NU 545 Unit 2 Study Guide

BRAIN
1. Review the anatomy of the brain. Which portion is responsible for keeping you awake, controlling
thought, speech, emotions and behavior, maintaining balance and posture? Wake: pineal body of
epithalamus Arousal is mediated by the reticular activating system, which regulates aspects of attention and
information processing and maintains consciousness. (pg 457).Thought (pg 456) prefrontal area for goal
behavior and memory recall limbic region. Speech pg 457 inferior frontal gyrus broca speech area. Emotions and
behavior is the limbic system and prefrontal cortex p 459 the cerebellum is responsible for balance and posture,
temporal lobe p 457. The prefrontal area is responsible for goal-oriented behavior (e.g., ability to concentrate),
short-term or recall memory, the elaboration of thought, and inhibition of the limbic areas of the CNS. The
prefrontal areas mediate several cognitive functions, called executive attention functions (e.g., planning, problem solving,
setting goals).
2. Know the function of the arachnoid villi. p.466Arachnoid villi protrude from the arachnoid space, through
the dura mater and lie within the blood flow of the venous sinuses. CSF is reabsorbed by means of a pressure
gradient between the arachnoid villi and the cerebral venous sinuses. The villi function as one-way valves
directing CSF outflow into the blood but preventing blood flow into the subarachnoid space.
3. Where is the primary defect in Parkinson’s disease and Huntington’s? p.564 The main disease feature is
degeneration of the basal ganglia (corpus striatum, globus pallidus, subthalmic nucleus, and substantia nigra)
involving the dopaminergic nigrostriatal pathway.
Huntington Disease - where is the primary defect? (p.564) The principal pathologic feature of HD is severe
degeneration of the basal ganglia, particularly the caudate and putamen nuclei and the frontal cerebral cortex.
The degeneration of the basal ganglia leaves enlarged lateral ventricles.
4. What is the function of the CSF? Where is it produced? Where is it absorbed? p.465-466 The function of
the CSF is to protect the brain and spinal cord structures. The intracranial and spinal cord structures float in the
CSF protecting them from jolts and blows. The buoyant properties of the CSF also prevent the brain from
tugging on nerve roots and blood vessels. The choroid plexuses are the structures that produce CSF;. . It is
reabsorbed into venous circulation through the arachnoid villi. These are primarily located in the superior sagittal
sinus. Made in the blood and after CNS returns to the blood. CSF is reabsorbed by means of a pressure gradient between
the arachnoid villi and the cerebral venous sinuses.
5. Review blood flow to the brain. p.467-469 The brain receives about 20% of the cardiac output or 800 to 1000
ml of blood flow per minute. Carbon dioxide serves as a primary regulator for blood flow within the CNS as it is a
potent vasodilator. The brain derives its arterial supply from two systems: the internal carotid arteries and the
vertebral arteries. The collateral blood flow to the brain is provided by the circle of willis.
PAIN
6. What is the gate control theory of pain? P. 485 Pain transmission is modulated by a balance of impulses
transmitted from large, myelinated A-Delta (responsible for well-localized, sharp pain sensations) and small,
unmyelinated C fibers. (GCT) explains that a balance of impulses conducted to the spinal cord, where cells in the
substantia gelatinosa function as a spinal gate, regulates pain transmission to higher centers in the CNS. the synaptic
connections between the cells of the primary-and secondary order neurons located in the substantial gelatinous and
other Rexed laminae function as a pain gate.
7. Know the type of nerve fibers that transmit pain impulses. Pain impulses - nerve fibers that transmit them
(p.486) medium-sized A delta Aδ fibers transmit pain impulses. Nociceptors (primary order neurons) are free nerve
endings in the afferent peripheral nervous system that selectively respond to different chemical, mechanical, and
thermal stimuli. Nociceptors are categorized according to the stimulus to which they respond and by the
properties of the axons associated with them.
A-delta fibers: lightly myelinated, medium-sized fibers that are stimulated by severe mechanical deformation
and/or by extremes of temperature. These fibers rapidly transmit sharp, well-localized "fast" pain sensations and
are responsible for casing reflex withdrawal of the affected body part from the stimulus.
C-fibers: polymodal; stimulated by mechanical, thermal, and chemical nociceptors. They slowly transmit dull,
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aching, or burning sensations that are poorly localized and longer lasting.
A-beta fibers: large myelinated fibers that transmit touch and vibration sensations. They do not normally
transmit pain but do play a role in pain modulation.
The cell bodies of the primary-order neurons, or pain-transmitting neurons, reside only in the dorsal root ganglia just
lateral to the spine along the sensory pathways that penetrate
8. Where in the CNS does pain perception occur? p.487Fig 16-4 p.489 The substantia gelatinosa is a structure
involved in pain transmission. Pain perception is the conscious awareness of pain. Three systems interact to
produce the perception of pain and individual responses to pain.
The cognitive-evaluative system overlies the individual's learned behavior concerning the experience of pain and can
modulate the perception of pain and is mediated only through the cerebral cortex.
9. Know different clinical descriptions of pain (acute, chronic, neuropathic); pain threshold/tolerance
clinical descriptions of pain; pain threshold/tolerance (p.491-492). Categories of pain 16-2. According to the
specificity theory, a direct relationship exists between the intensity of pain and the extent of tissue injury. Chronic pain is
often associated with a sense of hopelessness and helplessness as relief becomes more elusive and the timeframe more
protracted. The pain is perceived as meaningless, and depression is often a concomitant finding, as either a result of the
chronic pain state or as a contributor to its development. Individuals often psychologically respond to acute pain with
fear (e.g., fear of diagnosis, fear of continued pain), anxiety, and a general sense of unpleasantness or unease.
Acute pain arises from cutaneous, deep somatic, or visceral structures; these include acute visceral, acute somatic, and
referred.
10.Know endogenous opioids. p.490 a family of morphine-like neuropeptides that inhibit transmission of pain
impulses in the spinal cord, brain, and periphery. Play a role in various CNS, GI, immune system, and other
organ system disorders. The synthesis and activity of β-endorphins is concentrated in the hypothalamus and the
pituitary gland and act as strong µ-receptor agonist.
4 types: enkephalins, endorphins, dynorphins, endomorphins.
11.What are the two types of fibers that transmit the nerve action potentials generated by excitation of any
of the nociceptors. two types of nerve fibers that transmit these action potentials (p.486) The nerve action
potentials generated by excitation of any of these nociceptors travel along these two fiber types to reach the
spinal cord. Nociceptive transmission occurs more quickly in Aδ fibers than it does through C fibers. (1) Aδ
fibers carry well localized, sharp pain sensations and are important in initiating rapid reactions to stimuli (fast
pain). (2) The small unmyelinated C fibers are polymodal and are stimulated by mechanical, thermal, and
chemical nociceptors. They are responsible for the transmission of the diffuse burning or aching sensation that
follow (slow pain). Visceral pain is poorly localized because of fewer nociceptors in the visceral structures. The variable
nature and distribution of nociceptors affect the relative sensitivity to pain in different areas of the body; the tips of the
fingers have more nociceptors than the skin on the back, and all skin has many more nociceptors than the internal organs
including bone.
HEAT BODY TEMPERATURE
12.What is the relationship between epinephrine and body temperature? P.496 Epinephrine causes
vasoconstriction, stimulates glycolysis, and increases metabolic rates, thus increasing heat production.
Epinephrine and norepinephrine produce a rapid transient increase in heat production by raising the body's basal
metabolic rate.
13.Know mechanisms of heat production and heat loss. (p.496-497) Using a fan: convection causes the transfer
of heat through currents of gases or liquids. Sweating may cause as much as 2.2 L of fluid per hour to be lost. Radiation
refers to heat loss through electromagnetic waves.
Mechanisms of Heat Production:
1) Chemical Reactions of Metabolism—these processes occur in the body core (primarily the liver) and are in
part responsible for the maintenance of core temperature.
2) Skeletal Muscle Contraction—Skeletal muscles produce heat through two mechanisms: gradual increase in
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muscle tone and production of rapid muscle oscillations-shivering.

3) Chemical Thermogenesis—results from the release of epinephrine and norepinephrine that produce a rapid,
transient increase in heat production by raising the body's BMR. Produces a quick, brief rise in BMR, whereas
hormone thyroine triggers a slow, prolonged rise. Occurs in brown adipose tissue that is rich with mitochondria
and blood vessels and is essential for non-shivering thermogenesis.
Mechanisms of Heat Loss:
1) Radiation—refers to heat loss through electromagnetic waves. If the temperature of the skin is greater than the
temp of the air, the skin will lose heat to the air.
2) Conduction—refers to heat loss by direct molecule-to-molecule transfer from one surface to another. The
warmer surface loses heat to the cooler surface.
3) Convection—the transfer of heat through currents of gases or liquids.
4) Vasodilation—diverts core-warmed blood to the surface of the body.
5) Decreased muscle tone—to ↓ heat production, muscle tone may be moderately ↓ and voluntary muscle
activity curtailed
6) Evaporation—evaporation of body water from the surface of the skin and the linings of the mucous
membranes is a major source of heat reduction.
7) Increased pulmonary ventilation—exchanging air with the environment through the normal pulmonary
ventilation provides some heat loss, although it is minimal.
8) Voluntary mechanisms—response to high body temps, people physically stretch out.
9) Adaptation to warmer climates—the body of an individual who moves from a cooler to a warmer climate
undergoes a period of adjustment.
14.Know heat exhaustion and heat stroke? p.500
Heat Exhaustion—The result of prolonged high core or environmental temperatures. Causes the hypothalamic
response of profound vasodilation and profuse sweating.
Heat Stroke—Potentially lethal consequence of a breakdown in control of an overstressed thermoregulatory
center. Brain cannot tolerate temps over 104.9. The regulatory center may cease to function appropriately.
Prolonged high environmental temperatures that produce dehydration, decreased plasma volumes, hypotension,
decreased cardiac output, and tachycardia cause heat exhaustion.
Heat stroke is caused when the core temperature reaches or exceeds 40.5° C (104.9° F), the brain may be preferentially
cooled by maximal blood flow through the veins of the head and face, specifically the forehead. Symptoms of heat stroke
include high core temperature, absence of sweating, rapid pulse, confusion, agitation, and coma, and complications
include cerebral edema and degeneration of the CNS.
SLEEP
15.Define the different stages of sleep. 502-504 Normal sleep has two phases that can be documented by EEG:
REM and non-REM, or slow wave sleep.. REM sleep is also known as paradoxic sleep because the
electroencephalographic (EEG) pattern is similar to the normal awake pattern.
NREM sleep is divided into 3 stages, based on changes in EEG patterns
REM sleep accounts for 20% to 25% of sleep time and is characterized by desynchronized, low-voltage, fast activity that
occurs for 5 to 60 minutes approximately every 90 minutes, beginning after 1 to 2 hours of non-REM sleep.
The hypothalamus, as a major sleep center, secretes hypocretins (orexins), which are neuropeptides that promote
wakefulness and rapid eye movement (REM) sleep, as well as appetite, energy consumption, and pleasure or reward
In adults: Sleep time is decreased. Sleep takes longer to initiate
EYE
16. Discuss disorders of the conjunctiva of the eye. 507 & 508 Conjunctivitis may be caused by bacteria,
viruses, allergies, or chemical irritations.
17. Which part of the brain controls movement of the eye? 509, and Fig 16-13 occipital lobe pg 508, superior
colliculi pg 459.. The visual cortex is located in the occipital lobe. The superior colliculi are involved with voluntary
and involuntary visual motor movements. The abducens nerve affects control over the motor fibers to the lateral rectus
muscle and the proprioceptor fibers from the same muscle to the brain, allowing the eyes to move laterally.
18. Know which part of the brain controls pupillary changes. α1 stimulation leads to pupil dilation. In
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evaluating the oculomotor nerve, the pupils are examined for size, shape, and equality; pupillary reflex tested
with a pen light (pupils should constrict when illuminated); and ability to follow moving objects. The oculomotor
CN (III) is involved in this manifestation of pupil dilation
ALZHEIMERS
19. Characteristics of Alzheimer’s disease. Memory loss, Increased irritability, Anxiety and depression
Alzheimer disease and other forms of dementia have a slow onset. Mental status changes are memory loss and
behavioral changes that include irritability, agitation, anxiety, restlessness, and depression. Neurofibrillary tangles
characterize Alzheimers. Acetylcholine is reduced in alzheimers. Amyloid plaques and neurofibrillary tangles are also
found. Brain cell loss in Alzheimer disease is widespread throughout the brain, typically beginning in the hippocampus
and frontal lobes but progressing widely. Cell death in Alzheimer disease leads to reduced size of the brain, with wider
sulci and enlarged ventricles.
BRAIN & HEAD INJURIES
24.Know the characteristics of closed head injury. Closed head injury - characteristics(p.582, 588) Closed
(blunt) trauma is more common and involves either the head striking a hard surface or a rapidly moving object
striking the head. Brainstem is responsible for when a person loses cerebral function, the reticular activating system
and brainstem can maintain a crude waking state known as a VS. Stupor is a condition of deep sleep or unresponsiveness
from which a person may be aroused or caused to open his or her eyes only by vigorous and repeated stimulation.
20.What part of the brain must be functioning for cognitive operations? Level of arousal is activated by the
reticular activating system p 525. Pre frontal lobe is responsible for goal oriented behavior p452. The neural
systems that are essential to cognitive function are: (i) attentional systems that provide arousal and maintenance of
attention over time; (ii) memory and language systems by which information is communicated; and (iii) affective or
emotive systems that mediate mood, emotion, and intention. The five categories that are critical to the evaluation
process for neurologic functioning include: LOC, pattern of breathing, size and reactivity of pupils, (4) eye position and
reflexive response, and skeletal muscle motor responses.
19.Discuss the types of mid-brain dysfunction and its physical symptoms. Midbrain dysfunction types and
physical symptoms (p. 459, 558, & 565)
The midbrain is part of the brainstem and is composed of three structures:
1.) corpora quadrigemina (composed of the superior and inferior colliculi),
2.) tegmentum (containing the red nucleus and substantia nigra)
3.) basis pedunculi.
midbrain dysfunction causes pupils to be pinpoint size and fixed in position is the pontine dysfunction. The tegmentum,
corpora quadrigemina, and cerebral peduncles are parts of the midbrain.
20.Know the best prognostic indicator of recovery of consciousness and functional outcome after a brain
event. p. 533, 582, 584, 587-588) Evaluation is based on history, LOC using the Glasgow Coma Scale, imaging
(CT, MRI, PET), and assessment of vital parameters (ICP and EEG). (p. 584)
21.Know vomiting with which CNS injuries. Vomiting is due to disruptions in the medulla oblongata.
Vomiting with CNS injuries (p.533) Yawning, vomiting, and hiccups are complex reflex-like motor responses
that are integrated by neural mechanisms in the lower brainstem. Vomiting, yawning, and hiccups are complex
reflexlike motor responses that are integrated by neural mechanisms in the lower brainstem. Vomiting often
accompanies CNS injuries that involve the vestibular nuclei. Vomiting can be caused by an impingement on the fourth
ventricle. It can also be the result of brainstem compression from an increase in intracranial pressure.. Vomiting is due to
disruptions in the medulla oblongata..
22.Know patterns of breathing with head injuries. P530 Cheyne-Stokes respirations occur as a result of CO2
levels in the blood. Ataxic breathing occurs as a result of dysfunction of the medullary neurons. Central
neurogenic patterns occur as a result of uncal herniation. Normal respirations are based on the levels of oxygen
(O2) in the blood.
The existence of regular, deep, and rapid respirations after a severe closed head injury is indicative of neurologic injury to
the lower midbrain. Central reflex hyperpnea, which is a sustained deep and rapid but regular respiratory pattern that is
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the result of central nervous system (CNS) damage or disease, involves the lower midbrain and upper pons. This
neurologic injury is observed after increased intracranial pressure and blunt head trauma.
Level of consciousness is the most critical clinical index of nervous system function or dysfunction. An alteration in
consciousness indicates either improvement or deterioration of a person's condition.
Breathing becomes deep and rapid but with normal pattern is called Central neurogenic hyperventilation is a sustained,
deep, rapid, but regular, pattern (hyperpnea) of breathing.
SEIZURES
23.Define seizure and status epilepticus. What is the medical significance? Know benign febrile seizures.
An explosive, disorderly discharge of cortical neurons is a seizure. Seizure (p.550) sudden, transient disruption
in brain electrical function caused by abnormal excessive hypersynchronous discharges of cortical neurons.
Benign febrile seizure(p.679) . Status epilepticus (p.553) in adults is a state of continuous seizures lasting more
than 5 minutes, or rapidly recurring seizures before the person has fully regained consciousness from the
preceding seizure, or a single seizure lasting more than 30 minutes. Status epilepticus is a true medical emergency
because a single seizure can last longer than 30 minutes, resulting in hypoxia of the brain. Its the experience of a second
or a third seizure and often subsequent seizures before the person fully regains consciousness. What are the greatest
concerns when treating a person is in status epilepticus: Cerebral hypoxia and Aspiration. A complex partial seizure
results is impaired consciousness, as well as the inability to respond to exogenous stimuli. Partial seizures only involve
neurons unilaterally. They often have a local (focal) onset. Consciousness may be maintained. Although the history may
be supplemented with the remaining options, it remains the pivotal tool for establishing the cause of a seizure disorder.
Focal (partial) Jacksonian seizures most often begin in the face and fingers and then progressively spread to other body
parts. In generalized seizure, consciousness, is almost always impaired or lost. Febrile seizures are characterized by an
acute respiratory or ear infection is usually present. Simple febrile seizures are rare in infants before 9 months of age or
in children older than 5 years of age. The convulsion occurs with a rise in temperature higher than 39° C (102.2 °F). The
convulsion is short (15 minutes or less).
24.Define dyskinesia. Types? Characteristics? Unnatural movements that occur w/ variety of CNS
dysfunctions which alter muscular innervation; neurotransmitter dopamine plays a role in motor function.
Hyperkinesia: excessive movement (chorea, athetosis, ballism, hyperactivity, wandering, akathisia, Parkinsonian
Tremor, asterixis, cerebellar, rubral, myoclonus)
Paroxysmal dyskinesia: abnormal, involuntary movements that occur as spasms
Tardive dyskinesia: involuntary movement of the face, trunk, and extremities. Usually occurs as a side effect of
prolonged use of first or second generation antipsychotic drugs that cause denervation hypersensitivity, thereby
mimicking the effect of excessive dopamine.
Tardive dyskinesia is the involuntary movement of the face, trunk, and extremities. The other terms do not describe
involuntary movements of the face, trunk, and extremities. The antipsychotic drugs cause denervation hypersensitivity,
which mimics the effect of too much dopamine.
Hypokinesia: a loss of voluntary movement despite preserved consciousness and normal peripheral nerve and
muscle function. Types of Hypokinesia include akinesia, bradykinesia, and loss of associated movement.
Akinesia: An absence, poverty or lack of control of associated and voluntary muscle movements. Is related to
dysfunction of the extrapyramidal system, as in Parkinsonism.
Bradykinesia : slowness of voluntary movement. All voluntary movements become slow, labored, and
deliberate. Difficulty in initiating, continuing, and performing synchronous and continuous tasks.
ICP
25.Know the stages of intracranial hypertension. p. 555-557 *NORMAL INTRACRANIAL PRESSURE
(ICP) = 5-15mmHg OR 60-180 mm H₂O. The RED font indicates the compensatory mechanisms for ↑ ICP.
Stage 1 intracranial hypertension is caused by the Displacement of cerebrospinal fluid, followed by compression of the
cerebral venous system. Dilated and sluggish pupils, widening pulse pressure, and bradycardia are clinical findings evident
of STAGE 3. Stage 3 intracranial hypertension exhibits clinical manifestations that include decreasing levels of arousal,
Cheyne-Stokes respiration or central neurogenic hyperventilation, pupils that become sluggish and constricted, widened
pulse pressure, and bradycardia.
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26.Know normal intracranial pressure. How does body compensate for increased ICP? Stage 1 is
characterized by an ICP that may not change because of the effective compensatory mechanisms, and there may
be few symptoms. Stage 2 is characterized by subtle and transient symptoms, including episodes of confusion,
restlessness, drowsiness, and slight pupillary and breathing changes. Stage 3 is characterized by decreasing levels
of arousal or central neurogenic hyperventilation, widened pulse pressure, bradycardia, and pupils that become
small and sluggish Stage 4 is characterized by cessation of cerebral blood flow.
Brain tissue hypoxia occurs as a result of increased intracranial pressure as it places pressure on the brain. Increased
intracranial pressure leads to intracranial hypertension.
Cerebral edema is an increase in the fluid content of brain tissue; that is, a net accumulation of water within the brain.
Increased permeability of the capillary endothelium of the brain after injury to the vascular structure causes vasogenic
edema.
A rise in intracranial pressure necessitates an equal reduction in the volume of the other contents. The most readily
displaced content of the cranial vault is cerebrospinal fluid (CSF)
27.Know the most critical index of nervous system dysfunction/function. p.529 Level of consciousness is the
most critical clinical index of nervous system function or dysfunction. An alteration in consciousness indicates
either improvement or deterioration of the individual's condition.
28.What is responsible for the tremors associated with PARKINSONS Disease? P. 567 The Parkinson tremor
appears to result from instability of feedback from the basal ganglia to the cerebral cortex caused by the loss of
the inhibitory influence of dopamine in the basal ganglia.
29.Define CONSUSSION Know the different grades of concussion. p.588
Mild concussion
• Grade I: Transient confusion and disorientation accompanied by amnesia (momentary); no loss of
consciousness; symptoms resolve within 15 min.
• Grade II: Transient confusion and retrograde amnesia that develops after 5-10 min (memory loss only of events
occurring several minutes before injury); symptoms > 15 min.
• Grade III: Any loss of consciousness (seconds or minutes); confusion and retrograde and anterograde amnesia
remain from impact and persist several minutes. concussion exhibits symptoms of confusion and retrograde amnesia
from the time of the impact.
Classic cerebral concussion
• Grade IV: any loss of consciousness (can last up to 6 hrs) accompanied by retrograde and anterograde amnesia.
Transient cessation of respiration can occur with brief periods of bradycardia, and a decrease in blood pressure occurs,
lasting 30 seconds or less. Vital signs stabilize within a few seconds to within normal limits. Evidence of a classic
concussion is the immediate loss of consciousness, which lasts less than 6 hours.
30.Know COUP and countercoup brain injuries and how they happen. p. 583 & Fig 18-2 p. 584 Focal brain
injury results from compression of the skull at the point of impact and rebound effects. May be a coup injury
(directly below the point of impact) or contrecoup (on the pole opposite of site of impact). When there is force
applied to the skull, an injury may occur to the corresponding location on the brain. The injury may be coup
(injury at site of impact) or contrecoup (injury from brain rebounding and hitting opposite side of skull). The
focal injury produces a contrecoup (on the pole opposite the site of impact) injury. The frontal portion of the brain is
opposite of the site of impact. Objects striking the back of the head usually result in both coup and contrecoup injuries
because of the irregularity of the inner surface of the frontal bones. Coup injuries occur directly below the point of
impact. Objects striking the front of the head usually produce only coup injuries (contusions and fractures) because the
inner skull in the occipital area is smooth.
31.Know most common primary CNS tumor. p. 629-630 Astrocytomas are a type of glioma and the most
common primary CNS tumor (50% of all brain and spinal cord tumors).
32.What happens to a patient after an acute spinal cord injury? Why is it life threatening? Describe the
clinical manifestations. Why would their temperature fluctuate? The pathophysiological cascade of
secondary spinal cord injury begins within a few minutes after injury. P 589. In the cervical region, cord
swelling, may be life threatening because of the possibility of resulting impairment of the diaphragm function
(phrenic nerves exit C3-C5) and vegetative functions mediated by the medulla oblongata. Following spinal cord
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injury relates to damage of the sympathic nervous system that causes faulty control of sweating and radiation
through capillary dilation. The hypothalamus cannot regulate body heat through vasoconstriction and increased
metabolism; therefore, the individual assumes the temperature of the air. A spinal cord injury results in disturbed
thermal control because the hypothalamus is unable to regulate a damaged sympathetic nervous system. This damage
causes faulty control of sweating and radiation through capillary dilation.
VEGETATIVE STATE VS BRAIN DEATH
33.Know diagnostic criteria for vegetative state and brain death. Diagnostic criteria for vegetative state (VS)
include the return of professed vegetative (autonomic) functions, including sleep-wake cycles and normalization of
respiratory and digestive system functions. p.534. VS is the complete unawareness of self or the surrounding
environment and a complete loss of cognitive function.
Ocular response to head turning
Brain death occurs when there is cessation of function of the entire brain, including the brainstem and cerebellum. With
brain death, ocular response to head turning does not occur and pupils are often fixed and dilated. The following criteria
determine brain death:
1. Completion of all appropriate and therapeutic procedures with no possibility of brain function recovery
2. Unresponsive coma: absence of motor and reflex movements
3. No spontaneous respirations (apnea): partial pressure of carbon dioxide in the arterial blood (PaCO2) rises above 60
mmHg without breathing efforts, providing evidence of a nonfunctioning respiratory center (apnea challenge)
4. No brainstem function: no ocular responses to head turning or caloric stimulation; dilated, fixed pupils; no gag or
corneal reflex
5. Isoelectric (flat) EEG: electrocerebral silence
6. Persistence of these signs for an appropriate period of observation
Brain Death diagnostic criteria(p. 533-534) An isoelectric, or flat, electroencephalogram (EEG) (electrocerebral
silence) for a period of 6-12 hours in a person who is not hypothermic and has not ingested depressant drugs
indicates that no mental recovery is possible and usually means that the brain is already dead. Brain death in
children has same criteria as adults but a longer observation period.
STROKE
34. Define and discuss the different types of stroke, which affected artery causes what data processing
deficits (agnosia, dysphasia, etc). 598-603. Occlusion of the left middle cerebral artery leads to the inability to
find words and difficulty with writing. CVAs are classified according to pathophysiology and thus are ischemic
(thrombotic or embolic), global hypoperfusion (shock), or hemorrhagic. ischemic strokes vary depending on
artery obstructed; Hypertension is the single greatest risk factor for stroke. Hemorrhagic strokes vary location and
size of bleed. Focal defects in 80% altered consciousness 50%. Acute stroke treatment: "time is brain"
⇒Treatment needs to begin within 6 hours of symptom onset. Thrombotic: Dehydration is a risk factor because it
increases blood viscosity and decreases cerebral perfusion. High-risk sources for the onset of embolic stroke are
atrial fibrillation (15% to 25% of strokes), left ventricular aneurysm or thrombus, left atrial thrombus, recent myocardial
infarction, rheumatic valvular disease, mechanical prosthetic valve, nonbacterial thrombotic endocarditis, bacterial
endocarditis, patent foramen ovale, and primary intracardiac tumors. Symptoms of an embolic stroke in only the right
anterior cerebral artery would include left-sided contralateral paralysis or paresis (greater in the foot and thigh) and mild
upper extremity weakness with mild contralateral lower extremity sensory deficiency with loss of vibratory and/or
position sense and loss of two-point discrimination. A lacunar stroke is associated with occlusion of a single, deep
perforating artery that supplies small penetrating subcortical vessels, causing ischemic lesions, not an embolus,
hemorrhage, or aneurysm. A lacunar stroke (lacunar infarct) is a microinfarct smaller than 1 cm in diameter. Because of
the subcortical location and small area of infarction, these strokes may have pure motor and sensory deficits.
35.Know all types of CEREBRAL EDEMA and what causes each type. 557-558. Vasogenic edema is
clinically important because the blood-brain barrier (selective permeability of brain capillaries) is disrupted, and
plasma proteins leak into the extracellular spaces. an increase in the fluid content of brain tissue, a net
accumulation of water within the brain. Types: Vasogenic, Cytotoxic, Interstitial. Vasogenic edema is clinically
important because the blood-brain barrier (selective permeability of brain capillaries) is disrupted, and plasma proteins
leak into the extracellular spaces.
36.Know characteristics of AV malformation. 604-605 In an arteriovenous malformation, arteries feed directly
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into veins through a vascular tangle of malformed vessels without a true capillary bed. AVMs occur as
frequently in males as in females, and occasionally are found in families. systolic bruit over the carotid in the neck,
the mastoid process, or (in a young person) the eyeball is almost always diagnostic of an AVM. vascular malformation is
characterized by arteries that feed directly into veins through vascular tangles of abnormal vessels is AVM.
NEURO DISEASES/CONDITIONS
37.Define and describe the pathophysiology, clinical manifestations and etiology of Multiple Sclerosis. 619-
620MS is a chronic inflammatory disease involving degeneration of CNS myelin, scarring or formation of
plaque, and loss of axons. MS is caused by an autoimmune response to self-antigens in genetically susceptible
individuals. S/S paresthesia, weakness, impaired gait, visual disturbances, urinary incontinence. A 23-year-old
female begins having problems with tiredness, weakness, and visual changes. Her diagnosis is multiple sclerosis (MS).
What is occurring in the patient's body. Demyelination of nerve fibers in the CNS. Is a demyelinating disorder
38.Define and describe the pathophysiology, clinical manifestations and etiology of Guillian Barre
Syndrome. p. 622-624) An acquired acute inflammatory demyelinating or axonal polyneuropathy with four
subtypes: Acute inflammatory demyelinating polyneuropathy, acute motor axonal neuropathy, acute motor and
sensory axonal neuropathy, and fisher syndrome (only 5% of cases). Acute inflammatory demyelinating
polyneuropathy (AIDP) accounts for most occurrences of Guillain- Barré syndrome (GBS). demyelination of the peripheral
nerves with sparing of the axons.
39.Define and describe the pathophysiology, clinical manifestations and etiology of Mysthenia Gravis. 624-
626 Pathophysiology: Myasthenia gravis results from a defect in nerve impulse transmission at the
neuromuscular junction. The main defect is the formation of autoantibodies (an IgG antibody) against receptors
at the ACh binding site on the postsynaptic membrane. Exertional fatigue and weakness that worsens with activity,
improves with rest, and recurs with resumption of activity characterizes myasthenia gravis. Multiple sclerosis (MS) is an
autoimmune disorder diffusely involving degeneration of CNS myelin and loss of axons
40.Define and describe the pathophysiology, clinical manifestations and etiology of Parkinsons disease. p.
564-568 Pathophysiology: The hallmark pathologic features of Parkinson disease are loss of dopaminergic
pigmented neurons in the substantia nigra (SN) pars compacta with dopaminergic deficiency in the putamen
portion of the striatum (the striatum includes the putamen and caudate nucleus).
41.Define and describe the pathophysiology, clinical manifestations and etiology of Huntington disease.
562-564 Huntington disease is manifested by chorea, abnormal movement that begins in the face and arms and
eventually affects the entire body. Huntington disease is manifested by chorea, abnormal movement that begins in the
face and arms and eventually affects the entire body. There is progressive dysfunction of intellectual and thought
processes.
TUMORS
most common primary CNS tumor. p. 629-630 Astrocytomas are a type of glioma and the most common
primary CNS tumor (50% of all brain and spinal cord tumors).
42.Know types of tumors and its site of development/origination (681 child; spinal cord tumors 633) page
627 Approximately 70% to 75% of all intracranial tumors diagnosed in adults are located supratentorially (above the
tentorium cerebella). Approximately 70% of all intracranial tumors in children are located infratentorially (below the
tentorium cerebelli). Astrocytomas are the most common primary CNS tumors (50% of all brain and spinal cord tumors).
The other options do not occur as frequently.
43.Know clinical manifestations and presenting signs of Creutzfeldt-Jacob (t547), meningitis (609), and
brain abscess (613) . Page 547 table. Page 676. The most common cause of bacterial meningitis in children under 5 is
Neisseria meningitidis. Viral meningitis Viral meningitis may result from a direct infection of a virus, or it may be
secondary to disease, such as measles, mumps or herpes. 1 in every 24 children with sickle cell disease develops
pneumococcal meningitis by the age of 4 years. Astrocytoma is the most common type of brain tumor in children. Two-
thirds of all pediatric brain tumors are found in the posterior fossa.
MOOD DISORDERS
44.What is schizophrenia? What part of the brain is associated with the S/S of this disorder? 642-647
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Schizophrenia is a serious psychiatric illness that strikes 1% of the population; equally prevalent in males and
females, emerging in young adults during late teens and early twenties. Schizophrenia may result from
neurodevelopmental defects.
Alterations are suspected in the brain structure that may be the result of neurodevelopmental defects. Researchers
believe that environmental factors may alter brain development; these factors include prenatal infection, prenatal
nutritional deficiencies, perinatal complications, hypoxia, and upbringing in an urban environment. Researchers also
hypothesize that an early brain defect may remain silent until that part of the brain is used.
In the dorsal prefrontal cortex of schizophrenic brains, glutamic acid decarboxylase, the major enzyme in gamma-
aminobutyric acid GABA biosynthesis, is diminished, which likely impairs synaptic performance and cognitive and
behavioral functions associated with this brain region.
45.Define depression and its types; know etiology and link to cortisol. 647-652 When emotional states, such
as sadness, become chronic and uncontrollable, individuals may be diagnosed with depression; there are two
major classifications of mood disorder: major/clinical depression & bipolar disorder.
Depression occurs with deficits in brain norepinephrine.
The monoamine hypothesis of depression suggests that a deficit in brain norepinephrine, dopamine, and/or serotonin is
the underlying cause of depression. HPA system activity is increased in a large percentage of individuals with major
depression (30% to 70% of those with major depression have chronic activation of the HPA system and elevated
glucocorticoid secretion). Environmental and genetic factors play large roles in the development of depression.
46.Know side effects of MAOIs. 652 MAOIs also may induce acute and heightened elevations in blood pressure (e.g.,
hypertensive crisis) after the intake of tyramine-rich foods, such as aged cheeses, sour cream, pods of broad beans,
pickled herring, liver, canned figs, raisins, and avocados.
47.How Does ECT (electroconvulsive therapy) treat depression? (p. 652) ECT is used when individuals fail
to respond to antidepressants or when they are severely depressed, pregnant, suicidal, or psychotic. ECT is used to
treat depression when individuals fail to respond to antidepressants or when they are severely depressed, pregnant,
suicidal, or psychotic. Monoamine systems are affected from ECT. Although the mechanism of action of ECT is not
clear, the procedure is known to produce alterations in only the monoamine systems.
46.Define generalized anxiety disorder. What is the underlying defect? Know characteristics. 655 Excessive
and persistent worries are the hallmarks in GAD. Worries about life events, marital relationships, job
performance, health, money, or social status.
Anxiety disorders are the most prevalent psychiatric illness.
Anxiety disorders are the most prevalent psychiatric illness, occurring in approximately 10% to 30% of the general
population. Many individuals with anxiety disorders develop major depression, and the high comorbidity of anxiety
disorders and depression suggests a common neural pathophysiologic basis linking these two mental illnesses. When
normal fear and anxiety mental states persist and become uncontrollable, an individual may develop an anxiety disorder.
47.Define panic disorder. What are the complications? 654 Panic disorder consists of multiple disabling panic
attacks and is characterized by intense autonomic arousal involving wide variety of symptoms: light headedness,
rapid heart rate, difficulty breathing, chest discomfort, generalized sweating, general weakness, trembling,
abdominal distress, chills or hot flashes. Gamma-aminobutyric acid (GABA) and GABA-benzodiazepine (BZ) receptor
system are inhibited in panic disorders. Panic disorder complication is the development of agoraphobia or phobic
avoidance of places or situations where escape or help is not readily available.
CHILDREN NEURO
48.Define encephalocele, meningocele, spina bifida, myelomeningocele. Where is the defect located in each?
p 664 a herniation or protrusion of the brain and meninges through a defect in the skull, resulting in a sac like
structure. Meningocele - p. 664 Type of spina bifida; saclike cyst of meninges filled with spinal fluid. When
defects of the neural tube closure occur, such as meningocele or myelomenigocele, an accompanying vertebral
defect allows the protrusion of the neural tube contents. This defect is called spina bifida (split spine).
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Myelomeningocele p. 665 Type pf spina bifida more common than meningocele and one of the most common
developmental anomalies of the nervous system; cystic dilation of meninges and protuberance of various
amounts of the spinal cord through the vertebral defect and assoc. w/ more severe complications than a
meningocele. An encephalocele refers to a herniation or protrusion of brain and meninges through a defect in the
occipital region of the skull, resulting in a saclike structure. A meningocele is a saclike cyst of meninges filled with spinal
fluid, a mild form of posterior neural tube closure defect. These can occur throughout the cervical, thoracic, and lumbar
spine areas. A myelomeningocele is a hernial protrusion of a saclike cyst (containing meninges, spinal fluid, and a portion
of the spinal cord with its nerves) through a defect in the posterior arch of a vertebra in the lower spine. When
meningocele and myelomeningocele occur, they are related to an accompanying vertebral defect called spina bifida A
vertebral arch defect. Until the myelomeningocele is surgically closed, cerebrospinal fluid (CSF) may accumulate, resulting
in further dilation and enlargement of the sac, which may risk more damage to the nervous system.
49.Know when the neural tube forms during embryonic development. P 660 During the FOURTH
gestational week then neural groove deepens, its folds develop laterally, and it closes dorsally to form the neural
tube, epithelial tissue that ultimately becomes the CNS. When meningocele and myelomeningocele occur, they are
related to an accompanying vertebral defect that allows the protrusion of the neural tube contents.
50.Know pathophysiology, clinical manifestations and etiology of cerebral palsy. 670-672 Cerebral Palsy is
the term given to a diverse group of nonprogressive syndromes that affect that brain and cause motor dysfunction
beginning in early infancy. It is a disorder of movement, muscle tone, or posture that is caused by injury or
abnormal development in the immature brain. Spastic cerebral palsy accounts for approximately 70-80% of cerebral
palsy cases. Ataxic cerebral palsy accounts for 5-10% of cerebral palsy cases. Dystonic cerebral palsy accounts for 10-20%
of cerebral palsy cases. Mixed cases account for 13% of cerebral palsy cases.
Dystonic cerebral palsy is associated with extreme difficulty in fine motor coordination and purposeful movements.
Ataxic cerebral palsy manifests with gait disturbances and instability. The infant with this form of cerebral palsy may have
hypotonia at birth, but stiffness of the trunk muscles develops by late infancy. Spastic cerebral palsy is associated with
increased muscle tone, persistent primitive reflexes, hyperactive deep tendon reflexes, clonus, rigidity of the extremities,
scoliosis, and contractures. Mixed cerebral palsy may have symptoms of each of the disorders.
51. Know pathophysiology, clinical manifestations and etiology of PKU. 673-674 Etiology—PKU is an
autosomal recessive, inborn error in the metabolism of amino acids. All newborns are screened. PKU is an inborn
error of metabolism characterized by the inability of the body to convert the essential amino acid, phenylalanine, to
tyrosine.
52.What nerves are capable of regeneration? 450-451 Myelinated axons ONLY in the PNS. Peripheral nerves
can repair themselves through axonal reaction. Regeneration is limited to myelinated fibers and generally occurs only
in the PNS