wk 2- neuro Flashcards
issues of neuropathy (sensory/motor)
loss of sensation
- repetitive trauma
-unaware of injuries
- loss of proprioceptive feedback - impacting muscle tone and posture, gait and foot structure
motor deficits
- reduce muscle tone, strength
- gait changes / loading issues
diagnostic approach
- locate lesion
- find pathophysiology causing lesion
nervous system made up of what systems
- CNS: brain and spinal cord
- PNS: Afferent (sensory), efferent (motor)
- somatic: voluntary nervous system
- autonomic nervous system: involuntary (regulates bodies organs
what controls movements and what makes up the motor pathway
motor cortex which involves upper and lower motor neurons when descending down the body
what controls regulatory actions
basal ganglia and cerebellum
the motor cortex controls what?
the contralateral side of the body
Upper motor neuron tracts where
cerebral cortex to anterior/ventral horn (spinal cord)
lower motor neuron tracts where
anterior/ventral horn (spinal cord) to peripheral nerve that synapses at neuromuscular junction
symptoms of an UMN lesion
- increased tone
- hyper reflexia
- babinski sign present
- no muscle twitching/spasicity
occurs when theres a lesion above anterior/ventral horn
examples of UMN lesion pathology
stroke
cerebral palsy
multiple sclerosis
symptoms of LMN lesion
-decreased tone
-hypo reflexia / absent
- no babinski sign
- muscle twitching/spasicity
exmaples of LMN lesion pathology
poliomyelitis
nerve entrapment
sensory pathways
3 main pathways
- Dorsal column-medial leminscal pathway: fine touch and vibration, crosses over in the
brainstem - Spinothalamic pathway: coarse touch & pressure,
pain and temperature; cross over in spinal cord 2-3
levels above entry - Spinocerebellar pathways: convey information re
muscle stretch to ipsilateral cerebellum
autonomic system is made up of
- parasympathic system- rest and digest
- sympathetic system- fight or flight
dermatomes/myotomes in the lower leg
L3- knee extensors
L4- ankle dorsiflexors
L5- long toe dorsiflexors
S1- ankle plantarflexors
S2- knee flexors
imaging/investigations for nerves
CT and MRI
nerve conduction tests
serum and CSF testing
seizure is
sudden, abnormal electrical discharge in the brain
epilepsy is
tendency to experience recurrent seziures
seizure classification
- simple partial/focal- no LOC
- complex partial/focal- Reduced consciousness
- generalised- LOC
stroke and clinical features
block of blood flow to the brain
F- face or mouth drooped?
A- can they lift arms up?
S- slurred speech? can they undertsand you
T- time is critical call 000 if any signs
cerebral palsy
impaired voluntary movement due to brain prenatal development malformations or peri/postnatal brain injury
manifests by age 2
non progressive
different presentations of CP
- spastic syndromes- causes weakness/stiffness in legs, resistance to passive movement. (70%)
-athetoid / dyskinetic syndromes- slow, writhing, worm like movements
- ataxic syndromes- weak, tremor, wide base
- combination of these is also common
other clinical features of CP
-misalignment of eyes
-normal intelligence in hemiplagia/paraplegia
-foot deformities: equinas, planovalgus, equinovarus
diagnosis of CP
neuro imaging (MRI)
blood tests- screen for metabolic disease
CP management
- stretching for ROM, strengthening muscles and facilitating correct movement patterns
- braces and orthoses
- spasticity medication - baclofen
- botulinum injections - prevent uneven muscle pulls/fixed contractures
- surgery tendon release/transfer to improve joint range/alignment
parkinsons
progressive, degenerative neurological disorder causing
parkinsonism (tremors, rigidity, postural instability, slow movement)
patho of parkinsons
degeneration or injury to dopaminergic circuits in the basal ganglia,
impacting direct and indirect pathways of motor function
risk factors for parkinsons
family history
male
head injury
pesticides exposure
rural living
clinical features of parkinsons
- resting tremor
- rigidty
- slow movement
- postural instability
- can be with dementia, autonomic or neuropsychiatric symptoms
friedreich’s ataxia
progressive loss of voluntary muscle coordination, obstructive cardiac hypertrophy, and development of DM
friedrecichs ataxia clinical features
-delayed motor milestones
-tendency to stagger / fall
-distal muscle weakness greatest in peroneal
-cavus foot type with contracture of digits
-wide base gait
difference between incomplete and complete injuries to the spinal cord
incomplete- partial preserving of function below level and bowel and bladder
complete- complete loss below including bowel and bladder dysfunction
spinal cord ASiA classification
grade A- complete loss of sensory and motor below level of injury
Grade B- incomplete sensory loss, complete motor loss below level
Grade C- incomplete motor, muscle strength less than 3/5
Grade D- incomplete motor, muscle strength 3/5 or more
Grade E- normal sensory and motor
Spina bifida
Congenital brith defect that occurs when the neural tube that forms the spinal cord does not close properly during foetal development
Types of Spina bifida
- Occulta
- Meningocele
- Myelomeningocele
Cauda equina
Acute onset of lower limb neurological symptoms (radicular pain, weakness, sensory changes) and urinary and bowel dysfunction
Emergency can lead to permanent changes
Radiculopathy
Nerve root compression
Symptoms of Radiculopathy
Pain
Numbness
Flaccid motor weakness- emergency if this symptom occurs to avoid permanent disability
MS affects what nerve fibres
Central nerve fibres
GBS affects what nerve fibres
Peripheral nerve fibres
MS
Thought to be linked to an immunological process
Disseminated patches of demyelination in the brain and spinal cord
-common in women around 20-40y
Clinical features of MS
- paraesthesia
-weakness
-clumsiness
-visual disturbances
MS diagnosis
MRI of brain and spinal cord
CSF analysis
MS management
Medicine
1. immunotherapy early during onset
2. cortciosteroids for relapses
3. neurpathic pain medicines for symptoms (antidepressants/anticonvulsants)
GBS
rapidly progressive but self limiting inflammatory polyneuropathy
involves the demyleination of peripheral nerves resulting in weakness and sensory loss in LMN
GBS clinical features
ascending, symmetrical weakness and paralysis (starts with lumbs then goes to arms) with associated parasthesia
GBS management
- hospital
-IV fluids
-respiratory support
-physical therapy
IV immunoglobin can shorten hospital stay
chronic peripheral polyneuropathy
symmetrical, bilateral parathesia in glove and stocking dsitrubition with feet affected first
burning sensation in feet, often at night
diagnosis of chronic peripherl polyneuropathy
loss of sensation distally
reduced vibration and propriception
hereditary peripheral neuropathy
CMT
CMT
autosomal dominant condition, that is slowly progressive sensory and motor peripheral neuropathy
doesnt affect lifespan
clinical features of CMT
-pas cavus
-hammer toes
-gait disturbances, foot drop
-equinovarus deformity
-muscle weakness
-stork leg appearance- due to distal wasting
-glove and stocking
-loss of reflexes
management of CMT
- braces/orthoses for foot drop
Peroneal nerve palsy
compression of the nerve against lateral fibula neck
common in thin patients who cross legs
clinical featues of peronela nerve palsy
weakness in dorsiflexion and eversion causing foot drop
sensory changes in lower limb that it innervates
myasthenia gravis
acquired autoimmune disorder
chronic, progressive weakness of of voluntary skeletal muscles
Motor neuron disease
incurable
neurodegenerative disease of motor neurons (UMN, LMN)
death usually within 3 years of diagnosis
clinical features of MND
limb weakness
progresses to trips falls
muscular dystrophy
two types
duchenne muscular dystrophy and
becker muscular dystrophy
X-linked recessive disorders
progressive proximal muscle weakness caused by muscle fibre degeneration
DMD is worse
MD management
- active/passive exercises
- braces/orthoses
- daily prednisone, extends period of mobilisaiton, improves lungs and heart function, improves survival with DMD
