
AID in NMJ
fatiguability weakness
especially dysarhtria, ptosis, diplopia, opthalmoplegia
triggered via infections/drugs (bblocks)
assox with THymoma
ix- clincal hx and exams
AChR Ab are 80% +ve
Nerve conduction study will say in NMJ
Tensilon test
Ice test-put ice on the ptosis- improve
Mx- Pysostigmine
acute-plasma exchange/ivIG
longterm- steroids, other immunosupressants (azathioprine etc)
check for Thymoma
Parkinsons Sx, Ix and Mx
Resting tremor, bradykinesia, Postural instability, Rigidity,
hypomemisaia
Parkisonian gait/shuffling gait
then later ANS (hypotense, urinary)
can be caused by parkisons (asymetric), PSP (symetrical and falls early), MSA (ANS features first Hypotense, Urinary)
other than parkinsons-poor response to levodopa
Drug- symetrical
ix- response to levodopa
DAT-scan (normal in drugs, abnormal in park +)
Mx- Levodopa
Younger-dopamine agonist -Ropiridole
SE
issue with impulse control (more dopamine agonist)
confusion, hypotension
Nausea and vomiting (settles in weeks)
drowsy
long term- dyskinesia, hallucinations, psychosis)
MS sx,ix,mx
AID -> central demyelination, brain/cord
focal neurology isolated in time and space- >2 events
Optical neuritis very common start
Bladder incontinence, numbness etc
Ix-MRI with contrast-show lesions all around
Bloods,LP-oligoband only in CNS for mimics
NEW -McDonald criteria- need to exclude ddx to diagnose MS-based on the 2 attacks differentiated in time/space OR imaging /LP (w/ 1 sx attack)-> earlier diagnoses
Mx-
relapse-check for infections, if none->Steroids to lower length (not improve MS)
DMARD-dymethyl fumarate, interferon, Fingolimod
Stem cell transplant
MS ddx
bilateral Optic neuritis-neuromyelitic spectrum disorder
Neurosarcoidosis
Acute disseminated encephelomyelitis (post infection neuro lesions)
What is Rapid afferent peripheral d
