Neurology 2 Flashcards
(301 cards)
what is the epidemiology of cauda equina syndrome?
- rare, occurring mainly in adults but can occur at any age
- occurs in around 2% of herniated discs
- common cause is lumbar disc herniation at L4/5 and L5/S1
what is the causes/risk factors of cauda equina syndrome?
- herniation of lumbar disc; most commonly at L4/5 and L5/S1
- tumours/metastases
- trauma
- infection
- spondylolisthesis
- post-op haematoma
what is the pathophysiology of cauda equina syndrome?
- nerve root compression caudal to the termination of the spinal cord at L1/2
- usually large central disc herniations at L4/5 or L5/S1 levels
- generally S1-S5 nerve root compression; important in bladder function
what is the clinical presentation of cauda equina syndrome?
- major difference between cauda equina and lesions
higher up in the cord is that leg weakness is flaccid and areflexic (LMN) and not spastic and hyperreflexic - bilateral sciatica
- saddle anaesthesia
- bladder/bowel dysfunction
- erectile dysfunction
- variable leg weakness that is flaccid and areflexic
what is sciatica?
sciatica is pain, numbness and a tingling sensation that
radiates from lower back and travels down one of the legs to the foot and toes
what are differential diagnoses of cauda equina syndrome?
conus medullaris syndrome, vertebral fracture, peripheral neuropathy, mechanical back pain
what is used to diagnose cauda equina syndrome?
- MRI to localise lesion
- knee flexion; test L5-S1
- ankle plantar flexion (downwards); tests S1-S2
- straight leg raising; L5,S1, root problem; people with acute disc can barely get leg off bed
- femoral stretch test; L4 root problem
what is treatment of cauda equina syndrome?
refer to neurosurgeon ASAP to relieve pressure or risk irreversible paralysis/sensory loss/incontinence!:
• microdiscectomy - may tear dura
• epidural steroid injection - more effective for leg pain
• surgical spine fixation if vertebra slipped
• spinal fusion reduces pain from motion and nerve root inflammation
what is multiple sclerosis? what areas of the nervous system does it affect?
- chronic autoimmune, T-cell mediated inflammatory disorder of the CNS in which there are multiple plaques of demyelination within the brain and spinal cord, occurring sporadically over years
- disease of the CNS with oligodendrocytes targeted, affects the white matter of brain
what is the epidemiology of multiple sclerosis?
- begins in early adulthood
- more common in females than males
- presentation is typically between 20-40yrs
- presentation after 60 yrs is rare
- more common in white populations
- more common the further from the equator you go; rare in tropical countries
what are the causes/risk factors of multiple sclerosis?
- not understood
- combination of genetic and environmental factors
- female
- white
- living far from equator e.g. southern and northern hemispheres
what are environmental factors for MS?
- exposure to Epstein-Barr virus (EBV) in childhood may predispose to the later development of MS in a genetically susceptible host
- low levels of sunlight and vitamin D may be a risk factor: early exposure to sunlight/vit D is important and vitamin D status relates to prevention of MS and fewer symptoms and fewer new lesions on MRI in established MS
what is the pathophysiology of MS?
- autoimmune mediated demyelination at multiple CNS sites resulting in discrete plaques of demyelination affecting the white matter
- T cells activate B cells to produce autoantibodies against myelin
- once T lymphocytes cross the blood-brain barrier they can cause a cascade of destruction to the neuronal cells in the brain
- this results in demyelination and conduction disruption along axons
- although the myelin sheath does regenerate, the new myelin is less efficient and is temperature dependant, and when exposed to high heat conduction through new myelin decreases drastically
- plaques of demyelination are perivenular (occur around a vein), occur everywhere in the CNS but have a predilection for distinct CNS sites
- PNS myelinated nerves are not affected since their myelin is Schwann cell based and these Schwann cells are unaffected since their myelin has different antigens to the CNS myelin produced by oligodendrocytes
- repeated demyelination leads to axonal loss and incomplete recovery between attacks
- poor demyelination healing results in relapsing and remitting symptoms
- multiple areas of sclerosis form along neurones which slow/block signal conduction thus impairing movement/sensation
what distinct CNS sites does perivenular demyelination tracts occur at in MS?
- optic nerves
- around ventricles of the brain
- corpus callosum
- brainstem and cerebellar connections
- cervical cord (corticospinal tract and dorsal columns)
what are types of MS?
- relapsing and remitting (80%)
- secondary progressive MS
- primary progressive MS (10%)
what are clinical features of relapsing and remitting MS?
- most common pattern of MS
- symptoms occur in attacks (relapses) with onset over days and typically recovery over weeks
- periods of good health or remission are followed by sudden symptoms or relapses
- patients may accumulate disability over time if they do not recover fully after relapses
what are clinical features of secondary progressive MS?
- follows on from relapsing and remitting MS
- late stage of MS that consists of gradually worsening symptoms with fewer remissions
- 75% of patients with relapsing-remitting MS will eventually evolve into a secondary progressive MS 35yrs after onset
what are clinical features of primary progressive MS?
- gradually worsening disability without relapses or remissions
- typically presents later and is associated with fewer inflammatory changes on MRI
what are the clinical presentations of MS?
- usually presents in young adults 20-40 yrs
- monosymptomatic initially, rarely polysymptomatic
- symptoms may worsen with heat/exercise as new myelin is inefficient and doesn’t perform well in heat (Uhthoff’s phenomenon)
- unilateral optic neuritis
- numbness of tingling in the limbs
- leg weakness
- brainstem demyelination
- cerebellar symptoms, disorders of balance, coordination and speech
- trigeminal neuralgia
- constipation
- spasticity and weakness can result in stiffness/tightness of muscles that can interfere with normal movement, speech and gait
- intention tremor
- bladder dysfunction
- sexual dysfunction
- cognitive decline
- amnesia
what is Uhthoff’s phenomenon?
- symptoms may worsen with heat/exercise as new myelin is inefficient and doesn’t perform well in heat
- occurs in MS
what are features of unilateral optic neuritis in MS?
- pain in one eye on eye movement
* reduced central vision
what are features of brainstem demyelination in MS?
- diplopia, vertigo, facial numbness/weakness, dysarthria or dysphagia
- clumsy/useless hand or limb due to loss of proprioception (often a dorsal column spinal plaque)
what are differential diagnoses of MS?
hereditary spastic paraplegia, cerebral variant of SLE, sarcoidosis or HIV
what is used to diagnose MS?
- diagnosis requires two or more attacks affecting different parts of the CNS; that is 2 CNS lesions disseminated in time and space i.e. cannot diagnose MS after one potential relapse
- exclude differentials with FBC, inflammatory markers, U+E’s, LFT’s, glucose, HIV serology, auto-antibodies, Ca2+ and vitamin B12
- MRI scan brain and cord
- lumbar puncture
- electrophysiology (delayed nerve conduction suggests demyelination)