Neuro 1

Medial aspects of frontal lobes, Contralateral hemiparesis, contralateral sensory loss, impaired cognition and decision making, aphasia (if left sided), incontinence

Most of lateral cerebral hemisphere, internal capsule, and basal ganglia

Contralateral hemiparesis, contralateral sensory loss, aphasia (left sided), homo hemianopsia, altered consciousness, neglect syndrome

Occipital lobe, medial aspect of temporal lobe

visual defects including homonymous central blindness and color blindness, memory impairment

Thalamus and cerebellum and brain stem

Sensory loss, mild hemiparesis, disturbances of gait, speech, swallowing and vision.

Epithalamus, hypothalamus, thalamus

roof of 3rd ventricle, connects with limbic system, secretes melatonin (associated with circadian rhythm)

major relay center. receives sensory afferent signals (2nd to 3rd order transition point), relay center for basil ganglia and cerebellum to cortex for integration, has crude touch, pain, temperature.

maintains homeostasis of body, ANS overseer, maintains behavioral patterns, behavior and emotional portion of limbic system, hormone synthesis

• Concerned with intellectual function such as
– Reasoning, abstract thinking
– Aggression
– Sexual behavior
– Olfaction (smell)
– Articulation of meaningful sound (speech – broca [frontal] & wernicke’s area[temporal?])
– Voluntary movement
• Central sulcus separates frontal lobe from parietal lobe

• Body sensory awareness
• Taste (postcentral gyrus)
• Use of symbols for communication (language)
• Abstract reasoning (math)
• Body imaging

• Formation of emotions
– Love
– Anger
– Aggression
– Compulsion
– Sexual behavior
• Non limbic portion
– Interpretation of language (Wernicke’s area)
– Awareness, discrimination of sound
– Major memory processing area

Occipital:
• Receiving, interpreting, discriminating visual stimuli from optic tract
• Associating visual impulses with other cortical areas

• Incorporates parts of frontal, temporal, parietal lobe (only occipital is missing)
• Oldest part of cortex in evolutionary terms
• Center for emotional behavior

→ Function: planning, programming voluntary muscle movement

subthalmic nucleus, substantia nigra (dopamine production), claustrum, corpus stratum (lentiform nucleus = globus palidus (inside), putamen (outside), caudate nucleus.

caudate nucleus, putamen, globus palidus

progressive dementia, chorea (involuntary movements)

tx: HALDOL

substantia nigra, depletion of dopamine

Stiff, shuffling gait, drool, flat affect, personality changes (can't coordinate movements)

REGLAN!!! Causes lead pipe syndrome making it very difficult to ventilate patient, also make sure they got their levodopa day of surgery - if not, give it!

Coordinates signals from muscle, joint, visual, auditory and equilibrium receptors with instructions from cortex

Composed chiefly of tracts into the cerebellum from medulla and cord
(pinocerebellar, vestibulocerebellar, reticulocerebellar tracts)

Composed almost entirely of tracts into the cerebellum from the pons
(pontocellebellar tracts)

Composed chiefly of tracts from dentate nuclei (out of the cerebellum) through the red nucleus of the midbrain to the thalamus

-Continuous with spinal cord within the foramen magnum.
-Lies in the posterior fossa canal.
-Contains the reticular activating system (RAS) responsible for maintaining conscious, alert state.
-When this system is depressed → lose consciousness
Midbrain → pons → Medulla

Contains nuclei of III, IV CN
Contains red nucleus and substantia nigra which help to control skilled muscular movements

Tegmentum contains red nucleus, substantia nigra

Pons or bridge lies below midbrain
Groups of neurons form sensory nucleus of V and VI, VII CN
Primary function is transmission of information from cerebellum to brainstem and between two cerebellar hemispheres
Important center for control of respiration

-Contains centers controlling heart rate, blood vessels, respiration, coughing, sneezing, swallowing, vomiting
-Contains nuclei of VIII, IX, X, XI, XII cranial nerves
-Contains pyramidal tracts (75% cross here)

-Network of nerve cells and fibers extending through the central core of brain stem
-Connects medulla, pons, midbrain with each other and spinal cord, thalamus, cortex
-Entire system called reticular activating system (RAS)
-Controls level of excitability of brain neurons and helps maintain consciousness and the waking state
-Inhibition of the RAS leads to sleep or coma

pineal gland, posterior pituitary, area postrema, supraoric crest, subfornical organ. Also the chemoreceptor trigger zone.

Tumors, trauma, hypoxia, and severe changes in CO2

Steroid dose - dexamethasone (decadron) solumedrol hydrocortisone etc immediately given preoperatively or upon arrival into ED with s/s of head trauma.

-Normal CPP=100 mmHg
-CPP=50=EEG slowing
-CPP=25-40, flat EEG
-CPP<20, irreversible tissue damage at normothermia

Linear between 20 - 80 mmHg CO2

30 seconds

hypoxemia, ischemia, hypercapnia, trauma, anesthetic agents

the effect when something increases CBF and decreases CMRO2, what volatiles do

CO2 is thought to create carbonic acid when combining with water and then dissociating into H ions which vasodilate cerebral vessels

When CMRO2 and CBF match in their direction (increase/decrease), What IV drugs do

• Reduce brain bulk if needed to decrease ICP
• Minimize retraction needed for tumor exposure
• Protection of patient from position related injury
o Nerve
o VAE
• Rapid emergence to allow neurological assessment
• Prevention of decreases in cerebral perfusion and CBF
o Prevent decreases in BP
o Prevent increases in ICP

Rationale: may cause cerebral edema or vasodilation

Rationale: May cause cerebral vasodilation

Rationale: May cause cerebral vasoconstriction of impaired oxygen delivery

Rationale: May decrease cerebral perfusion

Rationale: May cause increased cerebral edema

Rationale: May decrease cerebral perfusion or lead to cerebral dehydration

intracranial elastance, control of CBF and CMRO2, brain protection, early neurologic assessment, hemodynamically stable emergence

ICP rarely elevated, very vascular so plan fluids accordingly

compresses neural tissue, ICP varies - generally not elevated b/c of slow growth, supra/infra common, HYPERVASCULAR, anticipate lots of blood loss, variable edema, seizures common.

compresses neural tissue, rapid growth (if highly malignant), ICP will rise if malignant r/t rapid growth, supra/infra, HYPOVASCULAR, variable edema, seizures common

oligodendroglimon, medulloblastoma, ependymoma

s/s r/t endocrine dysfunction and compressing (optic nerve, CN3, 4, 6 and hypothalamus), slow growth, ICP may be elevated esp if invading 3rd ventricle and blocking CSF flow (hydrocephalus), transphenoidal approach, avascular, edema rare

Compresses pituitary gland (panhypopituitarism, DI) and optic chasm, slow growth, ICP may be elevated r/t hydrocephalus, not vascular, edema uncomon

Cerebellar compression symptoms, variable growth rate, posterior fossa hypertension possible, mostly occurs in cerebellum although posterior fossa or spinal cord also location, HYPERVASCULAR, massive blood loss, will have high HNH on presentation

Stretches CN8 (deafness, tinnitus), adjacent nerves (V, VII, IX, X) and if big enough can compress cerebellum (Ataxia), brain stem, and 4th ventricle (hydrocephalus) IX and X cranial nerve involvement may depress airway reflexes, vascularity variable, edema rare

s/s of compressing neuronal tissue, growth variable, but usually rapid, ICP varies, seizures common, everything else varies depending on growth, size and location.

AKA Dolls eyes; Hold eyelids open and turn head from side to side (r/o spinal injury) normal: eyes try to stay facing the top; abnormal: eyes do not turn in a conjugate manner. CN III, IV, VI

Instill ice water in ear. Normal: conjugate movement of eyes; abnormal: disconjugate movement of eyes CN VIII, VI

tight brain = hypercapnia, hypoxia, REM, ketamine, inhalation agents (high flow)

slack brain = hypocapnia, hypothermia, IV anesthetics, adequate O2

headache, irritability, N and V, papilledema, confusion

Loss of ability to think rapidly and clearly; impaired judgment and decision-making

disturbed LOC, hypertension, bradycardia, irregular respiration

cardiovascular collapse, coma, respiratory depression, dilated pupils, respiratory secondary to brain stem compression

Promotes lactic acidosis and worsens cellular injury during cerebral ischemia

Elevates, be sure to monitor

Ipsilateral side of tumor

YES! Will cause cerebral edema r/t decrease in serum osmolarity

OSMOTIC!!! Avoid hypotonic solutions as it will cause brain to swell.

improved surgical exposure, blood and irrigation drains from wound, face visible for cranial nerve VII stimulation, access to face and airway (disadvantages: hypotension, risk of VAE)

surgical exposure more difficult, blood and irrigation fluid puddle in wound, limited access to face and airway, decreased risk of VAE

intermediate surgical exposure, blood and irrigation drain, lmited access to face and airway, probable decreased risk of VAE

small reactive, regular

small and reactive

Sluggish, dilated, fixed

midposition and fixed

Loss of ability to think rapidly and clearly; impaired judgment and decision-making

Beginning loss of consciousness; disorientation to time followed by disorientation to place and impaired memory; lost last is recognition of self

Limited spontaneous movement of speech; easy arousal with normal speech or touch; may or may not be oriented to time, place, or person

Mild to moderate reduction in arousal (awakeness) with limited response to the environment; falls asleep unless stimulated verbally or tactilely; questions answered with minimum response

touch (high localization), touch (fine gradients), vibration, movement against skin, position sense (joints), pressure

pain, temperature, crude touch and pressure localization, tickle, itch, sexual sensations

Sensations from leg, arm, face

thigh, thorax, neck, fingers, shoulders, tongue, abdomen, hand.

(dorsal horns of spinal cord)

1. Send descending signals through lower pons/medulla
2. Second order nuclei send signals (enk and end) to dorsolateral columns in spinal cord
3. ENK and END work in the dorsal horns of the spinal cord to inhibit pain signals before they can be relayed to the brain.
3.

Causes cord neurons to release enk which causes inhibition of incoming C and alphaD fibers in dorsal horn

Blocks spinal cord withdraw reflexes from painful stimuli

Suppress pain signals at peripheral nerves at mu opioid receptors (where enk and endo work)

decreases release of glutamate and substance P from cfiber terminal

Terminating in blood pressure, motor control, and descending inhibition of pain

integrated motor, autonomic, and antinocioceptive responses such as orienting, defense, and confrontation

Emotional response to pain, terminated in hypothalamus and amygdala

legs, feet, trunk, arm, hand, face mouth (parallels somatosensory area 1)

distal portion of BA6, same topical org as primary motor cortex (mouth/face most lateral), cause more complex movements, sends signals to either primary motor cortex or thalamus and basal ganglia back to PMC

provides body-wide attitudinal movements, positional movements of head and eyes, background for finer motor control of the arms and hands by the premotor areas and PMC

Corticospinal tract (cortex to brain) - pyramidal - 30% from PMC, 30% from premotor and supplementary area, 40% SSI (posterior to central sulcus)

Alpha motor neurons - 16micrometers,
70m/sec velocity

- located in mesencehpalon, large # of direct fibers from primary motor cortex (from corticorubral tract), also from corticospinal, synapse in lower portion of red nucleus where betz cells live forming rubrospinal tract - PURPOSE: accessory route for transmission of relatively discrete signals from the motor cortex to spinal cord

through red nucleus - cross lower brain stem, close connections with cerebellum (balance), if you coordinate movements needing balance.

in pons, transmit excitatory signals to muscles to suppor body against gravity - signals from vestibular and deep cerebellar nuclei

works with pontine to control antigravity, promotes equilibrium

inhibits, provides counterbalance to muscle simulation so they aren't abnormally tense.

R/t lesion of mesencephalon blocking medullary reticular nuclei signals from cortex, red nuclei, and basal ganglia therefore there is unopposed rigidity b/c signals to tell it to stop and where to stop are blocked by lesion.

Spastic (unopposed spinal reflex triggering)

Flaccid

Don't cross over at medulla, larger automatic movements (e.g. swimming, riding bike), coordination to do things in correct order, emotional expression (smile or frown)

Mg, aminoglycocides, CCBs

Decreases, muscles already inhibited, don't need as much to block out Ca channels from opening.

Choline and acetate, choline is reabsorbed into presynaptic cleft.

Tell cord length

Tension

knee jerk via patellar tendon strike

Interneurons

Exaggerated SNS response (increased HR, BP

pentothiazines and butyrophones (inaspsine) antagonize dopamine

N2O, low dose volatile, narcotics well tolerated, these patient's have decreased plasma cholinesterase - give less succs, prone to aspiration r/t pharyngeal muscles

center of hypothalamus that opposes the desire for food.

causes extreme desire for food

Area of hypothalamus that controls renal excretion of water, when fluids too concentrated, neurons stimulated and cause release of ADH from neurohypophisis

cause pituitary release of oxytocin to contract uterus and produce milk. Also water conservation

movement overshoots intended ROM, cerebellar lesion

dysmetria - when doc asks you to point to their finger then point to nose, will pass point if there is a lesion here.

Cerebellar lesion, failure of progression, loss of perception of parts during rapid motor movement

Cerebellar lesion, lack of coordination of speech (failure of cerebellum to coordinate muscles of larynx, mouth, and respiratory system).

oscillating movements with overshoot, failure of damping system of cerebellum

tremor of the eyeballs, failure of damping.

loss of tonic signals from deep cerebellar nuclei - decreased tone on side of cerebellar lesion.

contains red nucleus and substantial nigra

controls excitability of brain neurons and helps maintain consciousness - where we want to anesthetize! when someone coming out of anesthesia, this is becoming active again

Avoid in pts with low cat stores, could precipitate adrenal crisis because they can't make NE r/t blockage of dopamine beta hydroxlase

constrict blood vessels, inhibit insulin

Some vasodilation, mainly negative feedback, inhibit NE release = e.g. agonist = precidex

increase HR, contractility, lipolysis,

dilate vessels, relax bronchioles, secrete insulin,

negative feedback

dilate splanchanic blood vessels, increase GFR and renal blood flow, increase contractility of heart

inhibit NE release

inhibits NE release = vasodilation

inhibits outflow of SNS in brain, vasodilation, sedation

promotes hyperglycemia and hypokalemia

Because b2 stimulates Na-K pump and if it is blocked, K will leave blood and go into the cell r/t concentration gradient.

.2 mcg/kg/min

inhibit breakdown of cAMP which causes vasodilation, increased contractility, good for LV failure patients.

SLUDGM = salivation, lacrimation, urination, defecation, increased GI motility

AKA PSNS - CN III, VII, IX, X, and S2 - S4

AKA SNS, T1 - L3

cortex, hippocampus, stomach = activated increases H+ ions, post op delirium may be causes here in hippocampus r/t low ACh

heart and lung, concerned with bradycardia here - will give anticholinergic (e.g. atropine)

Stimulation decreases NE release therefore causes and decreases HR and contractility

activates cGMP and promotes bronnchodilation and vasodilation

anterolateral of upper medulla that stimulates preganglionic vasoconstriction neurons, lateral increase HR and contractility

anterolateral area of lower medulla that inhibit upper area (vasoconstrictor)

nucleus tractus solarius receives input from CN IX and X

receive input from medial vasomotor center to decrease rate and contractility

input from baroreceptors, chemoreceptors, GI receptors, will get info from these places and decrease HR if needed via ventrolateral medulla

to CN IX and X, from aortic and carotid sinuses

works because you are stimulating baroreceptors in carotid sinus simulating drop in HR from vagal response

CN IX = carotid sinus, CN X = aortic sinus, travels to tractus solaris of medulla and will turn off vasoconstrictors causing vasodilation, and decreased HR and contractility

CN IX = carotid bodies, and CN X aortic bodies, transmit to vasomotor center via hering's nerves, senses lack of O2 and will increase HR or BP to get more blood to tissues.

traction on extraocular muscles, afferent CN V with reflexive efferent CN X = bradycardia, decreased SVR/BP

traction or pressure on structures within peritoneal or thoracic cavities = bradycardia, hypotension, apnea.

Increased HR in response to fluid over load (in conjunction with increased ADH and BNP and dilation of kidneys.

In DM, vagal denervation = orthostatic hypertension, resting tachycardia, decreased gastric emptying, cardiac dysrhythmias, absence of HR variability with deep breathing, postural syncope, silent MI, sudden cardiac death, early saiety, lack of sweating, nocturnal diarrhea,

Lesions T5 and above, will have SNS unapposed below lesion, PNS response above lesion (paroxysmal hypertension, bradycardia, cardiac dysrhty, vasodilation above lesion), from full bladder or incision,

Remove stimilus, direct vasodilators E.g. nipride.

Brain 80%, blood 12%, CSF 12%

45 - 50 mL/100g/min

White = 20 mL/100g/min, Gray = 80 mL/100g/min

100 - 150 mL

Basil ganglia, corpus callosum, medial surface of cerebral hemispheres, superior surface of frontal and parietal lobes = hemiplegia on the contralateral side of the body, greater in LOWER than upper

Frontal lobe, parietal lobe, temporal lobe, (cortical surfaces), aphasia in dominant hemisphere

Part of the diencephalon and temporal lobe, occipital lobe = contralateral hemiplegia greater in UPPER extremities than in lower, sensory loss, visual loss (homonymous hemianopsia)

elevates CSF and ICP by decreasing reabsorption of CSF back into blood, ICP = 37, or 4x normal

Block in aqueduct of sylvius, flattens brain against skull

blockage of fluid in SAP around basal regions or by arachnoid villa where fluid absorbed, fluid collects on the outside of brain and lesser extent the ventricles.

Lipid soluability, size of particle, charge of particle, and degree of protein binding in the blood

Immature glial cells, higher solubility in brain, makes them more susceptible to kernicterus

3 mL/100g/min

4.5 mL/100g/min

Between 50 - 150 mmHg MAP

Doubles cerebral blood flow

30 mmHg in tissues

60 mmHg

50 = low end, 100 = average, 150 = high end of CBF autoregulation

linear

HHITS = Hypoxemia, Hypercapnea, Ischemia, Trauma, Some Anesthetic agents

Decrease in MAP, CVP, PAOP, CO, and PaO2

~ 15%

hydrostatic pressure = (density)(force of gravity)(height of the fluid column)

18 mmHg

20%

30 mmHg, 5 - 11 seconds

present as seizures, hemiplegia, or aphasia, ataxia, syncope, deCORTicate rigidity (UPPER LESION- associate with cerebrum) MOST COMMON

less common

1. ataxia
2. nystagmus
3. dysarthria

cranial nerve palsy, altered LOC, altered respiratory patterns, deCEREbrate

Supratentorial lesion herniation

CO2 == POTENT VASODILATOR,

30 seconds

20 - 80 mmHg

trying to wash H+ out), but never works out that way - H+ ions depress neuronal activity - why the brain wants to increase blood flow and flush them out!

pyruvic or lactic acid buildup (from H+ ions), septic patients, trauma patients, any critically ill patients

4 - 6 hours

50 mmHg

10 - 12% decrease in CBF - more O2 available, less blood needed

5% per degree centigrade

between 30% and 50%

can kick in to help, but also can be severed and brain will still have ability to autoregulate

When MAP rises to exceptionally high levels (e.g. during strenuous exercise, SNS vasoconstricts intermediate and large vessels in the brain to prevent the super high pressures from reaching the tiny vessels preventing stroke.

induced hypothermia

600 - 800 mL/day

125 - 150 mL

supratentorial CSF pressure or pressure in lateral ventricle or SAS

- barbiturates, propofol, volatiles, etomidate,

Increase CBF, Decrease CMRO2, uncoupling effect

KETAMINE - don't give bad idea, also increases CMRO2 - no bueno

Decrease both!! Use to protect patient's brain!

improved CPP, less interference with EP, BETTER PRESERVATION OF AUTOREGULATION IN PATIENT VS VOLATILE

0.4 - 0.5% volatile, 50/50 nitrous/o2, adjunct IV meds for neuro protection

Increase and Increase, but not a significant amount the we don't use it

1 mac, rarely go over .5

shifts autoreg to left, lower does not as far of a shift.

giving benzo or thiopental prep can attenuate increases in ICP, auto regulation of hypo/hypertension is maintained at 70%, response to CO2 is not altered @ 70%

tight brain, unplanned TIVA (r/t progression of response), neurotrauma, neurological monitoring necessitates minimal influence of anesthetics

CBF up by 33% @ 1 MAC, CMRO2 dec by 23%, ICP goes up, volatile of choice because it facilitates CSF absorption, however still run low, MAC 1 still maintained CO2 responsiveness

immediate changes in CBF and delayed alterations in CSF dynamics and arterial CO2 tensions

Similar to ISO, has quick wash in and washout with minimal effect on cerebrospinal and cerebrovascular dynamics

decrease CBF, CMRO2, and ICP

little effect on CBF and ICP unless pt goes apneic and Co2 increases

NO! They do decrease CMRO2 and CBF BUT metabolites hang around too long and you want them to wake up for neuro exam

Routinely used during induction, use adjunct remi or su as they wear off faster

Does give slight increase in ICP, but is decent adjunct

All provide steady hemodynamics, predictable metabolism, CBF reduced by 25 mL/100g/min, CMRO2 reduced by 40 - 50%, great

use sparingly to prevent slow emergence and impaired neuro exam, however are neuro protective like barbiturates

flumazinel

Neo, ephedrine (namely at induction)

BEFORE - how EP works

TACHYPHYLAXIS! Pt can quickly build up tolerance to infusion, may have to titrate to achieve akinesia during case.

careful with volatile anesthetics

50% in gray, 20% in white (white is more sensitive)

somatosensory EP = spine surgery, tumor resection, brachial plexus repair, thoracic AAA repair

used to evaluate neuronal activity when blood supply to cord or actual tissue of cord is at risk for damage - e.g. hypotension at artery of dampowitz for supine spine or clamped during AAA repairs

contralateral side

Increased latency and decreased amplitude

LEAST - crank up those volatiles! Think that sometimes patient can hear you, but can't see you

MOST - limit meds I guess..

.5 MAC of des + N2O allowed adequate MEPs when compared to TIVA with proposal but in another case, propofol fent and light vec enhanced MEPs

Ketamine and etomidate

Sufentanil and Remifentanyl

Provides amnesia

Chest wall rigidity causing hypotension and bradycardia, difficulty ventilating

At the end, want to fill up brain if lesion removed and want to give patient back their respiratory drive, 50 in normal patient, 60 in pt with right shift (e.g. COPDer)

side to side, under falux cerebri (middle line), abnormal posturing and coma, usually precipitates other herniation (uncal)

uncus - innermost portion of temporal lobe, goes through tentorium (aka transtentorial), (up or down), can compress CNIII

will see pupillary changes and eye cast downward and out (in uncal herniation - CN VI and IV still intact)

herniation of cerebellum through foramen magnum - compression/destruction of medulla =

1. HR control
2. RR control

brain matter out through skull

140 - 180 - sugar is bad for the brain

30 - 33, too high too viscous, too low, not enough to perfuse brain

CHF and renal failure

YES

CBF = CPP/CVR

It is indicated when GCS is 3-8, after resuscitation, an abnormal CT scan, posturing.

Reduced by 50%

25 Et = 30 Pa, perfect, usually run around 28