Leukoencephalopathy
- Broad term for leukodystrophy-like diseases
- Characterized by dysfunction of the white matter of the brain
- Caused by imperfect growth or development of the myelin
sheath
- Made up of at least ten different
chemicals
- Each of the leukodystrophies is the result of a defect in the
gene that controls the production or metabolism of one (and only one) of the component molecules of myelin
- Can refer specifically to any of
these diseases:
Stroke imaging- http://www.radiologyassistant.nl/en/483910a4b6f14
- Do an un-enhanced CT first
- So you don't confuse contrast for blood
- Early CT signs
- Loss of grey/white matter differentiation
- Hyperdense artery
- Due to thrombus
- Some thrombi may look different to others
- Sulcal effacement
- Mass effect
- Can use "stroke window" to enhance grey/white contrast
- Infarct covering >1/3 of the MCA territory are likely to undergo haemorrhagic transformation
T2WI, DWI, ADC- ADC = Apparent Diffusion Coefficient
- In the acute phase T2WI will be normal, but in time the infarcted area will become hyperintense
- The hyperintensity on T2WI reaches its maximum between 7 and 30 days, then fades
- DWI is already positive in the acute phase and then becomes more bright with a maximum at 7 days
- DWI in brain infarction will be positive for approximately for 3
weeks after onset
- In spinal cord infarction DWI is only positive for
one week
- ADC will be of low signal intensity with a maximum at 24 hours
and then will increase in signal intensity and finally becomes bright in
the chronic stage
Caudate nucleusEye movements- Use the patient's words!
- "Jerky vision", not "Oscilloptia"
- Distinguish SYMPTOM from EXAMINATION FINDING
- e.g. Nystagmus => Oscilloptia
- First check HEAD POSTURE
- They'll turn their head to reduce the use of the weak muscle
- But a CN III palsy will cause a complete ptosis so they won't need to :)
- Check smooth horizontal movement first
- 1 m away
- Keep within the binocular field
- Go slow
- Pause at the sides
- Use something coloured
- NB comes from occipital lobe, so you need an object!
- If they have diplopia then the OUTSIDE image is the false one
Cranial nerves
- Bilateral innervation to the forehead is to protect eye closure
- => Best test is to screw the eyes up
- Smiling is a extrapyramidal pathway (emotive)
- => Doesn't accurately test CN function
- Trigeminal nerve => Muscles of mastication
- All have bilateral cortical representation
- Swallowing has bilateral cortical representation
- But takes a few days to kick in e.g. after a stroke
- La-la-la-la-la-la-la-la-la is good to check for a pseudobulbar palsy
- (Results from an UML lesion to the corticobulbar pathways in the pyramidal tract)
- SCREW EYES and PURSE LIPS
- Facial nerve
- Taste in front of tongue (corda tympani)
- Laccrimal ducts (greater superficial petrosal nerve)
- Stapedius muscle
- => Hyperacusis (raised sensitivity to LOUD noise)
- cf stethoscope test
- Bell's phenomenon
- Blink reflex
- Eyelids down, but also eyeball up
- => Can test even with ptosis
- Inspect the tongue AT REST
- As you would for other muscles
- Check movements later
- Check palatal deviation by looking at the median raphe, not the uvula
- Deviation
- Tongue is pushed to the weak side
- Raphe is pulled to the strong side
Notes
- Dehydration is the commonest cause of venous stroke
- Neck pain + Neurological deficit => Carotid dissection
- Bulbar palsy refers to impairment of CN IX, X, XI and XII which occurs due to a lower motor neuron lesion
- Either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem
- DHx: Give dose and WHEN STARTED
- Skin popping => Clostridium botulinum
- Don't forget handedness and job
- 70% of diagnosed TIAs weren't TIAs
- Torticollis
- Stiff neck associated with muscle spasm
- Usually SCM + splenius capitus
- Treat with Botox
- Ophthalmic branch goes all the way up to the ear-to-ear line
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