Summary MRCP Neurology related diseases

Basics
 Spinal cord
o Pain, temperature, crude touch (MIDDLE OF SPINAL CORD/MIDDLE OF COLUMN)
 Located in centre of spinal column
 Decussate/cross-over as soon as they enter spinal cord
 Disease of spinal cord affects CONTRALATERAL side
o Fine touch, vibratory sense, position (POSTERIOR COLUMN)
 Located in posterior spinal column
 Decussate at brain stem (medulla)
 Disease of spinal cord affects IPSILATERAL sidem
 Upper Motor Neurons (ANTERIOR AND ANTEROLATERAL COLUMN)
o Run down the corticospinal tracts
 80% decussate at the medulla and travel down ANTEROLATERAL COLUMN
 10% DO NOT decussate and travel down ANTEROLATERAL COLUMN
 10% travel down ANTERIOR COLUMN and decussate at the level they exit
o These tracts are found anteriorly and laterally
o Upper motor neuron signs (AKA pyramidal signs)
 Hyper-reflexia
 Hypertonia
 Babinski+
 Weakness
o Example  In Brown-Sequard Syndrome (spinal cord hemisection at particular spinal level)
 Lose CONTRALATERAL pain + temperature
 Lose IPSILATERAL fine touch, vibratory sense, position/proprioception
 Attain IPSILATERAL UMN signs (mainly)
 Lower Motor Neurons
o Connect UMNs to an effector (e.g. muscle)
o Types
 Alpha LMNs
 Innervate EXTRAFUSAL muscles  MUSCLE CONTRACTION; high in number
 Gamma LMNs
 Innervate INTRAFUSAL muscles  PROPRIOCEPTION; low in number
o LMN signs
 Hypo-reflexia
 Hypotonia
 Fasiculations
 Weakness
 Peripheral Nerves
o Motor  LMNs
o Sensory
 Aδ  Fast pain
 To mechanical or thermal stimuli
 Well localised; sharp
 C Fiber  Slow pain
 To chemical stimulation
 Poorly localised; throbbing/aching
o Autonomic  E.g. Bladder dysfunction, sexual dysfunction, constipation, abnormal BP/heartrate

 Pyramidal tracts  Consists of corticospinal tracts (bodily motor function) + corticobulbar tracts (motor
supply to cranial nerves)
 Extrapyramidal Sx (Bas Gang)  Akinesia (can’t initiate movement), Akathisia (can’t remain motionless)

,Neurological Investigations
 EEG

 NCS  For peripheral nervous system lesions
o Radiculopathy/proximal nerve lesions  Slow F-response
o Demyelination  Reduced conduction velocity, sometimes conduction block
o Axonal neuropathy  Reduced compound muscle action potential amplitude

 EMG

 Lumbar Puncture

 CT

 MRI  For CNS lesions
o Background:
 All human cells contain protons
 When protons placed in magnetic field, protons align
 After magnetic alignment, radiofrequency pulses produced to excite proton
 When radiofrequency stops, protons relax and release energy which can be transduced
onto MRI machine, and then translated to images

o Types: Relaxation times for protons vary, hence two image times are taken (T1 + T2)
 T1: Water is black  Ideal for defining NORMAL anatomy
 T2: Water is white (Water white 2 – WW2)  Ideal for defining ANY pathology where
tissue oedema is present (which is most things! E.g. stroke, inflammation, etc)

 Diffusion MRI: Measures diffusion of water into tissues allowing for detection of areas
where water diffusion is restricted (e.g. to study areas of demyelination [MS] + stroke)

 Diffusion-weighted Images: Like Diffusion MRI – best at looking at areas where
water movement has become restricted (e.g. best for acute stroke ONLY – can
see ischaemia within minutes of occurrence)

 Fluid Attenuated Inversion Recovery (FLAIR):
 Basically a T2 image that allows attenuation of fluid (e.g. CSF) so other images
around fluid can be visualised easier
o E.g. MS – ideal to attenuate CSF in ventricles to see periventricular
white matter lesions
 Picking the “inversion” time corrects allows one to attenuate any fluid to see
structures around fluid clearer
 The best image to look for quick pathology

 MRA or MRV: Look for abnormalities in arteries or veins (e.g. stenosis, aneurysm,
vertebral body dissection, [renal artery stenosis])

 Functional MRI: Visualisation of neural activity by detecting increased blood flow

o Contrast: Often Gadolinium (do NOT use if eGFR <30  systemic nephrogenic fibrosis)

,Spinal Cord
 Emergency intervention necessary when BACK PAIN present – RED FLAGS:
o Previous diagnosis of cancer  KPBLT (kidney, prostate, breast, lung, thyroid; multip myeloma)
 Metastatic disease causing spinal cord compression through direct compression OR
vertebral collapse
 First presentation of cancer in 20% of metastatic spinal cord compression (MSCC)

o Associated fever (e.g. osteomyelitis or abscess causing compression)

o Neurology:
 Bowel/bladder dysfunction (LATE features; bladder may be incont or retention!)
 Must do PR on these patients to assess anal tone
 Sexual dysfunction
 Focal neurology
 Lhermitte’s sign  Flexion of neck causes electric shock down spine + into limbs
 UMN signs in lower limbs (hypertonia, hyper-reflexia, +Babinski, weakness, clonus)
 LMN signs in upper limbs (hypotonia, hyporeflexia, fasciculations, weakness, atrophy)

Spinal cord compression  Emergency

o Symptoms (sensory and motor symptoms ALL can be present as per spinal tracts)
Low back pain  Sciatica  Cauda equina (spectrum)
 Tenderness on the spine  *MOST IMPORTANT SIGN FOR COMPRESSION
 Often cervical or thoracic
 Progressively worsening
 Aggravated by straining (e.g. passing stool, coughing)
 Nocturnal pain common

 Band-like back pain around abdomen typical of spinal cord compression  SENSORY
LEVEL where below this level sensation is lost
 Contralateral pain and temperature loss
 Ipsilateral vibration and position loss

 Upper motor neuron signs expected below the level of compression
 Hyperreflexia  no inhibition of reflexes from above
 Increased tone  no inhibition of tone from above
 Babinski sign+  upgoing plantar on brushing sole of foot (lateral  superior
 medial)
 Lower extremity weakness  motor neuron compression

 NB: Cervical lesions = quadriplegia, Thoracic lesions = hemiplegia

 Red Flags  As above

, o Causes
(NB: all causes may lead to a vascular/chemical process which produces oedema and subsequent
secondary spinal cord injury [hence use of Dexamethasone])

 Herniated/slipped disc (e.g. sciatica)
 Types:
o Non-central  Unilateral sciatica-type symptoms
o Cental  Spinal column involvement (cauda equina)

 Risk: High BMI, heavy lifting
 Bone disorders (e.g. osteoporosis [compression fracture], spinal stenosis [NEVER acute,
always chronic], Paget’s dis of bone)
 Spinal stenosis  SLR negative, better by leaning forward + rest
 Sciatic  SLR positive, not better by leaning forward

 Secondary malignancy (e.g. kidney, prostate, breast, lung, thyroid)
 Primary malignancy (e.g. myeloma)

 Inflammation (e.g. seronegative arthropathies e.g. AS)
 Infection (e.g. TB/Pott’s, epidural abscess, epidural haematoma, RA atlanto-axial)

o Management  Intervention FIRST then diagnosis AFTER (as more time is more morbidity)

 Treatment – ABCDE first (many patient come after severe trauma; immobilise C-spine)
 Dexamethasone  INITIAL treatment to reduce swelling/inflammation

 Radiotherapy  if from metastatic disease

 Surgical decompression  if from an abscess, haematoma, herniated disc

 Other  Catheter (urinary retention), VTE prophylaxis,

 Diagnosis
 X-ray/CT  X-ray 80% sensitivity so FIRST test; but CT done first some places
o 3 views  AP, lateral, odontoid
o Unconscious patient  CT brain + entire spinal cord

 Whole Spine MRI (if MRI CI’d, CT can be done)  Conduct in <24hr
o Lesions ABOVE L1 = Spinal cord compression
o Lesions BELOW L1 = Cauda equina syndrome

 Biopsy (to discover if metastatic disease)  necessary for radiotherapy
o Most accurate test

o DDx: Cauda equine syndrome due to above causes, Conus medularis syndrome, mechanical back
pain w/ prolapsed disc