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FNP 2.0 > Neurological System > Flashcards

Neurological System Flashcards

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1
Q

What is the function of the nervous system?

A

Responsible for the body’s ability to interact with the environment and regulate and control activities involving internal organs, muscles and glands.
The network is composed of complex structures that give off electrical and chemical signals between the brain and body’s organs and tissues

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2
Q

Describe the Central Nervous System

A

Consists of the brain and spinal cord.

Neurons are the basic structure

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3
Q

Describe the Peripheral Nervous System

A

Consists of:
Cranial Nerves: project from the brain and pass through a foramina in the skull
Spinal Nerves: Project from the spinal cord and pass through intervertebral foramina

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4
Q

What is the difference between Ascending Pathways and Descending Pathways?

A

Ascending pathways: Afferent pathway- carry sensory information TOWARDS CNS (skin)
Descending pathways: Efferent pathway- conduct signals along motor neurons to target muscles and glands: skeletal, cardiac, smooth muscle.

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5
Q

Describe Somatic Nervous System

A

Motor and sensory pathways regulating voluntary motor control of skeletal muscle

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6
Q

Describe Autonomic Nervous System

A

Motor and sensory pathways that are involved with regulation of the body’s internal environment (viscera) through involuntary control of organ systems
2 divisions: sympathetic and parasympathetic

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7
Q

Describes neurons

A

Electrically excitable cell and transmits electrical information between other neurons or to an effector organ. They detect environmental changes and initiates body responses to maintain a dynamic steady state.
Cell body: SOMA
Dendrites: Thin branching fibers of the cell. Receptive portion of the neuron. Sends impulses to the cell body
Axons: Long projections that carry nerve impules AWAY from cell body

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8
Q

Describe sensory neurons

A

Respond to stimuli such as TOUCH, SOUND, LIGHT, that affect the cells of the sensory organs.
Sends signals to the spinal cord or brain
Transmit via afferent (toward) pathway

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9
Q

Describe Motor neurons

A

Recieve signals from the brain or spinal cord to control everything from MUSCLE CONTRACTIONS or GRANDULAR OUTPUT.
Transmit via an Efferent (toward) pathway

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10
Q

Describe interneurons

A

Connect neurons to other neurons within the same region of the brain or spinal cord.

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11
Q

Describe Neuroglia

A

“Nerve glue”
General classification of non-neuronal cells that SUPPORT the neurons of CNS
- Astrocytes (fill the spaces between neurons and surround the blood vessels in the CNS)
-Oligodendroglia (deposit myelin with in the CNS)
-Microglia (Remove debris in the CNS)
-Ependymal cells (line the CSF filled cavities of the CNS)

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12
Q

Describe Nerve injury

A

Nerve injury: Injury in CNS causes permanent loss of damaged neurons
LOCAL: Occurs when the axon is severed.
ANTERGRADE: occurs at the distal axon.
RETROGRADE: Occurs at the proximal end of injured axon.
* If CELL BODY is injured = neuron will not regenerate, it will die.

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13
Q

Describe nerve regeneration

A

Depends on location of injury, type of injury, process of inflammatory response, scarring

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14
Q

Describe synapes

A

Neurons form points of conduct through synapes
- Axons (Axo-Axonic) - Axon to cell body (Axo-Somatic) - Axon to Dendrite (Axo-Dendritic) - Dendrite to Dendrite (Dendro-Dendrotic)
Presynaptic Neuron = Relay messages TOWARD the synapse
Postsynaptic Neuron = Relay messages AWAY from the synapse
Neurotransmitter is stored on presynaptic side of synaptic cleft and the receptor sites are on postsynaptic side

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15
Q

What are some neurotransmitters?

A

Neroephiniephrine, Acetylcholine, Dopamine, Histamin, Serotonin

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16
Q

Describe Acetylocholine (neurotransmitter)

A

Located: Many parts of the brain, spinal cords, neuromuscular, junction of skeletal muscle, ANS synapes
Effect: Excitability or Inhibitory
EXAMPLE: Alzheimers disease (decrease in # of acetylocholine secreting neurons) and Myasthenia Gravis ( muscle weakness d/t autoimmune response to acetylcholine receptors on postsynaptic terminal

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17
Q

Describe Norepinephrine (neurotransmitter)

A

Located: Many parts of the brain and spinal cord, some ANS synapes
Effect: Excitatory or Inhibitory
EXAMPLE: CNS: the sleep-wake cycle, mood, Cocaine/amphetamines overstimulation of postsynaptic neurons
PNS: sympathetic nerve transmission

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18
Q

Describe Serotonin (neurotransmitter)

A

Located: many areas of brain and spinal cord
Effect: Inhibitory
EXAMPLE: mood, anxiety, sleep induction, increased levels= schizophrenia

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19
Q

Describe Dopamine (neurotransmitter)

A

Location: Some areas of the brain and ANS synapes
Effect: Excitatory
EXAMPLE: Destruction of dopamine secreting neurons: Parkinsons disease. Drugs used to increase dopamine can induce vomiting/hallucinations

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20
Q

Describe Histamine (neurotransmitter)

A

Location: Posterior hypothalmus
Effect: Excitatory (H1 and H2) Inhibitory (H3)

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21
Q

What are the structural divisons of the brain?

A
  1. Forebrain (includes telecephalon and diencephalon)
  2. Midbrain (Connects pons to diencephalon and includes the corpora quadrigemia, tegmentum and cerebral peduncles
  3. Hindbrain (cerebellum, pons, medulla)
    - Brainstem = midbrain, medulla, pons
    - Brainstem connects hemisphere of brain, cerebellum and spinal cord
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22
Q

What are the regions of the brain?

A
  1. Frontal lobe
  2. Parietal lobe
  3. Occipital lobe
  4. Temporal lobe
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23
Q

Describe the functions of the Frontal Lobe

A

Goal-oriented behavior: ability to concentrate, short-term, recall memory, elaboration of thought and inhibition of Limbic (emotional) areas of CNS

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24
Q

Describe the function of the Parietal Lobe

A

Somatic sensory input (storage, analysis, interpretations of stimuli)
Function for both primary motor and primary sensory areas

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25
Q

Describe the function of the Occipital lobe

A

Visual association

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26
Q

Describe the function of the Temporal lobe

A

Primary auditory cortex
Sensory speech area= reception and interpretation of speech and dysfunction (aphasia, dysphagia)
memory consolidation and smell

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27
Q

Describe the function of dienchephon

A

Controls vital function, visceral activities, closely associated with Limbic system.
Epithalamus
Thalamus: Integrating center for afferent (sensory) impules to the cerebral cortex
Hypothalamus: maintains a constant internal environment and implement behavioral patterns, integrative centers control ANS function, regulate body temp, endocrine function and adjust emotional expression
Subthalamus: basal gangilia center for motor function

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28
Q

Describe function of the Midbrain

A 
Superior (vision): Voluntary/involuntary visual movement, ability for eyes to track objects in visual field
Inferior colliculi (Auditory): Positionin head to improve hearing
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29
Q

Describe functions of Hindbrain

A

Cerebellum: Conscious/unconscious muscle synergy, maintains balance/posture. Damage is characterized by ipsilateral (same side) loss of equilibrium, balance and motor corrdination
Pons: Transmits information from cerebellum to the brainstem between the 2 cerebellar hemispheres
Medulla Oblingata: Helps control HR, RR, CP, coughing, sneezing, swallowing and vomiting

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30
Q

Describe the function of the spinal cord

A

Connects the brain and the body
Conducts somatic and autonomic reflexes
Provides motor pattern control centers
Modulates sensory and motor function

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31
Q

Cranial Nerve I: Olfactory

A

Sensory: Carries impulses for sense of SMELL
EXAM: Person is asked to sniff aromatic substance and identify them

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32
Q

Cranial Nerve II- Optic

A

Sensory: carries impulses for vision
EXAM: vision and vision field tested with an eye chart and by testing point at which person 1st sees an object moving into visual field. The inside of the eye is viewed with an ophthalmoscope to observe blood vessels of the eye interior

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33
Q

Cranial Nerve III- Oculomotor

A

Motor fibers that direct eyeball; levator muscle of the eyelid, smooth muscle of the iris and cillary body and proprioception (sensory) to the brain from extraocular muscle
EXAM: pupils examined for size, shape and equality. Pupillary reflex tested with penlight and ability to follow moving objects

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34
Q

Cranial Nerve IV- Trochlear

A

Proprioceptor and motor fibers for superior oblique muscle of the eye (extraocular muscle)
EXAM: tested with CN III relative to ability to follow moving objects

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35
Q

Cranial Nerve V- Trigeminal

A

Motor/sensory for the face. Conduct sensory impulses from the mouth, nose, surface of eye and dura mater. Also contain motor fibers that stimulate chewing
EXAM: Sensation of pain, touch, temp tested with safety pin and hot/cold objects. Corneal reflex tested with wisp of cotton, motor branch tested by asking subject to clench teeth, open mouth against resistence and move jaw from side to side

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36
Q

Cranial Nerve VI- Abducens

A

Motor fibers to lateral rectus muscle and proprioceptor fibers from same muscle to brain
EXAM: tested with CN III, relative ability to move eyes laterally

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37
Q

Cranial Nerve VII- Facial

A

Mixed: motor fibers to muscle of facial expression and to lacriminal/salivary glands carry sensory fibers from taste buds of anterior part of tongue
EXAM: Anterior 2/3 of tongue tested for ability to taste SWEET, SALTY, SOUR and BITTER. Symmetry of face checked. Subject asked to close eyes, smile, whiste. Tearing tested with ammonia fumes

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38
Q

Cranial Nerve VIII- Vestibulocochlear (acoustic)

A

Sensory; vestibular branch transmits impulses for snes of equilibrium. Cochlear branch tranmits impulses for sense of hearing
EXAM: hearing checked by air/bone conduction by tuning fork. Vestibular tests

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39
Q

Cranial Nerve IX- Glossopharyngeal

A

Mixed. Motor fibers serve pharynx and salivary glands. Sensory fibers carry impulses from pharynx, posterior tongue (taste buds) and pressure receptors of caratoid arteries
EXAM: gag/swallow reflex checked. Persons asked to speak and cough. Posterior 1/3 of tongue may be tested for taste

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40
Q

Cranial Nerve X- Vagus

A

Sensory/motor impulses for pharynx, large part of this nerve is parasympathetic motor fibers that supply smooth muscle of abdominal organs. Receives sensory impulses for viscera
EXAM: Same as CN IX, both serve muscle of throat

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41
Q

Cranial Nerve XI- Spinal Accesory

A

Sensory/motor fibers for sternocleidomastoid and trapezius muscle and muscle of soft palate, pharynx and larynx
EXAM: Sternocleidomastoid and trapequis muscle check for strength by asking subject to rotate head and shrug shoulders against resistence

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42
Q

Cranial Nerve XII- Hypoglossal

A

Motor fibers to muscle of tongue and sensory impulses from tongue to brain
EXAM: ask persons to stick out tongue and any position abnormalities are noted

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43
Q

Describe sympathetic nervous system

A

Fight or Flight Response
Mobilizes energy store in time of needs
*Decreased peristalsis, increased blood sugar levels, temp and blood pressure, regulates vasomotor tone

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44
Q

Describe Parasympathetic nervous system

A

Rest and digest
Functions to conserve and restore energy
* Promotes rest/tranquility, decrease HR, enhances visceral function leading to digestion, controls pupil constriction and tears secretion, increase salivary secretion, contracts urinary bladder*

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45
Q

What are nervous system changes that happen with aging?

A

Structural changes: Decreased # of neurons, decreased brain weight/size, fibrosis and thickening of meninges, narrowed gyri and widened sulci, increased ventricles
Cellular changes: decreased myelin, deposition of lipofuscin, presence of senile plaque, mulitple neurofibrillary tangles, lewy body
Function changes: diminished sensory function, sleep disturbance, memory impairments

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46
Q

What are the theories of pain

A
  1. Specificity Theory: proposes that pain and touch are carried on distinct pathways that project to distinct brain centers
    Useful for specific injuries and acute pain (not chronic, cognitive/emotional elements)
  2. Pattern Theory: proposes that any somatic sense organs respond to a dynamic range of stimulus intensities. Limited (does not account for all types of pain experiences)
  3. Gate Control Theory: integrates and builds upon features of other theories to explain the complex aspects of pain perception and pain modulation. Pain transmission is modulated by a balance of impulses conducted to the spine where cells in the substantia gelatinsoa act as a gate
  4. Neuromatrix Theory: Advancement of the gate control theory and proposes that the brain produces patterns of nerve impulses drawn from various inputs. This includes genetic, sensory-discrimination, affective-motivational, evaluative-cognitive experiences.
    Feelings of pain felt in the absense of inputs from body (phantom limb pain)
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47
Q

What is the clinical description of pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of damage.
Nociceptive pain: pain with normal tissue injury from KNOWN cause
Somatic: fracture, thermal, trauma/ visceral: bowel obstruction
Nonciceptive pain: Neuropathic pain and Central/peripheral
Neurophysiologic pain: Nociceptive pain (somatic, visceral, referred), Neuropathic (central pain, peripheral pain)
Neurogenic pain: Neuralgia, constant
Temproal pain: acute or chronic
Regional pain: Abdomen, chest, HA, low back, orofacial, pelvic, joint
Etiologic pain: cancer, dental, inflammatory (infection, trauma), ischemic, vascular, postoperative

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48
Q

What are some chronic pain syndromes?

A

Persistent low back pain- poor mm tone, inactivity, mm strain, exercise
Myofascial pain syndrome- mm spasm, tenderness, stiffness, as disease progresses = pain becomes generalized
Chronic postoperative pain- disruption or cutting of sensory nerves
Cancer pain- advanced disease, treatment, coexisting disease
Deafferentation pain-damage of peripheral nerve. Burning pain triggered by various stimuli (cold, light touch or sound)
Hyperesthesia- increased sensitivity and decreased pain threshold to tactile and painful stimuli
Hemiagnosia-loss of ability to identify source of pain on 1 side of body. Associated with stroke
Phantom limb pain
Complex regional pain syndrome- associated with limb injury, surgery or fracture

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49
Q

Nociceptive pain (Aute pain)

A

< 3 months
Clinicals symptoms: increased HR, HTN, diaphoresis, dilated pupils, and axiety
Acute somatic: pain is sharp and localized on A Delta fibers. Pain is dull, aching, throbbing and poorly localized on C fibers
Acute visceral: pain is poorly localized. Aching, gnawing, throbbing or intermittent cramping, N/V, hypotension, restlessness and shock
Referred: pain in an area is removed or distant from its point of orgin

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50
Q

What is thermoregulation?

A

Temperature regulation. Achieved through heat production, heat conservation, and heat loss.
Peripheral thermoreceptors in skin and abdominal organs
Central thermoreceptors in the spinal cord and trigeminal ganglia

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51
Q

What are the mechanisms for heat loss?

A
  1. Radiation: loss through electromagnetic waves from surfaces with temp that is higher than surrounding air
  2. Conduction: by direct transfer from one surface to another, so that warmer surface loses heat to cooler surface
  3. Convection: Transfers of heat through currents of gas or liquid, exchanges warmer air at body’s surface with cooler air in surrounding space (fans/wind)
  4. Vasodilation: Diverts core-warmed blood to surface of body with heat transferred by conduction to skin surface and from there to surrounding environment.
  5. Evaporation: Body water evaporates from surface of skin and linigng of mucus membrane. Major source of heat reduction connected with increased sweating in warmer surroundings
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52
Q

What are the mechanisms for heat production?

A
  1. Chemical reactions of metabolism: ocurrs during ingestion and metabolism of food and while maintaining body at rest. occurs in body core
  2. Skeletal mm contraction: gradual increase in mm tone or rapid mm oscillation (shivering). Controlled by posterior hypothalamus
  3. Chemical (nonshivering) thermogenesis: epinephrine and norepinephrine are released and produce rapid, transient increase in heat production by raising basal metabolic rate. Quick, brief effect that counters heat loss through conduction or convection.
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53
Q

What is the pathogenesis of fever?

A

Febrile response or pyrexia that is temporary resetting of the hypothalamic thermostat to a higher level in reponse to pyrogenic cytokines and exogenous pyrogens.
Exogenous pyrogens: pathophysiologic mechanism of fever to begin here, which is produced by pathogens
Pyrogenic cytokines: produced by phagocytic cells as they destroy micoorganisms within the host

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54
Q

What are the benefits of fever?

A
  1. aids infectious response
  2. kills many organisms
  3. decrease the serum levels of iron, zinc and copper (all needed for bacterial replication)
  4. promotes lysosomal breakdown and autodestruction of cells (preventing viral replication of infected cells)
  5. Body switches from burning glucose to a metabolism based on lipolysis and proteolysis (depriving bacteria of a food source)
  6. heat increase lymphocytic transformation and motility of polymorphonuclear neutrophils (immune response)
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55
Q

What are some disorders of temperature regulation?

A
  1. Hyperthermia
  2. Hypothermia
  3. Trauma
56
Q

What is hyperthermia?

A

Elevation of the body temp without an increase in the hypothalamic set point.
Causes derve damage, coagulation of cell proteins and death

57
Q

What core body temperature will result in convulsions or death in hyperthermia?

A

Convulsions: 41c (105.8F)
Death: 43C (109.4F)

58
Q

What are the different types of hyperthermia?

A

Therapuetic: used to destroy pathologic microorganisms or tumor cells by facilitiating the hosts natural immune process or tumor blood flow
Accidental: Heat cramps- treat with administration of dilute salt solution through oral/paternal routes
Heat exhaustion: causes profound vasodilation and profuse sweating that leads to dehydration, decrease plasma volume, hypotension, decreased cardiac output and tachycardia. Treatment- person to stop and lie down. Rest, drink cool fluids
Heat stroke: overexposure to environmental heat, impaired physiologic mechanism for heat loss. Symptoms: core temp is >40C, 104F. no sweating, rapid pulse, confusion, agitation and coma.
Malignant hyperthermia: potientally lethal hypermetabolic complication of rare inherited mm disorder that is triggered by inhaled anesthetics and depolarizing mm relaxants. Most commen in children and adolescents. Treat with withdrawal of provoking agent, body cooling therapy and drugs that antagonize the ryanodine receptor. Temp may rise 1C, 1.8F every 5 minutes.

59
Q

What is Hypothermia?

A

Core body temp < 35C (95F)
Produces depression of the CNS, RR system, vasoconstriction, alterations in microcirculation and coagulation, ischemic tissue damage.

60
Q

What are the different types of hypothermia?

A
  1. Accidental: high energy ATP are depleted. Sudden immersion in cold water or prolonged exposure to cold environments.
    Children and older adults at high risk d/t thermoregulatory mechanisms are immature or altered.
    Peripheral vasoconstriction shunts blood away from the cooler skin to the core in an efor to decrease heat loss. Produces peripheral tissue ischemia.
  2. Therapeutic: ATP storage is preseserved. Used to slow metabolism and preserve ischemic tissue after brain trauma or duing brain surgery, aftrer cardiac arrest and neonatal hypoxic encephalopathy.
61
Q

What is the treatment for accidental hypothermia?

A

Mild: passive rewarming may be sufficient
If core temp is >30C (86F): active rewarming may be required
-Active rewarming = Warm water baths, warm blankets, hearting pads, warm oral fluids
Core rewarming: Admin of warm IV solutions, warm gastric lavage, warm peritoneal lavage, inhaled warm gases
Extreme cases: exchange transfusions, warming blood in a pump oxygenator circut, mediastinal lavage.
Rewarming should proceed no faster than a few degrees per hour.

62
Q

What are the 2 phases of sleep?

A
  1. Rapid eye movement (REM) sleep

2. Non-rapid eye movement (NREM) sleep

63
Q

Describe REM sleep

A

Begins about 1-2 hours after NREM starts.

paradoxical sleep, memorable dreams, loss of voluntary mm control

64
Q

Describe NREM sleep

A

Parasympathetic acitivity increases: decreased HR, RR, BP, temp and mm tone.
3 stages: N1= light sleep. Slow eye movements. Last about 10-12 minutes
N2= slow eye movement, cycle lasts about 30-60 minutes
N3 = no slow eye movement. 12-23% of sleep time spent here

65
Q

What are the neurotransmitters for sleep/wakefulness?

A

Wakefulness = brainstem and basal forebrain serotonin, norepinephrine, dopamine acetylcholine, glutamin
The production of these neurotransmitters decrease with sleep
Sleep = GABA, galanin
NREM sleep = melanin-concentrating hormone, adenosine, prostaglandin D2, nitric oxide and cytokines
REM sleep = ACh, GABA, glutamate

66
Q

Pediatrics sleep patterns

A

Newborns sleep 16-18 hrs per day
53% is REM sleep and 23% NREM
Infant sleep cycle is about 50-60 minutes
They enter REM immediately
Children develop adult sleep patterns between ages 3-5
Sleep is important for growth and neurocognitive development

67
Q

Advanced age sleep patterns

A

Total sleep time is decreased
Longer time is needed to fall asleep, awaken more frequently through the night
time in REM is decreased
Causes for changes in sleep patterns: physical ailments, lack of daily routine, circadin rhythm changes, medications and lifestyle changes

68
Q

What are common sleeping disorders?

A
  1. Dysomnia (intrinsic and extrinsic sleep disorders and circadin rhythm disorders)
  2. Parasomnia (arousal and sleep wake transition disorders and REM sleep disorders)
  3. Medical/psychiatric
  4. Proposed sleep disorders
69
Q

What is dysomnia disorder?

A

Difficulties in initiating or maintaining sleep or excessive sleepiness.

70
Q

Name some dysomnia disorders

A
  1. Insomnia
  2. Obstructive sleep apnea syndrome
  3. Restless leg syndrome
  4. Obesity Hypoventilation
  5. Circadian rhythm disorder
  6. Hypersomnia
  7. Narcolepsy
71
Q

Insomnia

A

Inability to fall asleep or stay asleep; accompanied by fatigue during wakefulness- may be mild, moderate or severe.
Transient (lasting few days to months)
Results in hyperarousal, decreased cortical GABA, increased arousal during REM sleep and dysregulation of sleep-wake cycle.

72
Q

Restless leg syndrome

A

Unpleasant sensations (prickling, tingling, crawling) that occur at rest and are worse in the evening/night.
Person feels the urge to move legs for relief.
More common in women with iron deficiency.
Familial tendency.
*Related to diurnal variation in iron transport across the blood-brain barrier and loss of dopamine

73
Q

What is the treatment for RLS

A

Alpha-2 Delta drugs (gabapentin)
Dopamine agonist
Iron administration

74
Q

Obstructive sleep apnea syndrome

A

Disorder of breathing during sleep, related to an upper airway obstruction associated with reduced blood oxygen saturation and hypercapnia.
Most common sleep disorder

75
Q

What are the risk factors for obstructive sleep disorder

A

Obesity, males, older age, postmenopausal women

76
Q

How is obstructive sleep apnea scored?

A

Using the Apnea Hypopnea Index (AHI): represents apnea (total airway closure) or hypopnea (partial airway closure) episodes per night.

77
Q

AHI scoring:

A

Normal: 0-5 abnormal sleep episodes
Mild: 5-15 abnormal sleep episodes
Moderate: 15-29 abnormal sleep episodes
Severe: >30 abnormal sleep episodes

78
Q

Obstructive sleep apnea results from:

A

Partial or total airway collapse related to pharyngeal anatomy or decreased pharyngeal dilator mm tone

79
Q

Symptoms of Obstructive sleep apnea disorder

A

Obstruction to airway recurring at night causes loud snoring, gasping, multiple apneic episodes that last 10 seconds or longer.
Hypercapnia, low oxygen saturation that leads to polycythemia, pulmonary hypertension, HTN, right-sided CHF, dysrhythmias, cyanosis and peripheral edema

80
Q

Treatment for obstructive sleep apnea

A

Continuous positive airway pressure (treatment of choice)
Surgery of upper airway/jaw
CHILDREN: adenotonsillar hypertrophy is cause of OASD and adenotonsillectomy is treatment of choise

81
Q

Circadian rhythm disorder

A

Rapid time-zone change (jet lag)
Changes in sleep schedule with an advance or delay of 3 hours or more in sleep time
changes in total sleep time from day to day that desynchronizes rhythm

82
Q

What are the neuropsychologic symptoms of sleep deprivation?

A
  1. Impact on performance through cognitive functions (attention, learning, memory, vigilance)
  2. Decreased speed of mental processing
  3. Abnormal activation in the prefrontal cortex, parietal lobe, thalamus, temporal lobes shown on functional neuroimaging
  4. Task performance decreases as sleep debt accumulates
83
Q

Parasomnia

A

Arousal and sleep wake transition disorders and REM sleep disorders

84
Q

What are common arousal disorders?

A
  1. Sleep walking (somnambulism)
  2. Night terrors
  3. Confusional arousal
  4. Rearranging furniture
  5. Violent behanior
    6, Bruxism (grinding teeth)
  6. Sleep enuresis
85
Q

What neural systems are essential for cognitive function?

A
  1. attentional systems that provide arousal and maintenance of attention over time
  2. memory and language systems by which information is communicated
  3. affective or emotive systems that mediate mood, emotion, and intention.
86
Q

What are 2 direct components of consciousness?

A
  1. Arousal (state of awakeness)

2. Awareness (content of thought)

87
Q

Describe arousal (awakeness)

A

regulates aspects of attention and information processing and maintain consciousness.
Infection, vascular alterations, neoplasms, traumatic injury, congential alterations, degenerative changes, polygenic traits and metabolic disorders can cause alterations in arousal.

88
Q

Supratentorial disorders (alteration in arousal)

A

produce changes by either diffuse or localized dysfunction.
Diffuse dysfunction = caused by disease processes affecting the cerebral cortex or the underlying subcortical white matter (encephalitis). Disorders outside the brain, but within the cranial vault can also produce diffuse dysfunction (neoplasm, closed-head trauma)
Localized dysfunction = directly impair function of the thalamic or hypothalamic activing systems. Primariily masses ( bleeding, infarcts, emboli, tumors)

89
Q

Infratentioral disorders (Structural alteration in arousal)

A

Produces a decline in arousal by 1. direct destruction of the reticular activating system and its pathway (accumulation of blood/pus, demyelinating disorders) 2. The brainstem may be destroyed by direct invasion or indirect impairment of its blood supply (cerebrovascular disease) (tissue compression)

90
Q

Metabolic alterations in arousal

A

produce a decline by alterations in delievery of energy substrates as occurs with hypoxia, electrolyte disturbances, and hypoglycemia.
metabolic disorders caused by the liver or renal failure = alterations in neuronal excitability because of failure to metabolize or elliminate drugs/toxins.

91
Q

Psychogenic alterations in arousal (unresponsivenesss)

A

Uncommon, may signal general psychiatric disorders.

Despite apparent unconsciousness, person is physiolocally aware and the neurologic exam is normal

92
Q

What are 5 patterns of neurologic funcation to evaluate arousal?

A
  1. level of consciouness
  2. pattern of breathing
  3. pupillary reaction
  4. oculomotor responses
  5. motor responses
93
Q

What are the levels of altered consciousness?

A
  1. confusion- loss of ability to think rapidly and clearly; impaired judgement and decision making
  2. disorientation- Beginning loss of conscniousness; disorientation to time, then place and impaired memory; lost last is recognition of self
  3. lethargy- limited spontaneous movement of speech; easy arousal with normal speech/tough; may not be oriented to time, place, person
  4. obtundation- mild-moderate reduction in arousal with limited response to environment; falls asleep unless stimulated. minimal response to Q
  5. Stupor- a condition of deep sleep/unresponsiveness from which person can be aroused or open eyes at vigorous/repeated stimuli. response is often withdrawal or grabbing at stimulus
  6. light coma- assosicated with purposeful movement on stimulation
  7. coma- no verbal response to external environment to any stimulil; noxious stimuli (deep pain or suctioning) yeilds motor movement
  8. deep coma- associated with unresponsiveness or no respone to any stimuli
94
Q

What are the patterns of breathing?

A
  1. Normal- neural center in forebrain produces a rhythimc breathing pattern.
  2. Posthyperventilation- RR stop after hyperventilation has lowered the Paco2 level below normal. Rhythmic breathing returns when the Paco2 returns to normal. Location of injury: diffuse bilateral metabolic or structural diseae of cerebellum)
  3. Cheyne-Stokes RR- abnormal thythm of ventilation (periodic breathing) with alternating periods of hyperventilation and apnea (crescendo-decrescendo pattern) Damaged brain has higher Paco2 levels and stimulate ventilation. Paco2 decreases below normal and breathing stops until carbon dioxide reaccumulates and repeats the cycle. Cases seen in opiate or sedative drug overdose
95
Q

What are the patterns of breathing?

A
  1. Central reflex hypernea- sustained deep rapid but regular patter. Decreased Paco2 and a corresponding increase in PH and increased P02
  2. Apneusis- Prolonged inspiratory cramp (a pause at full inspiration). Common variant is a brief end-inspiratory pause of 2-3 seconds, alternating with an end-expiratory pause. Damage to RR control mechanism at pontine level, pontine infarction.
  3. Cluster breathing- Cluster of breaths has a disordered sequence with irregular pauses between breaths. Dysfunction in lower pontine and high medullary areas
  4. Ataxic breathing- completely irregular breathing occurs with random shallow and deep breaths and irregular pases. Rate is slow. Dysfunction of medulla
  5. Gasping breathing pattern (agonal gasps)- A pattern of deep “all-or-none” breathing is accompanies by slow respiratory rate. Indicative of a failing medullary RR center
96
Q

What is the pattern response after assessment of motor responses

A
  1. purposeful (defensive or withdrawal of limbs to noxious stimuli)
  2. inappropriate or not purposeful (generalized motor movement, posturing, grimacing or groaning)
  3. not present (unresponsive, no motor response)
97
Q

Abnormal motor response- Decorticate posturing

A

Upper extremity flexion, lower extremity extension. Slow developing flexion of arm, wrist and fingers with abduction in upper extremity and extension, internal roation, and plantar flexion of lower extremity.
Location of injury: hemispheric damage ABOVE midbrain releasing meduallry and pontine reticulospinal systems.

98
Q

Abnormal posturing: decerebrate posturing

A

Upper/lower extremity extensor response. Hyperextension of the vertebral column with clenching teeth, extension, abduction and hyperpronation of the arms; hyperpronation of the arms and extension of lower extremities.
Location of injury: Associated with severe damage involving midbrain or upper pons

99
Q

What are the forms of neurologic death?

A
  1. Brain death

2. Cerebral death

100
Q

Describe brain death

A

Occurs when brain damage is so extensive that it can never recover (irreversible) and cannot maintain the body’s internal homeostasis.
This includes irreversible cessation of function of the entire brain, including the brainstem and cerebellum.

101
Q

What is the criteria for brain death?

A
  1. Completion of all appropriate diagnostic and therapeutic procedures with no possibility of brain function recovery
  2. Unresponsive coma (no motor or reflex movements)
  3. No spontaneous respiration (apnea)
  4. No brainstem function (ocular responses to head turning, dilated, fixed pupils, no gag or corneal reflex
  5. Isoelectirc (flat) EEG
  6. Persistence of these signs for an appropriate observation period
102
Q

Describe cerebral death

A

Irreversible coma. The death of the cerbral hemispheres exclusive of the brainstem and cerebellum. Brain damage is permanent, person is unable to respond behaviorally significantly to the environment.
Brainstem may maintain internal homeostasis (body temp, CV functions, RR and metabolic functions)
May present in a coma, persisten vegetative state, minimally conscious state.

103
Q

Describe awareness (content of thought)

A

All cognitive functions, including awareness to self, environment and affective state (moods)

104
Q

What are some alterations in awareness/

A

Selective attention deficits, memory, nondeclarative memory (unconscious), amnesia, image processing and detection

105
Q

Selective attention disorders

A

Temporary, permanent or progressive. Seizure activity, parietal lobe contusions, subdural hematomas, stroke, gliomas/metatastic tumors, late Alzheimers dementia, frontotemporal dementai and psychotic disorders.

106
Q

Describe unilateral neglect syndrome

A

Failure to report, respond or orient to visual, auditory or tactile stimuli that are presented contralateral to a brain lesion. Given that this failure is not primary sensory/motor disorders.
Most cases, right parietal cortex is injured and the left side of the body/space is ignored.

107
Q

Describe memory

A

Recording, retention and retrieveal of information. 2 types of long term memory:
Declarative: learning and remembrance of spisodic memories (personal hx, events and experiences) and semantic memories (facts/information)
Nondeclarative (unconscious): memories for action, behavior or skill that become automatic

108
Q

What are some conditions that cause acute confusional states or delirium?

A
  1. Drug intoxication
  2. Alcohol or drug withdrawal
  3. Metabolic disorders (hypoglycemia, thyroid storm)
  4. Brain trauma or surgery
  5. Postanestesia
  6. Febrile illness or heat stroke
  7. Electrolyte imbalance, dehydration
  8. Heart, kidney, liver failure
109
Q

Describe Dementia

A

An acquired deterioration and a progressive failure of many cerrebral function of many cerebral functions that includes impairment of intellectual processes with a decrease in orienting, memory, language, judgement and decision making.
Person may exhibit alterations in behavior (agitation, wandering, aggression)

110
Q

What are some reversible causes of dementia

A

Infection: encephalitis, meningtitis, neurosyphilis
Normal pressure hydrocephalus: Chronic subdural hematoma, nutritional deficiencies
Drug intoxication: alcohol, sedatives
Metabolic disorders: Thyroid abnormalities, chronic hepatic encephalopathy, cerebral vasculitis, sarcoidosis
Tumors: Frontal and temporal love, pseudodementia of depression
Medial side effects: Anticholinergics, antihypertensives, antihistamines

111
Q

What are some irreversible causes of dementia?

A

Neurodegenerative disorders: Alzheimers, Dementia with Lewy bodies, frontotemporal dementia, pick disease, Huntington disease, Parkinson disease
Vascular disease: Vascular dementia, Multi-infarct, Amyloid angiopathy
Infection: Creutzfeldt-Jakob Disease, postencephalitic dementia, dementai assosicated with HIV

112
Q

Pathophysiology of dementia

A

Neuron degeneration, compression of brain tissue, atherosclerosis of cerbral vessels and brain trauma.
Genetic predisposition = neurodegenerative diseases: alzhiemers, huntington and parkinson
CNS infections = HIV, prions in Creutzfeldt-jakob disease lead to nerve cell degeneration and brain atrophy

113
Q

Describe Alzheimers Disease

A

Mental status: memory loss, disorientation to place and time, loss of facial recognition
Neurobehavior: Initially normal; progressive cognitive, language, abstraction and judgement impairment
Neurologic exam: Initially NORMAL

114
Q

Describe Creutzfeldt-Jakob disease

A

Mental status: Variable, frontal/executive, focal cortical, memory
Neurobehavior: depression, anxiety, decreased cognitive function and memory loss
neurologic exam: Myoclonus (quick, involuntary muscle jerk), rigidity, parkinsonism

115
Q

Describe dementia with Lewy Body

A

Mental status: Initially affects concentration and attention, then memory or cognition loss but unpredictable levels of ability, attention, or alertness. Delirium prone
Neurobehavior: Visual hallucination, depression, sleep disorder, delusion, transient loss of consciouness
neurologic exam: Parkinsonism, changes in walking or movement may present first

116
Q

Describe Frontotemporal disorders/degeneration/dementia

A

Mental status: PPA variant, language loss with talking less and speech becoming hesitant, or loss of understanding language, which may precede memory loss, spares drawing
Neurobehavior: Behavioral variant FTD, loss of empathy, apthay, increased inappropriate or decline in personal or social conduct, loss of judement and reasoning, hyperorality, euphoria, depression
Neurologic exam: Caused by CBD and PSP variants

117
Q

Describe Huntington disease

A

mental status: N/A
Neurohavior: Apathy, loss of interest early, impaired cognition, judgement, and memory occur later
Neurologic exam: Chorea, bradykinesia, dystonia

118
Q

Describe vascular dementia

A

mental status: Frontal/executive, cognitive slowing, memory can be intact
Neurobehavior: often but not always sudeen, usually within 3 months of a stroke, variable, apathy, falls, focal weakness, delusions, anxiety
Neurologic exam: Usually motor slowing, spasticity; can be normal or may have symptom improvement with stroke recovery

119
Q

Risk factors for Alzheimers disease

A

Greatest risk: age and family HX
DM, midlife HTN, hyperlipidemia, midlife obestity, smoking, depression, cognitive inactivity or low education attainment, female gender, estrogen deficit at time of menopause, physical inactivity, head trauma, elevated serum homocysteine and cholesterol levels, oxidative stress and neuroinflammation.

120
Q

What are some protective factors for Alzheimers disease?

A

lifelong activity, presence of apoE2 and antioxidant substances, omega-3 fatty acids, estrogen replacement at time of surgical menopause, low-calorie diet, and nonsteroidal anti-inflammatory agents.

121
Q

Pathophysiology of Alzheimers disease

A

Early onset: autosomal dominant and linked to 3 genes with mutations on chromosome 21.
Late onset: genetic- apolipoprotein E gene-allele 4 on chromosome 19: interferes with amyloid beta clearance from the brain and processed into neurotoxic fragments found in the plaques and tangles in the brain.
Sporadic late onset is most common and does not have a specific genetic association.
Accumulation of extracellular neuritic plaques containing a core of abnormally foled amyloid beta and tau proteins, intraneuronal neruofibrillary tangles and degeneration of basal forebrain cholinergic neurons with loss of acetylcholine. Failure to process and clear amyloid precursor protien results in accumulation of toxic fragments of amyloid beta protein that leads to formation of diffuse neuritic plaques, disruption of nerve impulse transmission and death of neurons.

122
Q

Stages and symptoms of Alzheimers disease.

A

Mild cognitive Impairment = Cognitive: mild memory loss, particularly for recent event (episodic memory) and new information (semantic memory). Functional: possibly depressed (vs apthay), mild anxiety
Early stage = Cognitive: measureable short-term memory loss, difficulty planning, disorientation to location. Functional: mild IADL problems
Middle stage = Cognitive: significant forgetfulness, easy to get lost, may dress inapporpriate, hallucincation. Functional: IADL dependent, some ADL problems
Late stage = Cognitive: little cognitive ability, language not clear, personality change, does not recognize family members, wantering, repetitive behavior. Functional: ADL dependent, incontinent, difficulty eating.
End stage = Cognitive: no significant cognitive function, loss of word speech. Functional: nonambulatory/ bedbound, unable to eat

123
Q

How to diagnose Alzheimers disease?

A

Clinical hx, including mental status exam (mini-mental status exam, clock drawing, geriatric depression scale), CSF analysis, brain imaging of structure, blood flow and metabolism, and course of illness (over the span of 5 years or more)
Genetic suspectibility test for PSEN1, PSEN2, APP are used to screen early-onset

124
Q

Treatment for Alzheimers

A

Treatment is directed at using devices to compensate for impaired cognitive function- memory aides, maintaining unimpaired cognitive functions, and maintaining or improving general state of hygiene, nutrition and health.
Cholinesterase inhibitors for mild-moderate cases
N-methyl-D-aspartate receptor antagonist blocks glutamate activity and may SLOW PROGRESSION from moderate-severe

125
Q

What cranial nerve with cause Bell’s Palsy?

A

Cranial nerve VII (facial)

126
Q

What is the patho for Bell’s Palsy?

A

Etiology is unknown.
Inflammatatory reaction compressing the facial nerve in the fallopian (facial) canal of the middle ear followed by demyelinating neural change.
Symptoms: unilateral facial weakness and inability to smile or whistle
May be caused by reactivation of herpesvirus in CN VII geniculate ganglia or an autoimmune response.

127
Q

Glasgow Coma Score

A

Score Best eye response Best verbal Response Best Motor response
1 No eye opening No verbal response No motor response
2 Eye opening to pain Incomprehensible sounds Extension to pain
3 Eye opening to verbal command Inappropriate words Flexion to pain
4 Eyes open spontaneously Confused Withdrawal from pain
5 N/A N/A Localized pain
6 N/A N/A Obeys Commands

128
Q

Results from Glasgow score

A

Mild brain injury: 13 or higher
Moderate brain injury: 9-13
Severe brain injury: 8 or less

129
Q

Describe traumatic brain injury

A

Alternation in brain function or other evidence pathology caused by an external force
Most common: falls for children and older adults followed by unintentional blunt trauma and motor vehicles accidents
Can be classified as PRIMARY and SECONDARY
PRIMARY: caused by direct impact or injury and can be focal, affecting one area of the brain or diffuse, involving more than one area of the brain
SECONDARY: indirect consequence of the primary injury and includes systemic responses and a cascade of molecular and chemical events that affect the brain.

130
Q

Describe focal brain injury

A

Caused by closed (blunt) trauma or open (penetrating) trauma

131
Q

Describe neural tube defects

A

Posterior defects:

  1. Anencephaly: The skull and much of the brain in missing. Pathologic mechanism unknown.
  2. Encephalocele: A saclike herniation of vaious amount of brain and meninges protrude through a defect in the skill; requires surgery to correct
  3. Meningocele: Saclike cyst of meninges filled with spinal fluid
  4. Myelomeningocele: Contains neural tissue, spinal cord or nerves
132
Q

What is congential hydrocephalus?

A

Imbalance between the production and reabsorption of CSF
Ventricular enlargement and increased intracranial pressure (dilates the ventricles and pushes or compresses brain tissue against the skull)
Obstructive hydrocephalus is most common; congenital aqueductual stenosis.

133
Q

Describe Cerebral Palsy

A

Disorder of movement, muscle tone or posture that is caused by injury or abnormal development in the immature brain.

134
Q

Risk factors for cerebral palsy

A

prenatal or perinatal cerebral hypoxia, hemorrhage, infection, genetic abnormalities, or low birth weight

135
Q

Describe pyramidal/spastic cerebral palsy

A

Results from damage to corticospinal pathway (upper motor neurons) and is associated with increased muscle tone, persistent primitive reflexes, hyperactive deep tendon reflexes, clonus, rigidity of extremities, scoliosis and contractures.

136
Q

Describe extrapyramidal/nonspastic cerebral palsy

A

caused by damage to cells in the basal ganglia, thalamus or cerebellum and includes 2 types: dyskinetic (movements are stiff, uncontrolled, abrupt and reptitive resulting in difficult fine motor coordination and purposeful movements and ataxic (gait disturbances and reflects cerebellar involvement)

137
Q

Describe Phenylketonuria (PKU)

A

inborn error in the metablisim of amino acids, characterized by phenylalanine hydroxylase deficiency and results in inablility of the body to conver essential amino acid phenylalanine to tyrosine.
Autosomal recessive disorder characterized by mutation of phenylalanine phdroxylase gene.
Elevated serum phenylalanine levels results in developmental abnormalities of the cerebral cortical layers, defective myelination and cystic degeneration of gray and white matter.
TX: reduction of dietary phenylalanine, must continue for life.

FNP 2.0 (2 decks)

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