π’ Mini Neuro Tweetorial #1
π§ Cortex (Grey cells/axons. Processes. Coms to/from other neurones. Some Higher functions are lateralised).
π§ LT cortex dom in RT hander
π§ LT cortex dom in 50% LT handers
What happens if cortical destructive lesion bullet/tumour/bleed/infarct ??
R cortical π§ damage causes a clinical subset of 4 things.
πL Sided Weakness FACE|ARM|TRUNK|LEG ALL same side
πL Hemisensory reduction/Loss
πL Homonymous Hemianopia (No vision to LT. Pt looks RT)
πRight Higher function loss: Extinction/Anosognosia
L cortical π§ damage causes a clinical subset of
πR Sided Weakness FACE|ARM|TRUNK|LEG all same side
πR Hemisensory reduction/Loss
πR Homonymous Hemianopia (No vision to RT. Pt looks LT)
πLeft Higher function loss: Language(Dysphasia)
Subcortical π§ Damage (Nuclei and Myelinated axons)
πContralateral sensory/motor/ataxia
πNo Higher functional loss or hemianopia.
πUsually due to white matter pathologies
Brainstem: Midbrain Pons Medulla MPM
MIDBRAIN
πV shaped MR/CT. Limbs of V cerebral peduncles which hold C/spinal fibres.
πSubstantia nigra and red nucleus [Think Colors !].
π3rd/EW nucleus and below this 4th CN.
π3rd exits ant btwn V limbs.
π4th exits pstrly to C/L SO.
Lesion in Midbrain: subset of
π Ipsilateral III and C/L hemiparesis (Weber syn)
π Ipsilateral rubral tremor
π Ipsilateral IV
Pons: looks swollen on CT/MR as axons++ to and from cerebellum traverse. A bridge "pons" over CSF in IVth ventricles behind. Separates it from cerebellum behind. Contains
π Corticospinal fibres
π CN 5,6,7,8. 6/7 lie close
π Axons to/from cerebellum
π Sensory fibres
π MLF
A lesion will cause a subset of
π Contralateral Hemiparesis arm/leg/trunk
π Ipsilateral 5/6/7/8 nerve lesion - especially ipsilateral facial weakness and LR palsy
π Internuclear ophthalmoplegia
π Ipsilateral cerebellar symp/signs
Medulla
Small oval. Corticospinal fibres cross anteriorly. CN 9,10,11,12. Symp trct. Nclus ambig. sensory fibres
Classic Lat med PICA occlusion. Get DWI
π Vertigo Hiccups, Dysphagia, Dysarthria
π I/L Horner's syn
π Ataxia
π Pain altered I/L face
π Loss pain/temp C/L arm/leg
Basically for Brainstem remember its basically
Cranial nerve palsy + C/L weakness so neuro on both sides. This was all done at one sitting without books so basically a brain dump so please forgive any omissions but generally hope its ok. I will do more later.
WRT Cortex the simple concept point I neglected to state is that the right brain receives sensory input (touch/vision) from left side of your world and outputs all motor to the left side of your world and vice versa.
Mini Neuro Tweetorial #2 : Cord and Cauda
Spinal Cord
π Starts at Foramen magnum.
π Ends at lower edge of L1 vertebra
π So can LP below L1.
π Whole cord C8/T12/L5/S5/C1 31 nerves.
π 7 Cervical vert but 8 nerves. C1 goes over the top.
π Cord much shorter than the canal.
π Cord has corticospinal tract (CST)
π CST is Upper motor neuron (UMN).
π CST Synapses at anterior horn cell to form
π Motor Roots which are Lower motor neuron (LMN)
π These exit cord anterior. Forms root.
π Exits canal at foramina
π In cord we correlate clinical findings primarily with dermatomal and myotomal level. Secondarily with side.
πWe need to know our myotomal /dermatomal landmarks
π Highest dermatome ? C2 back of head
π Lowest dermatome ? S5 Perianal
NHS management 101
If u are not complaining then u are overstaffed. You will lose assets
If you are complaining then you are at peak efficiency and assets sweated
If u r complaining + metrics worsening + adverse event. you might need help but first will be told to get a move on
contd:
If there are patients in corridors during surge then you have enough beds. Ride it out
If there are never patients in corridors during surge then you have too many beds
If there are patients in corridors frequently then sweat your discharge process. Might need more beds.
The weakness is that over staffed departments with staff learned in the art of complaining don't get touched as too much work to analyse the metrics and redeploy assets. Managers only around for 1-2 years so pass the parcel.