Cerebral Palsy Flashcards
What is cerebral palsy?
Group of neurodevelopmental disorders due to upper motor neuron lesion affecting movement and posture
When can cerebral palsy occur?
Before, during and after pregnancy up to the first few years of life
What is the pathophysiology of cerebral palsy?
Hypoxia-ischaemia of the brain
Acute energy failure >tissue acidosis and loss of ion homeostasis, Na+, Ca2+ accumulate
> Osmotic swelling, cell lysis
> Releases glutamate and free radical - cytotoxic and exacerbate injury
> Excitotoxic cascade - overactivation of glutamate receptors cause high level Na+ and Ca2+ influx and can’t be tolerated
>Initiates multiple destructive pathways, activates proteases, lipases, endonucleases
> Damages dendrites, kills neurons, degrades structures, cause ROS production
> Oxidative stress, damage to DNA, membranes
What measures can reduces chances or severity of CP?
Therapeutic hypothermia: slows metabolic rate, allows normal oxygenation and BF to injured cells, supresses pathways leading to delayed cell death
Magnesium sulfate: given to pre-term mothers, prevents glutamate-induced Ca2+ entry - prevents cell lysis, and excitotoxic cascade
What are the different types of CP?
Spastic
- Hemiplegic
- Quadriplegic
- Paraplegic
Dyskinetic
Ataxic
How are the different forms of CP caused?
Spastic: damage to cerebral motor cortex > hypertonicity, weakness
- Hemiplegic: UMN lesions in one entire side of cerebral motor homunculus
- Quadriplegic: UMN lesions in entire motor homunculus bilaterally
- Paraplegic: UMN lesions in medial motor homunculus bilaterally
Dyskinetic: UMN lesions in basal ganglia
Ataxic: UMN lesions in the cerebellum
What can cause CP during pregnancy?
Premature birth: inadequate time for brain development
- Can lead to PVL - inadequate BS to tissue around ventricles
- Can lead to Isolated intraventricular haemorrhage, fragile capillaries rupture and bleed into ventricles
Intrauterine infections: Toxoplasmosis Gondi, Rubella, Cytomegalo virus, Herpes simplex virus - directly insult to brain
Hypoxic/ischaemic insult:
- Placental issues
- Stroke
- Injury to unborn baby head
What can cause CP during or after birth?
Hypoxic-ischaemic insults:
- Umbilical cord compression
- Complications of labour
- Acute ischaemic stroke
Intracerebral haemorrhage
Meningitis/encephalitis
What are the risk factors of CP?
Prematurity: 32 weeks or earlier, low birth weight, or multiple pregnancies, underdeveloped lungs, immunity etc.
Genetic susceptibility: some genetic mutations increase risk
Smoking/drinking/drugs during pregnancy = premature birth
How does spastic CP present?
Subtypes: hemi, di and quadriplegia
Muscle spasticity: tight, stiff muscles
Increased muscle tone: increased tension and resistance to movement
Scissoring gait (diplegic)
Tiptoe walking
How does dyskinetic CP present?
Dystonia: abnormal muscle tone > muscle spasm, abnormal posture
Chorea: sudden, involuntary jerky muscle movement
How does ataxic CP present?
Shakiness
Uncoordinated
Clumsy
Wide based gait - due to lack of balance
What are the relative prevalence of different forms of CP?
Spastic: 80%
Dyskinetic: third most common type
Ataxia: rare
Mixed: second most common
What are the two types of muscle fibres in muscles?
Extrafusal fibres: cause contraction
Intrafusal fibres: proprioception, aligned with extrafusal fibres
What are the different muscle fibre types innervated by?
a-motor neurons innervate extrafusal
Y-motor neuron innervate intrafusal
Intrafusal fibres are innervated by both afferent and sensory neurons (sensory and motor)
What are golgi tendon organs?
Proprioceptors innervated by type lb afferent
Located in series between muscle fibre and macroscopic tendon
What is alpha-gamma coactivation?***
Muscle starts at certain length encoded by firing of la afferent fibres
When muscle is stretched, muscle spindle stretches and la afferent fibres fire more frequently
When muscle released, and contracts, spindle becomes slack, reduces la afferent to fall silent
Muscle spindle becomes insensitive to further stretch. To restore sensitivity, Y-motor neurons fire and cause spindle contraction, become taught, able to signal muscle length again
What are the extrapyramidal tracts, and what are their function?
Originate in the brain stem, to spinal cord
Controls automatic control of musculature - tone, balance, posture, reflexes, locomotion
Rubrospinal
Reticulospinal
Vestibulospinal
Tectospinal
What are the pyramidal tracts and what is their function?
Originate in the cerebral cortex, carrying motor fibres to the spinal cord and brain stem
Control voluntary control of musculature
Corticospinal
Corticobulbar
What are UMN?
Relay impulses that control/modulates LMN from the brain
What are UMN lesions and what do they cause?
Damage to motor neurones above the cranial nerves or anterior/ventral horn of the spinal cord
Hypertonia/spasticity - stiffness - increased firing rate from alpha/gamma neurones
Clonus -abnormal reflex>involuntary and rhythmic contractions
Hyperreflexia - loss of inhibitory signals from descending pathways so myotatic stretch reflex is exaggerated
Up-going babinski’s - toes point up and fan out
Paresis - muscle weakness
What are LMN?
Efferent neurone that connects CNS to muscle
What are LMN lesions, and what do they cause?
Injury to LMN lead to loss of function of LMN that supplies muscles
Hypotonia - degeneration of alpha neurons decrease muscle tone as they are the only neurones innervating them
Hyporeflexia - lack of alpha neurones weaken the myotatic stretch reflex
Fibrillation and fasciculations - damaged alpha neurons leave remnants of the axon near muscle fibres and can still generate spontaneous AP to cause muscle contraction
Muscle atrophy - alpha neuron damage, muscle fibres are deprived of trophic factors > atrophy
SOMATIC NS
What does this scan show?
Periventricular leukomalacia
Common in premature babies, or babies with low birth weight
White matter tract (leuko) surround the ventricles of brain are deprived of blood and oxygen, leads to softening (malacia)
