Brain Flashcards
Oculomotor
- CN III
- Motor
- Bedside test = eye movement, pupil constriction
Trochlear
- CN IV
- Motor
- Bedside test = eye movement
Trigeminal
- CN V
- Motor & Sensory
- Bedside test =
V1- Opthalamic = somatic sensation to face
V2 - Maxillary = somatic sensation to
anterior 2/3 tongue
V3- Mandibular = muscles of mastication
Abducens
- CN VI
- Motor
- Bedside test = Eye movement
Facial
- CN VII
- Motor & Sensory
- Branches: temporal, zygomatic, buccal,
mandibular, cervical - Bedside test =
facial movement except mastication
eyelid closing
taste anterior 2/3 tongue
Vestibulocochlear
- CN VIII
- Sensory
- Bedside test = hearing & balance
Glossopharyngeal
- CN IX
- Both
- Bedside test = somatic sensation & taste to
posterior 1/3 tongue
Vagus
- CN X
- Both
- Bedside test = swallowing
Accessory
- CN XI
- Motor
- Bedside test = shoulder shrug
Hypoglossal
- CN XII
- Motor
- Bedside test = tongue movement
How does hyperventilation affect CBF?
- CO2 dilates cerebral vessels, decreases CVR, increases CBF, increases ICP
- Hyperventilation constricts cerebral vessels, increases CVR, decreases CBF, decreases ICP
Goal: PaCO2 30-35 mmHg
How do NTG & nitroprusside affect ICP?
- cerebral vasodilators
- increase CBF
- increase ICP
How does head position affect ICP?
- HOB > 30 degrees facilitates venous drainage away from brain
- Neck flexion/extension compresses jugular veins, reduces venous outflow, increases CBV, increases ICP
- Head down increases CBV & ICP
How does mannitol reduce ICP?
- osmotic diuretic
- increases serum osmolarity
- “pulls” water across BBB toward IV space
- problems:
- if BBB disrupted, manitol can cause
cerebral edema - transiently increases blood volume,
increase ICP & stress a failing heart
- if BBB disrupted, manitol can cause
Anterior circulation of brain
- supplied by internal carotids
- aorta –> carotid a. –> internal carotid a. –> circle of willis –> cerebral hemispheres
Posterior circulation of brain
- supplied by vertebral arteries
- aorta –> subclavian a. –> vertebral a. –> basilar a. –> posterior fossa structures & cervical spinal cord
Circle of Willis
When should tPA be given?
< 4.5 hours after symptom onset
Relationship b/t cerebral hypoxia & hyperglycemia
During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue & is associated w/ worse outcomes.
In context of cerebral aneurysm, how is transmural pressure calculated?
transmural pressure (TP) = MAP - ICP
increased TP –> risk of rupture
S/S SAH
- intense HA “worse of my life” (most common)
- LOC (50%)
- focal neuro deficit
- N/V
- photophobia
- fever
-Meningismus
incidence of cerebral vasospasm
25% of patients w/ SAH
When is cerebral vasospasm following SAH most likely to occur?
4 - 9 days following SAH
Cerebral vasospasm treatment
Triple H therapy
1. Hypervolemia
2. HTN
3. Hemodilution (Hct 27-32%)
Hydration supports BP & CPP, while also reducing blood viscosity & CVR
Nimodipine shown to reduce M&M–increases collateral flow
Aneurysm ruptures while undergoing endovascular coil placement. What do you do?
- Patient is heparinized
- If aneurysm ruptures, give protamine 1 mg per 100 U heparin
-lower MAP to low/normal range
GCS
Tx for pt w/ intracerebral bleed on warfarin
- FFP
- prothrombin complex concentrate
- recombinant factor VIIa
Tx for pt w/ intracerebral bleed on plavix
- platelets
- recombinant factor VIIa
2 common ways of reducing ICP that should be avoided in pt w/ TBI
- Hyperventilation (worsen ischemia)
- Steroids (worsen neuro outcome)
Is N2O safe in pt w/ TBI?
No, pt may have other injuries-pneumothorax . N2O can rapidly expand pnemo
Grand Mal SZ
- Generalized tonic-clonic
- tonic = whole body rigid
- clonic = repetitive jerking
- respiratory arrest & hypoxia
-Tx: propofol, diazepam, thiopental
Focal Cortical SZ
Localized to a particular cortical region
- motor or sensory
- no LOC
Absence (Petit mal) SZ
- loss of awareness but remains awake
- common in children
Akinetic SZ
Temporary LOC & postural tone
- fall, head injury can result
more common in children
Status Epilepticus
-SZ activity last > 30 min or 2 grand mal SZ w/o regaining consciousness b/t
- resp arrest
- Tx:
1. phenobarbital
2. thiopental
3. phenytoin
4. benzos
5. propofol
6. GA
Etomidate & SZ
- Causes myoclonus
- not associated w/ increased EEG activity in pt w/o epilepsy
- increases EEG activity in pt w/ SZ d/o
Alzheimer’s dz patho
- development of diffuse beta amyloid-rich plaques & neurofibrillary tangles in brain
- dysfunctional synaptic transmission (nicotinic Ach)
- apoptosis
Alzheimer tx
Cholinesterase inhibitors
1. Tacrine
2. Donepezil
3. Rivastigmine
4. Galantamine
How do cholinesterase inhibitors interact w/ sux?
increase DOA
Parkinson’s dz patho
- destruction of dopaminergic neurons in basal ganglia
- decreased dopamine + normal Ach = increase Ach
- suppression of corticospinal motor system
- overactivity of extrapyramidal motor system
What drugs increase extrapyramidal s/s in Parkinson’s pt?
Drugs that antagonize dopamine:
1. metoclopramide
2. butyrophenones (haloperidol, droperidol)
3. phenothiazines (promethazine)
AVOID
Most common eye complication in the perioperative period
Corneal abrasion
Most common cause of vision loss in the perioperative period
Ischemic optic neuropathy (ION)
Ischemic optic neuropathy patho
- ischemia of optic nerve
- venous congestion in optic canal reduces perfusion
- central retinal & posterior ciliary arteries high risk
- increased IOP can compress vessels & reduce O2 to retina
Ocular perfusion pressure = MAP - IOP
Surgical procedure that presents most risk of ION?
**Spinal surgery in prone position
Other risk factors:
prone
wilson frame
long anesthesia time
large blood loss
low ratio of colloid to crystalloid resuscitation
hypotension
male
obese
DM
HTN
smoking
old
atherosclerosis
