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
Ischemic stokes
Thrombotic-deficit progresses over time, usually large vessel
Atherosclerosis and inflammation are common causes
Embolus- deficit worse at onset, common in MCA
Hemorrhagic type stroke
Subarachnoid- bleeding into space between arachnoid and pia Mater, aneurysm 85% of time, AVM rupture, sudden deficit, progresses rapidly
Intracerebral- bleeding in parenchyma, basal ganglia, putamen most common, HTN, anticoagulation, sudden onset, progress rapidly
Migraines
4-72 hours in duration, unilateral or bilateral, +- aura
Etiology-genetic, environmental, increased risk for epilepsy, MDD, GAD, CVD, stroke
Triggers reduce migraine threshold
Pathos is unclear
Phases
-Premonitory-symptoms before HA
-migraine aura- visual, sensory, motors, symptoms before HA
-HA-throbbing pain with fatigue, n/v, dizzy
-Recovery - irritability, fatigue, depression-May last days
Cluster HA
Unilateral, severe, stabbing, throbbing, sudden onset; short duration
-associated with ptosis, tearing, nasal congestion
More common in males
Occur related to release of vasoactive peptides, neurogenic inflammation and pain activation
Tension HA
Bilateral pain (band pressure), gradual onset
Generic? Episodic or chronic
Central-trigeminal hypersensitivity
Peripheral-myofascial afferent sensitivity
Anterior horn to the spine
Motor neurons, carry motor stimuli to control skeletal muscles
Posterior horn’s to the spine
Sensory neurons, carry sensory signals to brain
Pediatric related changes
Milan develops into teenagers, making recovery from injuries easier, reflexes are markers of healthy nervous system development change within the first year
Aging related changes
Decreased neurons, Milan and dendritic processes with synaptic connections, decrease in brain, weight and size, atherosclerosis, increase blood brain barrier permeability, functional changes decrease in DTR, taste, smell, color, detection, sleep, disturbances, impaired memory
Stages of increased ICP
5 to 15 is normal manipulation of brain blood cerebrospinal fluid plus or minus a mass
Stage one compensation for controlling cerebral blood flow
Stage too early signs of elevated ICP confusion, restlessness, and lethargy this is where you want to Intervine
Stage three brain injury begins hypoxia, hypercarbia loss of autoregulation
Stage four herniation of brain tissue from area of high-pressure to area of low pressure
Autonomic function
Visceral functions of the body
HR, arterial, gut, bladder, smooth muscle tone, sweating, piloerection
Coordination of brain, spinal cord, hypothalamus, visceral reflexes
Can be broken down into two more categories,
sympathetic fight or flight, direct messaging Oregon and parasympathetic rest and digest. Ganglia delivers message.
Sympathetic stress response
High blood pressure and heart rate increase blood flow to muscles decrease blood flow to GAN kidneys increase blood coagulopathy increase glucose glycogenolysis in liver and muscle, increase muscle strength and mental activity
Major components of the cranial vault
Cranium, meninges, parenchyma, and neurological cells
Cranium
Consist of the frontal, occipital, parietal, temporal ethmoid, sphenoid, coronal, suture, sagittal, sutures, anterior fontanelle, posterior fontanelle, skin, periosteum and bone
Meninges
From Outer to in
Dura arachnoid pia
Parenchyma
Gray matter unmyelinated
White matter myelinated
Blood brain barrier
Cellular structures that selectively inhibit certain potentially harmful substances in the blood from entering the interstitial spaces of the brain or CSF tight junction sites
Glucose, lipid soluble molecules, electrolytes, chemicals, plus or minus antibiotics make it harder to treat infections chemotherapy
CSF
Produced by the choroid plexus, average, 35 mL per milliliter of 500 mL per day reabsorb through arachnoid villi responsible for cushion in shock absorbent of the brain high in salt concentration
Monroe, Kelly, principal
Hemodynamics for increased ICP
Cranium consist of brain, blood and CSF and something has to give
Trauma Mastro can increase pressure brain hast to stay the same but blood and CSF have to decrease to make room can cause further issues such as hypoxia when can no longer compensate increased ICP
Anterior cerebral artery
Fed by middle cerebral artery
Supplies, the basal ganglia, medial, cerebral hemispheres, superior surface of frontal and parietal lobes
Middle cerebral artery
Fed by posterior cerebral artery
Supplies blood to frontal lobe, parietal, lobe, cortical surface temporal lobe
Vertebral basilar artery
Fed by posterior cerebral artery
Supplies blood to posterior cerebral hemispheres, occipital, lobe, cerebellum, and brainstem
Circle of Willis
Fed from base of brain
Assist in regulating differential blood flow to the brain
If one Karadas not working, still able to perfused brains, such as in ECMO
Frontal lobe
In charge of behavior, personality, abstract, thinking motor control
If disordered can result in abnormal personality
Temporel lobe
At the temples
Function includes hearing, crude, vision, smell, and taste
Parietal lobe
On top and sides of head
In charge of language, interpretation of somatic experiences, motor control, special relation, and body position
Occipital lobe
In the back of the head in charge of visual and spatial orientation
Wernicke area
In the parietal lobe in charge of sensory speech, if abnormal cannot interpret language leads to aphasia and dysphasia
Brocas area
In the frontal lobe in charge of motor speech, impaired causes inability to talk expressive aphasia
Brainstem
Bottom portion of brain leading to spinal cord
Composed of the middle brain, medulla pons connect the brain to cerebellum
Thalamus
Center of the brain relays impulses to send to, and from cerebral cortex
Hypothalamus
Below the thalamus and charger, regulatory temperature, hunger and hormones
Basal ganglia
In charge of motor, control and tone, if disordered increase muscle tone and motor control issues
Reticular activating system
In charge of consciousness in the sleep wake cycle
Medulla
Part of the brain stem in charge of respiratory center vasomotor, cardiac control, nucleus for nerves, 9, 10, 11,12
If disordered results and respiratory distress requiring ventilation
Pons
Located in the brain, stem nuclei for cranial nerves five through seven nerves to head and neck
Acetylcholine
In charge of muscle tone and gland secretion
Excites, but not inhibitory and parasympathetic nerve endings like in vagal response decreased amount causes Alzheimer’s
Norepinephrine
Monoamine class
Controls mood, wakefulness integration
Excites CV system sympathetic
Dopamine
Monoamine class
In charge of mood, integration and movement
Inhibitory decrease causes Parkinson’s disease
Serotonin
Monoamine class
Modulates pain at level, spinal cord, wakefulness sleeping mood
Inhibitory
Glutamate
Amino acid
Controls integration
Excitatory
Glycine
Amino acid
In charge of integration
Inhibitory
GABA
Amino acid
In charge of wakefulness awareness and integration
Inhibitory
Epidural, intracranial hemorrhage
Blood between the Dura in school by convex shape, associate with skull fracture, tearing of middle meningeal artery, acute worthy of symptoms possible
Subdural, intracranial hemorrhage
Leading between the Dura, an arachnoid matter, tear in bridge in vain, crescent shaped, maybe bilateral depend on mechanism symptoms depend on severity
Intracerebral hemorrhage
Leading the parenchyma and ventricles, penetrating arteries, trauma, Stroke and tumor
Subarachnoid hemorrhage
Leading between the arachnoid and pia matter, blood in the circle of Willis, cisterns and fissures
Due to aneurysm rupture, most of the time
Major depressive disorder
Mood disorder, most common all ages women over men after adolescence
Increases risk for cardiovascular disease, obesity, diabetes, and thyroid issues
Symptoms include depressed or irritable mood loss of interest or pleasure 5% weight change in a month, insomnia or hypersomnia psycho motor agitation or retardation fatigue loss of energy, doing a worthlessness or guilt, poor concentration, or indecisiveness, suicidal ideations, and death 5+ symptoms were 2+ weeks are diagnostic
Bipolar disorder
Mood disorder
Increased risk for cardiovascular disease, obesity, diabetes, thyroid issues
Two types
Type one at least one manic episode does preceded by a hypomania or major depressive episode
Type to one major depressive episode for 2+ weeks at least one hypomanic episode for at least four days
All classic signs of depression with manic symptoms including elevated mood irritable mood, inflated self-esteem, decrease need for sleep, excessive talking racing or credit thoughts distractibility increase goal orientated activities, excessive risky activities, 3+ symptoms for one week are diagnostic
Dopamine
In charge of attention, motivation, concentration, memory, and cognition
Can cause mood issues
Serotonin
Impulsivity, obsessive, thinking, compulsive behavior, eating and sexual function
If abnormal can result in a mood or anxiety disorder
Norepinephrine
Alertness, vigilance, learning, sleep, rest, fight, or flight
If abnormal can result in a mood or anxiety disorder
Mood disorders
Can be do to genetics strong association, bipolar length of chromosome, 18 and 22
Can be neurochemical monoamine hypothesis of depression, deficits in monoamine, transmitters and metabolites in CSF is underlying cause of depression, decreased dopamine, causes fatigue, low energy and motivation decrees norepinephrine causes depletion planning, and concentration decrease serotonin depletion proceeds depression
Neuro endocrine
Or Nuro, anatomic, decrease, serotonin, receptors and transport binding sites norepinephrine receptor, alterations, smaller amygdala results and recurrent depressive episodes, smaller hippocampus from chronic stress? Decrease, prefrontal cortex, cerebral blood flow, degreees glucose metabolism.
Mood disorder, Neuro endocrine causes
Chronic stress, active HH PA, which increases glucocorticoids and up to 70% of patients or activates the immune system increasing pro-inflammatory cytokines specifically interleukin one and six and TNF alpha, causes continued secretion of HPA, hormones and metabolism of mono amine neural transmitters increase neural damage with lots of synapses, decreased level of neuron regulated growth factors all together decreases neurotransmitter levels
Social anxiety
Fear and avoidance in social situation, such as speaking, reading, eating in Public parties speak into authority, figures, engaging in formal, socialization, more common in children, increase activity in the limbic and frontal cortex areas reduction of serotonin and GABA in the amygdala role of oxytocin? Antianxiety effects and promote social attachment. Trust empathy.
Generalized anxiety
Fear and worry about life events, more common in women onset typically early 20th but lessons with age causes, restlessness, muscle tension, irritability, elite fatigue, difficulty, concentrating, difficulty sleeping
Causes can be genetic high Family concordance abnormal norepinephrine and serotonin systems in the amygdala particular on the right side?
PTSD
Exposure to threat of dead, serious injury or sexual violence, develops hours to years after event for diagnostic cluster, is reexperience, avoidance negative cognition in mood arousal
Pathos dress alterations in neural structures, such as the amygdala and prefrontal cortex, and neural transmitters
Changes how memories are stored, retrieved and extinguished
Substance use disorders
Causes can be genetic up to 70 jeans associated early exposure, increases misuse
Psychological, ADHD, anxiety, depression, bipolar are more likely to use
Biological how body processes or processes substance
Social culture due to peer pressure
Environmental stress parental use
all addictive substances produced pleasurable surges of dopamine that act and reward center basal ganglia
Amygdala and prefrontal cortex makes stopping difficult support conditioning associated rewarding hi with other cues in life, such as friends, drinking a place, etc.
