Neuro Flashcards
Diffuse axonal injury
Whiplash
Shearing and stretching of axons
Not associated with increased ICP
severity depends on location and amount of shearing force
Coup and counter coup
Cord concussion
Spinal cord injury that causes temporary dysfunction of cord function
Cord contusion
Spinal cord injury that results in bruising of neural tissue causing swelling and temporary loss of function
Cord compression
Spinal cord injury that results in pressure on cord chasing ischemia and must be relieved
Laceration
Spinal cord injury that results in tearing of cord tissue, spectrum of injury and severity
Transaction
Spinal cord injury that causes severing of cord with permanent loss of function
Quadriplegic
C6 or higher trans section
Paraplegic with arm function
T6 or lower
Paraplegic with trunk function
L1 or lower
Secondary TBI complications
Hypotension, hypoxia, cerebral ischemia, impaired auto regulation of blood flow, cerebral edema, increased ICP, excitotoxicity, oxidative stress, vascular injury and BBB dysfunction, inflammation, neural death
Goal to manage or prevent
Hyperthermia
Hypoglycemia
Hypercarbia
Hyponatremia
Hypotension
Every patient with primary TBI is a risk. For secondary TBI
Post concussive syndrome
Occurs with mild TBI
HA, dizzy, fatigue, anxiety, irritability, photophobia, insomnia, depression, inability to concentrate
Can last weeks to months
24 hour of close observation then symptoms management
Chronic traumatic encephalopathy
Progressive dementia associated with repeated brain injury like sports, blasts
Neurofibrillary tangles present in brain
Violent behavior, loss of control, depression, suicide, memory loss, cognitive changes
TBI
Alterations in brain function cause by external force like fall, MVC
4 types
Closed, open, focal, diffuse
Closed TBI
Dura remains intact no visible brain
Open TBI
Skull fracture and break in dura exposing cranial content
Focal TBI
Direct impact, Scalp lac, skull fracture, contusion, hemorrhage
Diffuse TBI
Acceleration and deceleration
Concussion, diffuse axonal injury
Delirium
Acute confusional state acute onset with fluctuating cognitive impairment and varying states of awareness
Disruptions of neural networks-reticular activating system
Altered level of transmitters (metabolic disturbances and meds)
Inflammatory cytokines
Dementia
Chronic onset with slow cognitive decline with no impairment of awareness
Neuron degeneration compression of brain and vascular changes?
Alzheimer’s
Neural plaque formation (amyloid deposits) insoluble filaments disrupts neuron impulse
Loss of neurons and synapses in cerebral cortex and hippocampus (memory function)
Atrophy with decreased weight and volume, loss of neurotransmitters
Early onset-autosomal dominant
Late onset- ? Amyloid deposition, atherosclerosis, inflammation, oxidative stress?
Bacteria meningitis
Infection of pia mater, arachnoid villli, subarachnoid space, Ventricular system and CSF
Common pathogens- Neisseria meningititdis and strep pneumonia
Enter through nasopharyngeal cross mucosal membrane; enter blood stream, travel to cerebral vessels, cross BBB. Infect meninges
Inflammatory symptoms like meningeal irritation change in LOC. focal neuro deficits, sz, rash
Dx-labs (CSF with increased WBC, +pmns, low glucose and high protein)
Viral meningitis
Limited infection of the meninges
S/s dependent on virus
Virus reaches meninges via hematogenous spread
S/s More mild than bacterial-HA, photophobia, mild neck pain, fever, malaise
Encephalitis
Acute febrile illness with CNS (meningeal) involvement
Common cause
Bites- mosquito, ticks, fleas
HSV type 1
Post live virus vaccination
Auto immune
Significant neurological deficits
CSF “normal”
Febrile simple seizure
6 months to 5 years
Less than 15 minutes
1 seizure per 24hrs
Generalized
Post ictal with return to baseline and normal neuro
Febrile complex seizure
Any age
15 minutes or more
Multiple szs
Generalized or focal
Post ictal May not fully return to baseline
Focal seizure
Local, small, twitching, staring
Generalized seizure
Diffuse tonic clonic, across body
Role of sodium in seizure
Too high or low can result in seizures
Parkinson’s
Basal ganglia degeneration->low dopamine generating cells -> more areas of brain loose ability to generate dopamine
Resting tremor, rigidity, bradykinesia, postural instability
Degeneration of locus coruleus ->lack of NE -> behavior symptoms such as MDD, cognitive slowing
Multiple sclerosis
Chronic inflammation with degeneration of the CNS myelin, scarring and loss of axon
Progressive or relapsing and readmitting
Diffuse Injury
? Autoimmune or post infection ? Like mono
Parenthesis, weakness, impaired gait, visual changes, urinary incontinence
Myasthenia gravis
Mind to ground progressive weakness (descending)
Defect in nerve impulse transmission at neuromuscular junction r/t acetylcholine receptors antibodies
Autoimmune associated with SLE, RA, thyroidtoxicosis,
Improve with administering anticholinergics, steroids, immune suppressants
Guillaine barre
Ground to brain paralysis (ascending)
Demyelinating disorder caused by humor and cell mediated reaction that is directed at peripheral nerves
Post infectious or post immunization
Improves with descending pattern
30% with residual effects
Cerebral palsy
Disorder of movement, muscle tone and posture
+- cognitive disability and sz
Permanent but not progressive
Spectrum
Before age 3 70%, prior to birth
Prenatal, perinatal, post natal etiologies
5 Ps of CVA
Parenchyma
Pipes
Perfusion
Penumbra
Prevent complications
CVA
Opposite side manifestations
Middle artery-visual, sensory issues
Vertebral artery- swallow, speech, pain, temp, muscle weakness, gait, balance
Posterior artery-vision; depth perception
TIA
Deficits sudden most common is unilateral, weakness, limb parenthesis
Resolves in less than 60 minutes
No evidence of infarct but high risk for CVA in 3 months
Reversible neurological deficit
Deficits sudden and reverse in less than 24 hrs
Lacunar stroke
Deficits progress 24-26 hours
Motor hemiplegia, hemiseonsory, dysarthria, ataxia
Small lesions in penetrating arteries leading to vascular dementia