Disorders of the Central and peripheral nervous systems Flashcards
Traumatic Brain injury
- Primary TBI: caused by the direct impact or injury
- secondary: is the indirect consequence of the primary injury; includes a cascade of cellular and molecular brain events as well as systemic responses
Primary brain injury
- focal: affects one area of the brain (more than 2/3 of head injury deaths)
- diffuse axonal injury (DAI): Affects more than one area of brain
- -account for greatest # of severely disabled survivors
TBI: Closed blunt trauma
- head strikes a hard surface, or a rapidly moving object strikes the head
- dura remains intact; brain tissues aren’t exposed to the environment
- causes focal (local) or diffuse (general) brain injuries
- more common than open trauma injuries
TBI (Open) penetrating trauma
- injury breaks the dura and exposes the cranial contents to the environment
- causes primary focal injuries
Glasglow coma scale
- mild: GCS of 13-15 (mild concussion)
- moderate GCS: 9-12 (structural injury such as hemorrhage or contusion)
- severe GCS: 3-8 (cognitive/physical disability or death)
- hallmark of severe brain injury: Loss of consciousness for 6 or more hours
Focal brain injury
- coup injury: injury at site of impact
- contrecoup injury: injury from brain rebounding and hitting opposite side of skull
Focal brain injury manifestations/tx
- force of impact usually produces contusions
- contusions: blood leaks from an injured vessel bruising brain
- loss of consc. usually less than 5 minutes
- tx; control ICP, and surgery
- smaller the area of impact the greater the severity of injury
Contusions
- epidural (extradural) hematoma: bleeding between dura matter and skull, usually arterial and w/ skull fracture
- subdural hematoma: blood between dura and brain, usually venous
- intracerebral hematoma: bleeding w/in brain
Spinal cord injury
- individuals at risk are young adult men
- causes: MVAs, falls, violence, sports
- extent of injury: in order of occurance (incomplete quad, complete paraplegia, incomplete para, complete quad)
Primary spinal cord injury
- initial mechanical trauma and immediate tissue destruction
- damaged by shearing, compression or penetration
- may occur in absence of vertebral fracture or dislocation
- occurs when an injured spine is not adequately immobilized immediately following injury
Secondary spinal cord injury
- pathophys cascade of vascular, cellular and biochemical events
- begins w/in a few minutes after injury an continues for weeks
Mechanisms of secondary SCI
- microscopic hemorrhages, edema, ischemia, extitotoxicity, inflammation, oxidative damage, an activation of necrotic an apoptotic cell death
- cord swelling makes it hard to determine which changes are permanent
- -if injury cervical area then it can become life-threatening
Manifestations of SCI
- normal activity of spinal cord ceases at and below level of injury
- spinal shock
- neurogenic shock
spinal shock
- loss of continuous discharge from brain or brainstem and inhibition of suprasegmental impulses
- complete loss of reflex function, flaccid paralysis, sensory deficit, loss of bladder and rectal control
- transient drop in BP and poor venous circulation
- loss of thermal control, causes body to assume air temp
- resolving when reflexes return and bladder relaxes
Neurogenic shock
- loss of sympathetic outflow
- vasodilation
- Hotn
- brady
- hypothermia
- loss of supraspinal control and unopposed parasympathetic tone mediated by the intact vagus nerve
Autonomic hyperreflexia (dysreflexia)
- syndrome of sudden massive reflex sympathetic discharge associated w/ spi at thoracic level of T6 or above
- supraspinal control of sympathetic nervous system is disrupted
- -imbalance is present between sympathetic and para
- involves stimulation of sensory receptors below level of cord lesion
- results in uncompensated cardiovascular response
- somatic and sensory stimulation
Autonomic hyperreflexia (dysreflexia) manifestations
- HTN
- Brady
- pounding HA, blurred vision, sweating above lesion, flushing skin, piloerection, nasal congestion, nausea
- life threatening
- TX: elevate HOB, stimulus should removed, administer nitroglycering, paste above level of lesion, Ca channel blockers (nifedipine)
SPI tx
- spine immobilization is an immediate intervention
- decompress and surgical fixation
- coricosteroids w/in 8 hrs of injury to decrease secondary cord injury
- therapeutic hypothermia
- nutrition, lung function, skin integrity, bladder and bowel management
- rehab
Multple sclerosis
- progressive, chronic, inflammatory, demyelinatnig autoimmune disorder of CNS
- occurs in grey and white matter
- degeneration of myelin sheath in CNS neurons, scarring, and loss of axons
- most affected: women
- clinically isolated syndrome: precursor to MS
Manifestations of MS
- Relapsing and remitting
- primary progressive MS
- Secondary progressive MS
- Progressive relapsing MS
Tx of MS
- No cure
- immunotherapy
- immune system modulators
- vit D
- Stem cells
- continuous monitoring
Myasthenia gravis
- chronic autoimmune disease (IgG) antibody produced against acetylcholine receptors on the post-synaptic membrane
- defect in nerve impulse transmission at the neuromusclar junction
- autoantibodies, complement deposits, and membrane attack complexes destroy acetlycholine receptors sites (AChR), causing decreased transmission of the nerve impulse
Classifications of MG
- Neonatal myasthenia
- ocular myasthenia
- generalized AChR myasthenia
Clinical manifestations of MG
- exertional fatigue and weakness that worsens w/ activity, improves w/ rest
- weakness and fatigue of muscles of eyes, throat, diplopia, difficulty chewing, talking and swallowing
Myasthenic crisis
-severe muscle weakening, leading to respiratory distress
Cholinergic crisis from MG
-resembles myashenic crisis but weakness occurs 30-60 min after taking anticholinergic medication