Nervous System Flashcards
What are clinical manifestations of increased ICP?
Diminished cognitive functioning, headache, N/V, seizures, papilledema (edema of the optic disk) causing blurry vision, unsteady gait, loss of sphincter control
What are 2 mechanisms that can cause brain cell death?
Anaerobic metabolism
Deterioration of ion gradients
How does anaerobic metabolism lead to cell injury and death?
Mitochondrial dysfunction -> anaerobic glycotic pathways -> pyruvate coverts to lactate -> H ions lead to acidosis affecting neuronal integrity (cell membrane) -> deterioration of ion gradients -> K leaves, Na, Cl, and Ca enter the cell leading to edema (water follows Na), injury and death
Excessive glutamate can be released because of impaired membrane integrity. How can too much glutamate lead to cell injury/death?
Glutamate binds to NMDA receptor, allowing calcium to enter the cell. Too much calcium can kill it
NMDA receptor activation stimulates nitric oxide production, can lead to free radicals and reactive nitrogen species
What is reperfusion injury and what does lipid peroxidation lead to?
When oxygen reenters cells, it can produce reactive oxygen products that behave as free radicals
Cell membranes may undergo lipid peroxidation which will impair cell membrane, this predisposes the cell to inflammation and more free radicals
What is brain herniation? What is it caused by? How can it be assessed early?
Protrusion of brain tissue through an opening in the supporting dura of the brain. Caused by increased ICP.
Early assessment check pupil reflex (CN 2/3). Changes in size, shape, reactivity is an early indicator of increased ICP and possible brain herniation. Eye movements (CN 3,4,6) can also be affected by increased ICP.
What are ways to check Oculovestibular reflex?
Doll’s eyes
Cold calorics test
Absence of reflex indicates brainstem dysfunction
Primary traumatic brain injury: Focal vs. polar vs. diffuse?
Focal: localized to site of impact
Polar: due to acceleration-deceleration impact resulting in double injury (opposite to focal injury)
Diffuse: Widespread axonal injury due to movement of brain in the skull
Concussion vs. Contusion
Concussion: mild TBI, alteration/loss of consciousness less than 30 min, **no damage on CT, symptoms: headache, N/V, dizzy, fatigue, blurred vision, cognitive/emotional disturbance
Contusion: CT/MRI reveals an area of brain tissue damage (necrosis, laceration, bruising)
Intracranial Hematoma: Epidural vs. subdural vs. subarachnoid
Which effect veins/arteries?
Epidural: arterial injury, rapid onset of symptoms, followed by a period of normal cognition, then consciousness deteriorates again
Subdural: Involves bridging veins, slower onset, increased ICP 2-10 days later
Subarachnoid: rupture of bridging veins, blood spreads to CSF causing meningeal irritation, hydrocephalus, vasospasms, ischemia
What is secondary injury of TBI?
Body’s response to initial injury which may cause more harm, includes ischemia, hypoxia, vasogenic/neurogenic edema increasing ICP, vessels may re-bleed or spasm
What is the most likely cause of hemorrhagic stroke? Where does it normally occur?
Hypertension
Occurs within the brain parenchyma (supportive brain tissue), usually in the basal ganglia or thalamus
Morbidity/mortality is higher in hemorrhagic than ischemic
Homonymous Hemianopsia: Know where blindness would be based on where lesion is. R optic nerve lesion, midline chiasm lesion, R perichiasm lesion, R optic tract lesion
Review picture on slide 50
Lesion on R optic nerve: R eye blind
Midline chiasm lesion: blind periphery
R perichiasm lesion: R nasal blindness
Lesion on R optic tract: L homonymous hemianopia (blind on L half of both eyes)
Broca vs. Wernicke’s aphasia?
Broca: “BE” = broca expressive aphasia, poor articulation and vocabulary
Wernicke’s: Receptive aphasia, impaired auditory comprehension and speech that doesn’t make sense
What are the most common causes of subarachnoid hemorrhage?
Cerebral aneurysms and AVMs (arteriovenous malformations)
Where do most cerebral aneurysms occur?
Sacular/berry aneurysms are most common at areas of bifurcation in the circle of Willis (this is where flow is more turbulent)
What are symptoms and treatment of cerebral aneurysm?
Symptoms: sudden severe headache with meningismus (triad including photophobia, N/V, and stiff neck)
Treatment: surgery- clipping or embolization, vasospasm managed by keeping blood volume and pressure normal to high and calcium channel blockers
What is arteriovenous malformation?
Failure of capillary system to develop. Arterial blood is shunted to venous system and vessels enlarge, making a high risk of rupture and hemorrhage
Leads to seizures and neurological dysfunction
What is meningitis?
Bacteria (most common is streptococcus pneumoniae) enters and colonizes in the nasopharynx, then moves to blood and CSF
It damages the BBB causing edema and increased ICP and neuronal necrosis
The big problem is the accumulation of neutrophils because they degranulate and destroy brain tissue, nerves, and vessels
Diagnostics will show increased neutrophils in the CSF during an LP
What is encephalitis?
Inflammation of the brain caused by a virus which attacks the arachnoid and CSF via the respiratory or GI tracts or inoculation by insect bites
What is a brain abscess composed of?
The core of the abscess is infected full of neutrophils and tissue debris. Fibrous gliosis form due to immune response on glial cells creating scar tissue
How can anticonvulsants help people with seizure disorders?
People with seizure disorders have hyperactive or hypersensitive neurons. Anticonvulsants can target Na or Ca channels or enhance GABA
What are some pathologic features of Alzheimers?
Degeneration of neurons in temporal and frontal lobes, brain atrophy (synapse loss, neuron loss), amyloid plaques (A-beta 42 causes aggregation), neurofibrillary tangles (tau proteins)
With Alzheimers, will CSF Amyloid-beta 42 increase/decrease? Will tau in CSF increase/decrease? Will FDG (shows glucose metabolism) increase/decrease?
CSF A-beta 42 DECREASES (if it is not in the CSF, it is in brain tissue causing aggregation) CSF Tau INCREASES (it normally does not dissociate to form insoluble tangles, should not be in CSF) FDG DECREASES (decrease in synaptic activity)
