Functional Localisation Flashcards
CNS lesion inspection
limb posture
CNS lesion tone
increased spasticity (velocity dependent increased tone)/clonus (persistent ankle jerk)
CNS lesion pattern of weakness
Decreased hemisphere: contralateral hemiplegia
Spine: below lever of lesion. pyramidal pattern
CNS lesion reflexes
increased
CNS lesion plantar response
extensor
CNS lesion sensory
hemisphere: hemisensory
spine: below the level of the lesion
PNS lesion inspection
(distal) wasting/ fasciculation (damage to motor nerves)
PNS tone
Decreased
- Excessive flopping of foot in log rolling
- Foot dragging up bed
PNS pattern of weakness
Decreased
Peripheral neuropathy: Distal weakness
Root/ plexus (C5-T1 for upper)/ mononeuropathy: dependent on innervated muscles
PNS reflexes
decreased
PNS plantar response
flexor (if no sensation then there may be a muted response)
PNS sensory
peripheral neuropathy: glove and stocking
root/plexus/mononeuropathy: dependent (root= dermatomal)
NMJ inspection
additional ptosis or ophthalmoplegia
NMJ tone
normal or decreased
NMJ pattern of weakness
normal
fatiguability
NMJ reflexes
normal or decreased (only if long-standing process with wasting and weakness)
NMJ plantar response
flexor
NMJ sensory
none
muscle lesion inspection
proximal wasting
tone inspection
normal or decreased
pattern of weakness muscle
decreased strength
proximal weakness
symmetrical
difficulty rising from chair without using arms
reflexes in muscle pathology
normal or decrease
plantar response in muscle pathology
flexor
sensory in muscle lesion
none
how to examine NMJ
> demonstrate you understand fatiguability
- Fixed horizontal gaze for 20 seconds (looking for start of drooping, particularly on one side, then look to see if one eyelid is lower than other)
- Fixed horizontal gaze for 20 seconds, then report if there is any double vision, both horizontal and vertical, are images getting further apart?
- Sustained counting (dysarthria) West register street, count to 50, repeat west register street
- Shoulder abduction before and after repetitive movements, do 20 movements on one side then test for shoulder abduction again. Is there now weakness on one side?
- Also examine for facial weakness- test CN VII, test for neck weakness
nature of essential tremor
Postural
Generally symmetrical
History of relatively young onset, 50% have FHx of the same.
Should be a response to alcohol.
nature of cerebellar tremor
Action/intention tremor
May be asymmetrical or symmetrical (depending on pathology)
nature of extra-pyramidal tremor
Rest
Asymmetrical
tone in tremor
essential- normal
cerebellar- reduced/normal
extrapyramidal- increased
cerebellar features
DANISH
D ysdiadokinesis A taxia N ystagmus I ntention S lurred speech H eel shin
how to examine for dysdiadokineses
rapid alternating movements- difficulty trying to initiate movements
examination for ataxia
(ask patient to walk, is there a wide based short stepping gait. Are they able to heel toe walk?)
how to examine for nystagmus
just test horizontal movements, follow finger.
Might be physiological nystagmus at extremes of gaze but should be symmetrical.
Look for saccadic eye movements- look ahead eye movements, look quickly from fist to palm- looking for jerkiness and an intention tremor of eyes
how to test for intention tremor
finger nose testing
examination in resting tremor
- Bradykinesia- one side and then the other. Pincer grasp in air, 20 times.
- Rigidity- Supinator pronator movements. If not certain use synkinesis- movement of another body part. Tap with one hand while testing tone on other side. Cogwheeling.
- Tremor- rest hands down on knees, is there a pill rolling tremor. If they are suppressing it, get them to count backwards.
- Postural instability- shuffling gait, bit of difficulty turning, reduced arm swing.
Test of retropulsion, stand with back to couch- sit, stand up and then give them a pull backwards.
where does VZV lie
sensory ganglion
what does HSV cause
viral encephalitis (temporal lobe)
what does polio affect
anterior horn cell
what can measles cause
subacute sclerosing panencephalitis
what does JC virus cause
pml
what is bright in T1 sequence
fat
what is bright in T2 sequence
demyelination and CSF
common presentations of MS
optic neuritis
transverse myelitis
treatment of MS
acute: steroids
long-term; immunomodulatory treatments (copaxone/IFN/tysabri)
subdural haematoma
crescent moon shape, might cross midline.
Venous haemorrhage. Most common mechanism- trauma.
May be insidious, worsening headache
extradural haematoma
lens shape, arterial bleed.
Mechanism: trauma or after surgery.
Acute presentation: skull fracture and altered mental status.
subarachnoid haemorrhage
subarachnoid space, anywhere where there is CSF there is blood.
Predominately arterial.
Acute onset worst headache of life.
Spontaneous ruptures of peri-aneyurysms around circle of willis. Can be traumatic.
intraparenchymal haemorrhage
blood within the hemispheres themselves.
Mechanism: high blood pressure, AV malformation, tumour.
Arterial or venous.
Acute sudden onset nausea, vomiting
monroe kellie hypothesis
CPP= MAP- ICP
cushings reflex
- Raised ICP= low cerebral blood flow, cerebral ischaemia, acidosis
- Sympathetic response= vasoconstriction, raised MAP to increase CPP
- Baroreceptors in the neck lead to reflex bradycardia
- HIGH BP and BRADYCARDIA= cushings reflex
