UMN + LMN Flashcards
What part of the nervous system does UMN and LMN affect?
UMN= CNS i.e. efferents with cell bodies in higher centres LMN= PNS i.e. efferents with cell bodies in spinal motor nucleus or CN motor nucleus
What are the causes of UMN lesions?
Stroke
Traumatic brain injury
Spinal cord injury
Multiple sclerosis
What is the reasoning behind UMN signs?
UMN normally act as inhibitors of primitive LMN actions
== loss of UMN means signs related to excessive LMN activity
What are the signs associated with UMN lesions?
Rigidity and hypertonia= LMN constantly activated w/o inhibition
Hyperflexia= hyper-sensitised reflexes i.e. increased activity of gamma-MN means there’s increased tension in intrafusal fibres which means they are more sensitive for detecting changes in muscle length
Minimal atrophy= no loss of neurotrophic factors
Absent fasciculations
Hemiparesis (one side)
Paraparesis (LL)
+ve Babinski reflex= plantar extension rather than flexion in response to stroking of sole of foot i.e. due to CST lesion meaning loss of excitation of distal flexors so extensors dominate
Clonus= involuntary rhythmic muscle contractions
Chorea= uncoordinated and involuntary movements
What is spastic paraparesis? What are examples of conditions that can cause it?
Bilateral UMN signs associated with legs
Causes:
- MS i.e. MS plaques on the brain
- cervical myelopathy i.e. narrowing of spinal column
- malignancy
- MND i.e. can present with mixed UMN + LMN signs
- syringomyelia i.e. out pouch of fluid compressing SC
- vit B12 deficiency
- HIV myelopathy
What are the most common causes of peripheral nerve damage/LMN damage?
Diabetes Alcoholic peripheral neuropathy B12 deficiency Drugs Guillain-Barré syndrome
What are the common signs associate with LMN lesion?
Flaccid/weakness
Atonia= loss of alpha-MN means loss of mechanism to stimulate extrafusal fibres= decreased tone
Areflexia = loss reflex arc due to loss of myotactic stretch efferent
Atrophy= loss of neurotrophic factors
Fasciculations= spontaneous firing of alpha-MN
Sensory disturbances= peripheral spinal nerves are mixed nerves meaning that some sensory function also likely to be lost
How can you differentiate between Bell’s palsy and complete CNVII palsy? What is the pathology causing each of these?
Bell’s = NOT forehead sparing due to loss of bilateral innervation of forehead as LMN contain contributions from both sides of cortex
Stroke= loss of unilateral UMN so the contralateral muscles of facial expression lost but part of bilateral innervation of frontalis remains to enable wrinkling of forehead
What are the different parts of the PNS which can be involved in LMN lesion?
NMJ
Anterior horn
Nerve root
Plexus
Nerve
Muscle
What sign indicates anterior horn cell problems and what condition is it a red flag sign for?
Wide spread fasciculations
MND= fasciculations in context of UMN signs is a red flag for MND i.e. anterior horn junction affected meaning MND has mixed presentation of signs
What is radiculopathy and what is the most common radiculopathy? How is it differentiated from single nerve damage?
Symptoms associated with nerve root damage
Sciatica i.e. unilateral pain, pins + needles and numbness in LL
effects a larger somatic and muscular distribution than single nerve
What causes Guillain-Barré syndrome and how would someone suffering present?
AI condition post-bacterial/viral infection where cross-sensitivity of infection leads to degeneration of axons in peripheral nerves
-ascending condition= distal to proximal
Would present with finger dysesthesia and proximal leg weakness 2-4 weeks post-infection
What are the 3 most common causes of NMJ disorders? Briefly describe their pathology.
Myasthenia gravis
-auto-antibodies attack AchR= decreased firing due to decreased receptors on post-synaptic membrane
Lambert-Eaton syndrome
-auto-antibodies targeting pre-synaptic calcium channels causing decreased Ach release from pre-synaptic neurones
Botulism
-decreased Ach release from pre-synaptic terminals
What are the characteristic symptoms of NJM disorder? What is the key difference with Lambert-Eaton syndrome that can act as differential?
Proximal symptoms
-weakness in shoulder and thighs
-numbness and tingling
-difficulty walking due to proximal leg weakness
Fatigable= increased weakness with use due to using up Ach
Muscle loss i.e. disuse or because of de-innervation
Muscle weakness decreases with use due to Ach build up in NJM to enable momentary increase in strength
What are indicators that deficits in function is due to a muscular problem? What causes muscular problems?
Proximal weakness i.e. shoulder or hip = feel HEAVY
No sensory impairment
Cuase:
- inflammation i.e. dermatitis or polymotic
- hypothyroidism
- flu
- drugs