the sympathetic nervous system and

the parasympathetic nervous system

blood vessal constriction

elevated blood pressur

enhance blood flow to skeletal muscle

increased heart rate and contractility

increased respiratory rate

smooth muscle relaxation

pupil dilation

sweat secretion

Start by quietly observing the patient's behavior. If the patient is sleeping, try to rouse him by providing an appropriate stimulus, in this order: 

1. auditory

2. tactile

 3. painful

what areas should be assessed to test cognitive function

9

time is usually disrupted first

orientation to person, last.

• optic (II)- check visual acuity

• oculomotor (III)- check pupil size

• trochlear (IV)- check downward and inward eye movement.

• abducens (VI)- lateral eye movement

Make sure that the patient's pupils constrict when exposed to light and that his eyes adapt to seeing objects at various distances. Ask the patient to follow your finger through six cardinal positions of gaze: 

1.left superior

2.left lateral

3.left inferior

4.right superior

5.right lateral

6.right inferior

ask the patient to: • wrinkle his forehead • raise and lower his eyebrows • smile to show his teeth • puff out his cheeks. 

Also, with the patient's eyes tightly closed, attempt to open his eyelids. As you conduct each part of this test, look for symmetry.

How would you assess the 

spinal accessory nerve (CN XI)?

Note shoulder strength and symmetry while inspecting and palpating the trapezius muscles. 

apply resistance from one side while the patient tries to return his head to midline position. Look for neck strength. Repeat on the other side.

How would you assess the 

hypoglossal nerve (CN XII)

have the patient close his eyes; then touch all the major dermatomes, first with the sharp end of a safety pin and then with the dull end. Proceed in this order: • fingers

• shoulders • toes • thighs • trunk.

start in the area with the least sensation and move toward the area with the most sensation.

using a wisp of cotton or tissue. Lightly touch the patient's skin; don't swab or sweep the skin.

A patient with peripheral neuropathy might retain the sensation for light touch after losing pain sensation.

If the patient's vibratory sense is intact, you do not need to test for the position sense

True or False?

True

If the patient's vibratory sense is intact, further testing for position sense isn't necessary because they follow the same pathway.

move the patient's shoulder through its passive range of motion (ROM); you should feel a slight resistance. 

When you let the patient's arm drop to his side, it should fall easily.

the patient has a wide-based, unsteady gait.

Deviation to one side may indicate a cerebellar lesion on the side.

localization or withdrawal

This means that the sensory and corticospinal pathways are functioning

Trauma

Brain swelling

Electrolyte changes

Opioid or benzodiazapine overdose

Heavy Metal poisoning

Anoxic brain injury

Best Motor Response

Best Verbal Response

 Best eye response

What is the Monroe-Kellie hypothesis

There is limoted space in the cranium if swelling occurs it will increase ICP with an increase in ICP the brian will be damaged

ICP - sum of all contents

CPP = MAP – ICP  

Hematoma

Tumor

Trauma

Changes in blood flow

Making too much CSF

irtability restlessness

or change in LOC

Hypertension

+/- Bradycardia

Irregular respiratory pattern

Headache

Nausea/Vomiting

Papilledema 

What is Cushing’s Triad and what does it indicate?

hypertension (widened pulse pressure), bradycardia, irregular respirations)-Late Sign

indectes the hernation of the brain and the displacement of the brainstem

Diabetes Insipidus

 Syndrome of Inappropriate Antidiuretic Hormone

 Cerebral Salt Wasting

What are the key S/S of  Diabetes Insipidus 

Severe intravascular dehydration

Inadequate ADH

High Urine Out

High Serum Sodium

Free water Replacement

DDAVP (Synthetic ADH)

• Caution with clients with CAD or HTN

Caution in clients with fluid and electrolyte imbalances- cystic fibrosis, renal disease as they can experience hyponatremia.

Notiphy the MD

Changes in blood pressure either high or low are Serious Adverse Effects

Hyponatremia may occure in your pt with DI if they are taking DDAVP.

True or False?

True

a Serious Adverse Effect of DDAVP is hyponatremia

Limit fluid intake 1 hour before and 8 hours after dose to decrease the risk of hyponatremia and water intoxication.

Establish baseline for weight, blood pressure and electrolytes and urine specific gravity

Monitor urine volume and Osmolality as well as patient electrolyte levels.

What are the key S/S of SIADH

Severe intravascular fluid volume overload

Too much ADH

Hypervolemia

Hyponatremia- r/t dilution

Oliguria- decreased urine output 

Sodium replacement

Fluid restriction

What are teh key S/S of Cerebral Salt Wasting

Dehydration

Neurogenic sodium loss

Hyponatremia

Hypovolemia

High Urine sodium and osmolarity 

Low serum sodium and osmolarity

How is Cerebral Salt Wasting treated?

Replace fluids and sodium

the ability of cerebral vessels to maintain constant perfusion pressure despite MAP

sensitivity to CO2 and PO2

Vasodilation with acidosis or hypoxia

Vasoconstriction with alkalosis or hyperoxygenation

PO² <50 causes ________ , to get more oxygen

hypoxia decreases ICP

True or False?

False

It is important to avoid hypoxia because increases ICP

Brain accepts 15-20% of cardiac output

If cardiac output is low then the brain will have decreased perfution.

Intraventricular catheter (ventriculostomy), 

Subarachnoid bolt,  

Subdural or epidural catheter or sensor, 

Fiberoptic transducertipped catheter

measures ICP

can drain or sample CSF

can place contrast

establishes a vol/pressure relationship

risk of infection

most invasive type of monitoring

Requires frequent transducer balancing or recalibration

Catheter may be occluded

Insertion difficult if ventricles are small, compressed, or displaced

CSF leakage

lower infection rates than is ventriculostomy

quickly and easily placed

Can be used with small or collapsed ventricles 

Requires no penetration of brain tissue

can have a dampened waveform

less accurate at high elevations

Requires frequent balancing or recalibration with position changes

 no access for CSF sampling

Is least invasive

decreased risk of infection 

easily and quickly placed

Increase in baseline drift over time means possible loss of reliability or accuracy 

no access for CSF drainage or sampling

Can be placed in subdural or subarachnoid space, in a ventricle, or directly within brain tissue 

Is easily transported

Requires zeroing only once (during insertion) 

 decreased risk for infection 

Provides good-quality ICP waveforms 

Requires no adjustment in level of transducer with patient's change of position

no access for CSF sampling or drainage 

Cannot be recalibrated after placement 

Requires periodic replacement of probe- it is easily damaged

give sedatives or analgesics during catheter insertion. 

Do baseline and serial neurologic assessments.

Measure patient's temperature at least every 4 hours.

Document ICP and CPP measurements, and response to stimulation

Monitor insertion site for bleeding, drainage, swelling, and CSF leakage.

Administer sedatives or analgesics- to decrease risk of catheter being dislodged by patient's movements.

Educate patient's family as indicated. 

Notify physician if ICP or CPP is not within specified parameters.

Notice character, amount, and turbidity of CSF drainage.

Monitor system and tubing for air bubbles, and flush or purge system as appropriate. 

Drain CSF as indicated for treatment of ICP elevation. 

Notify physician if CSF drainage is not within prescribed parameters.

Monitor quality of ICP waveform.

Zero or calibrate device per hospital or unit protocol. 

Level transducer at the foramen of Monro; external landmarks include the tragus of the patient's ear and the external auditory canal, among others; all ICP measurements should be made with the transducer at a consistent level relative to external landmarks.

Monitor quality of ICP waveform and drift 

over time.

Jugular venous oxygen saturation

used to reflect cerebral oxygen supply-and-demand balance.

↑ Sjvo2 = ↓ cerebral metabolic rate

↓ Sjvo2 = ↑ cerebral metabolic rate

decreased blood flow due to hypotension, vasospasm, or intracranial hypertension or as

a result of increased brain metabolic requirements due to fever or seizures.

considered hyperemic (high cerebral blood flow CBF compared with metabolic need).

or increases if the brain is so severely injured the neurons are unable to extract oxygen.

the calculation for cerebral O2 consumption; normal is 4-9 ml/dl

(cerebral metabolic rate) CMRO2 = CBF x ajDO2

What does  the Licox/Camino monitor do?

Early warning of differences between brain tissue oxygen supply and demand independent, sensitive outcome prediction

What is Hypothermic Therapy

Body temperature reduced to 32-34 degrees Celsius to decrease cerebral metabolic demand (used for cardiac and neurological events)

Maintained for 24 hours then re-warmed

What is a potential problem that may aries from using Hypothermic Therapy

Electrolyte shifts can cause problems

Ice packs in axilla, groin, neck

Ice packs, misting with water and fans blowing

Body suits that circulate cold water

Central line infusing iced fluids

Occurs immediately upon impact of mechanical force

Neurons are basically ripped apart

Intracellular pathologic cascade

Hypoxia, hypercapnea, systemic hypotension, vasospasms,

hyperoglycemia, hypoglycemia, acid-base imbalance, hyperthermia

Cytotoxic

Vasogenic

Ischemic

neuronal degeneration. Each neuron is equipped with a sodium pump to maintain fluid and electrolyte balance. Traumatic injury can cause dysfunction of this pump and consequent influx of sodium and water into the cells (causes cells to burst)

is due to a combination of cytotoxic and vasogenic processes.

____________  is the major cause of

reduced blood flow to the brain

Cerebral edema does not usually contribute to ↑ ICP.

True or False? 

False

It is a major contributor to increased ICP.

occurs between 1 and 18 hours after injury, peaking at day 3. 

by increasing the permeability of the blood-brain barrier

Benign tumors do not ↑ ICP as much as malignant tumors.

 True or False?

False

Neoplasms increasing cerebral contents and causing edema which increasing intracranial pressure. Any growing tumor benign or malignant is taken out if possible because of the effects on ICP

Classified based on the space they fill in the meninges or in the brain

(Subdural, Epidural, Subarachnoid, Intracerebral)

Increased fluid volume

Increased brain volume

Cingulate

Central 

Uncal

Tonsillar

Downward shift through foramen magnum

(impalement of the brain stem on the tentorium = death)

Impaired responsiveness

Arousal and content GCS

Pupillary response

Vital signs

Cranial reflexes

Physical Signs of injury 

Do NOT PLACE THE NG!!!! 

call the MD and question the orders.

If an NG is placed on a pt with a Basilar Scull Fracture

the NG may pearce the brain tissue.

What are the two man goals for the interventions of TBI

Maintain or Optimize Cerebral perfusion pressure CPP

Optimize cerebral oxygenation

Why might Hyperventilation be an intervention for a pt with a TBI?

It is not recomended to moniter ICP in a pt with a TBI because the moniter may cause further injury.

True or False

False 

It is important to moniter the ICP of a pt with a TBI

Why would Osmotic diuretics be used in a pt with a TBI

Why would your pt with a TBI need Sedative and paralytics ordered

↓ cerebral metabolic demand 

to prevent hypoxia that leads to vasodilation

Why might your pt with a TBI need Barbiturates ordered?

to reduces the risk of seizure activity

(seizures cause extremely high demands of O2)

Scull Fractures-

Coup-Contre Coup

Edema,Seizures

bleeding, edema and loss of barrier to cerebral tissue, and infection.

What are the S/S of a Basilar skull fracture

Battles sign- Raccoon eyes, bruising behind the ear 

Level of Consciousness- arousal

Orientation

Seizures

Papillary changes/visual problems

Vomiting

Change in Speech

Drainage from eyes, ears or nose

What is a Simple partial (focal) Seizure

Awake, Variable motor, sensory, autonomic or psychic sensations

What are the key features of a Complex partial Seizure

Eyes are open but nobody is home. Memory lapse/amnesia of the event

What are the key features of a  Absence Seizure

Immediate loss of awareness. "Blanking out". Often immediate alertness afterward.

What are the key features of a Tonic Clonic Seizure

Tonic phase 

What are the key features of a Tonic Clonic Seizure 

Clonic phase

Rapid contraction and relaxation of muscles- convulsions

Ranges from twitching to violent shaking. Eyes roll back. Incontinence

Poor cerebral perfusion during tonic-clonic seizures- very high oxygen usage

**Over time persons with seizures can exhibit similar symptoms as those who have had a small stroke

IV benzodiazepines, sedatives, paralytics and intubation often necessary to reoxygenate the brain

Your pt is in a Postictal State. What should you anticipate from your pt?

Variable amnesia with gradual awareness of the situation

Exhausted- Will often sleep afterward because of the massive energy expenditure.

Embarrassed

Levels need to be maintained

Cannot abruptly stop medication

Seizures that cause memory loss can cause patients to take multiple medication doses a day, sugest using a pill box.

AED- lowers calcium influx

Used to treat absence (petit mal) seizures

40-100mg/ml 

What are the Classifications of Brain Attack

What are the Risk Factors for Brain Attack

Modifiable

What are the Risk Factors for Brain Attack

Non Modifiable

Age, Gender, Race, and Genetic factors

***Cardiovascular risk factors may or may not me modifiable

How does the blood flow Change in a Brain Attack

If treatment happens quickly what areas can be revived?

the areas with a higher CPP and greater blood flow.

which restores varying levels of cerebral function

What is the progression of cellular changes during a Brain Attack

Starts as failure of neuronal activity and regional brain dysfunction

Progresses to Cytotoxic edema

influx of Na and Cl

Influx of Calcium (irreversible)

Anaerobic metabolism (↑ ph and vasodialation)

Progresses still too advanced cell damage and formation of toxins that damage surrounding tissues

What are the Treatment Targets for a Brain Attack

Rapid identification

Rapid travel to hospital and access to specialists

Rapid intervention

(Face Arm Speech Test)

Facial weakness

Arm weakness

Speech disturbance

ealy indications of a stroke

What is a HemorrhagicBrain Attack

Hemorrhage of :

Microvessel aneurysms from long standing HTN

Aneurysm #1 cause- larger vessel

AVM’s (Arteriovenous malformations)

What is the Pathophysiology of a Hemorrhagic Brain Attack

Bleeding leads to ischemia and vasospasm from blood irritation cellular changes as blood is toxic to the brain. 

4% within 24 hours and 1-2% per day for the fallowing month

Re-bleeding leads to vasospasm. These pts have poor outcomes. 

tight controle of BP

anticonvulsant therapy

Decompensate Fast!

Evacuation of hematomas

Shunting and drainage-ventriculostomy placed. May drain CSF

Antihypertensives (Preop control SBP keep <150 to prevent re-bleeding)

Anticonvulsants

Triple H Therapy- Hypervolemia, hypertension, and hemodilution 

to treat cerebral vasospasum

Triple H Therapy- used 4-12 days after initial hemorage 

Hypervolemia- 

hypertension- 

hemodilution 

What are the most common causes of  Ischemic stroke

Carotid stenosis

A fib without use of Coumadin

Coagulopathy's

Cancer

What is the Pathophysiology Ischemic stroke

Oligemia (reduction in blood flow) leads to 

Ischemia leads to

Cellular ischemic cascade leads to 

Infarction

Penumbra surrounds infarct

Cellar ischemic cascade repeats if blood flow not resored 

Disturbances in Ca lead to Lactic Acidosis causing O2 free Radicals to accumulate and leading to cell death

STAT noncontrast CT within 30 minutes of arrivial

Lumbar puncture

12 lead EKG

Chest x-ray

Carotid doppler Cerebral angiogram

Labs: CBC, Coags, Chem, ABG’s, toxicology

Do Not treat BP unless SBP > 220; DBP > 140; or Mean >130

(treat with labetotol, nipride or nicardipine)

Tissue plasminogen activator (TPA)

or Streptokinase

Heparin, Coumadin

Aspirin, Ticlid, Plavix

Blood pressure Tx SBP>185 DBP >110

Anticonvulsants

Osmotic agents and diuretics- to reduce ICP

What is the two most common causes of Spinal Cord Injury

Vehicle Crashes and falls make up over 70% of spinal cord injuries

ALL spinal column injuries are presumed _______ until proven otherwise 

Vertebral (bony) and spinal cord (neural tissue) injuries always occur together.

true or false? 

False

Vertebral (bony) and spinal cord (neural tissue) injuries may occur independently or concurrently

Spinothalamic- Pain and Temperature

Corticospinal- Voluntary Motor

What are the Classifications of Spinal Cord Injuries?

Complete- Transection of the cord

Incomplete- Partial Cord Injury

What is the best description of a Complete Spinal Cord Injury

is least likely to get better.

There is no function below the level of injury if the spinal cord injury is complete: No movement , No sharp/dull sensation , No hot/cold sensation

No vibration sensation, No sensation of light or deep touch , No sense of position of the arms or legs 

If your pt has a Complete Spinal Cord Injury at the level of C1-2 what is their prognosis?

If your pt has a Complete Spinal Cord Injury at the level of C3-5 what is their prognosis?

If your pt has a Complete Spinal Cord Injury at the level of C6 what is their prognosis?

What are the types of Incomplete Cord Injury

Anterior Cord Syndrome

Brown-Sequard Syndrome

Central Cord Syndrome

Posterior Cord Syndrome

Cauda Equina

Sacral Sparing

Your pt has an Anterior Cord injury what deficets would you expect this pt to have?

Motor paralysis

Lost pain & temp

Your pt has an Anterior Cord injury. What pathways will still work?

Touch, pressure, and position  remain intact

Your pt has posterior cord syndrome. what deficets would you expect this pt to have?

Touch and position is lost

Your pt has posterior cord syndrome. What pathways should remain intact?

Motor function and pain intact

-Rare

Your pt has central cord syndrome.  what deficets would you expect this pt to have?

Motor deficit:  Upper extremities weaker than lower extremities

Variable bladder dysfunction

What are the causes of central cord syndrome

Occurs when the middle part of the spinal cord is damaged.

Occurs with hyperextension injury. It also can be due to degenerative bone changes in the spine and/or narrowing of the spinal canal that surrounds the spinal cord.

Your pt has Brown-Sequard Syndrome.  what deficets would you expect this pt to have?

Ipsilateral- Motor paralysis ,Touch, pressure and position lost

Contralateral-Pain and temperature lost

Your pt has an cauda equina injury.  what deficets would you expect this pt to have?

Bowl and Bladder dysfunction

Pain radiating down both legs

Damage to the peripheral nerve roots below the first lumbar vertebra; some regeneration is possible

Your pt has a sacral sparing injury.  what deficets would you expect this pt to have?

Only have perianal sensation, rectal motor function, and great toe flexor activity

 Indicates possible non-complete lesion

What is a Sacral Sparing non-complete lesion

Your pt has upper motor neuron syndrome.  what deficets would you expect this pt to have?

Originate in the brain and connect to lower motor neurons

Damage to upper motor neurons produce spastic paralysis

What can cause upper motor neuron syndrome.

Seen in patients with cerebral palsy, in patients with neurodegenerative diseases such as multiple sclerosis, and in those who have experienced stroke, traumatic brain or spinal cord injury, or hypoxic encephalopathy at the level of the cortex, the internal capsule, the brain stem, or the spinal cord

Your pt has lowwer motor neuron syndrome.  what deficets would you expect this pt to have?

Lower motor neuron creates “reflex arc”

Loss of function creates flaccid paralysis

What is a Secondary Spinal Cord Injury

Brain and spinal injury extend from the initial insult

Injury after the primary injury: Ischemia, Electrolyte shifts, Inflammation

CT scan:  Better visualization of spinal cord and soft tissues

MRI:  Best for evaluating tumors and vascular infarct

What is the celluar prosses of Secondary Spinal Cord Injury

Ischemia: Gray matter ischemia within one hour of injury; may develop spinal shock due to edema and decreased perfusion

Electrolyte shifts: Na+ increases edema; Ca++ breakdown phospholipids and lead to damage cell membranes

Inflammation: Hypoxia causes formation of free radicals  which are neurotoxic

Stabilization allows for realignment and potential healing

Sometimes fusion is used to decrease pain

Hypothermic Therapy suppress 

many chemical reactions including......

free radical production, excitatory amino acid release, calcium shifts which lead to mitochondrial damage and apoptosis.

How does Hypothermic Therapy affect the HR

Decreases Heart Rate

How does Hypothermic Therapy affect the K concentaration

How does Hypothermic Therapy affect the gut motility

Decreases gut motility

How does Hypothermic Therapy affect the blood glucose concentrations

Increases blood glucose concentrations

How does Hypothermic Therapy affect the SVR

Increases SVR

How does Hypothermic Therapy affect the solubility of gases in the blood

Increases the solubility of gases in the blood

How does Hypothermic Therapy affect the clotting time

How does Hypothermic Therapy affect the risk of aspiration pneumonia

May increase the risk of aspiration pneumonia

How does Hypothermic Therapy affect diuresis

May causes diuresis

How does Hypothermic Therapy affect seizure activity?

May act as an anticonvulsant

How does Hypothermic Therapy affect WBC’s and platelets

May decrease the number and function of WBC’s and platelets

What drugs are use during the Acute Phase of SCI

Steroids:  Inhibit phospholipid break-down; decrease WBC infiltration

Gangliosides:  Stimulate nerve cell growth (best 72 hr)

Lazaroids:  Non-steroidals

What druges are used during the Non-Acute Phase of SCI

Vasodilators:  Autonomic dysreflexia

Antispasmodics: Decrease contracture and bladder spasm

Pain:  Dysesthesias (phantom pain) in those with paraplegia more often than in those with quadriplegia

C4-5:  Decreased diaphragmatic innervation

T7:  Decreased intercostal muscles leads to decreased tidal volume and cough 

What are the key features of Neurogenic shock?

Vasodilation (warm, decreased SVR)

Decreased output (CO, BP)

Decreased sympathetic response (HR)

hypothermia dispight felling warm

How is Neurogenic shock treated?

Treat bradycardia- eppi, atropine,levophed, isoproterenol

vasopressors- eppi, levophed, vasopressen

Fluid resuscitation 

warming measures,

a condition that can occur shortly after traumatic injury to the spinal cord.

the complete loss of all muscle tone and normal reflex activity below the level of injury.

How will a SCI change the function of the GI

Bowel and bladder incontinence

Bladder spasm

Increased parasympathetic innervation to gut increases pepsin and risk

of ulcer

Gastric distention and ileus

Hypermetabolism for at least 2 weeks post injury

What is Autonomic Dysreflexia

Irritation below the level of injury causes activation of the fight or flight response

As a result of sympathetic blockage at the injury, the only symptoms of fight or flight show up above the level of injury.

Severe hypertension

Flushed

Sweating

Treatment: Remove irritation