12.10.24 Teaching notes

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:

  • Progressive multifocal leukoencephalopathy

  • Toxic leukoencephalopathy

  • Leukoencephalopathy with vanishing white matter

  • Leukoencephalopathy with neuroaxonal spheroids

  • Reversible posterior leukoencephalopathy syndrome

  • Megalencephalic leukoencephalopathy with subcortical cysts

  • Hypertensive leukoencephalopathy

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 nucleus

Eye 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!

      • Can't do it voluntarily

  • 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

    • Esp. in kids

  • Neck pain + Neurological deficit => Carotid dissection

    • Esp. if young

  • 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