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Patho > Week 8 Neuro > Flashcards

Week 8 Neuro Flashcards

1
Q

Name and explain the three levels of somatic sensation

A
  1. first order: these detect the sensation and the threat level and transmit them to the CNS
  2. second order: in the spinal cord; transmits message to the brain; this processes nociceptive information and is related to gait theory
  3. third order: in the brain; relays info from the thalamus to the cerebral cortex; projects pain information to the brain where it can interpret what that pain means to you
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2
Q

explain gate theory

A

the pain messages encounter “nerve gates” that control whether these signals are allowed to pass through to the brain

Ex: shaking your thumb after slamming it is a gate that stops those nerves from sending signals to your brain

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3
Q

Explain the types of nerve tracts and what pain response they elicit

A
  1. A delta fibers: large, unmyelinated fibers; fast pain

2. C fibers: small, unmyelinated; slow wave pain

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4
Q

What are the mediators mentioned in the mechanisms of pain slide? (excitatory, inhibitory, and both)

A

Excitatory (these augment/drive pain messaging): glutamate, dopamine, substance P

Inhibitory (suppressors): GABA, serotonin, opioid peptides (endorphins, enkephalins)

Both: acetylcholine

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5
Q

Explain the difference between a dorsal root ganglion and a dermatome

A

Dorsal root ganglion: all somatosensory information from the limbs and trunk shares a common class of sensory neurons. Dorsal root ganglion feed dermatomes

Dermatomes: region of the body supplied by a single pair of dorsal root ganglion

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6
Q

Name and explain the different types of pain

A
  1. cutaneous: arises from superficial structures such as skin and subcutaneous tissues; causes sharp, burning pain and is easily localized (pain is here)
  2. deep somatic: diffuse, originates in deep body structures such as periosteum, muscles, tendons, joints, and blood vessels (the connective tissues)
  3. visceral: originates in the visceral organs; one of the most common pains produced by disease
  4. referred: pain is perceived at a site different from its point of origin
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7
Q

explain why referred pain occurs with visceral pain

A

The visceral organs have very few nociceptors. The brain wants to make sense of the pain so it creates pain somewhere else that the pain could occur at places that follow the same dermatome. The areas that referred pain typically occur at are the subcutaneous areas where there are more nociceptors

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8
Q

Explain the difference between pain threshold and pain tolerance

A

Pain threshold: point at which a stimulus is perceived as pain. Does NOT significantly vary among people or in the same person over time

Pain tolerance: the duration of time or intensity of pain that an individual will endure before initiating overt pain responses; this pain is individualized and varies greatly among people and in the same person over time

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9
Q

Define hyperesthesia

A

unpleasant hypersensitivity

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10
Q

Define hyperalgesia

A

increase painfulness

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11
Q

Define hypoesthesia/anesthesia

A

reduced/lost tactile

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12
Q

Define hypoalgesia/analgesia

A

reduced/lost pain sensation

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13
Q

Define allodynia

A

pain after nonnoxious stimulus

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14
Q

What are the differences between acute and chronic pain?

What would the clinical manifestations be?

A

Acute: protective mechanism that alerts an individual to a condition or experience that is immediately harmful to the body; lasts less than 3 months

Clinical manifestations of acute pain: SNS response; pathologic response (vital sign changes)

Chronic: serves no protective purpose; lasts at least 3 months and is poorly understood. This pain does not respond to usual therapy

Manifestations of chronic: persistent chronic pain leads to physiologic adaptation; may cause behavioral and psychologic changes

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15
Q

Explain neuropathic pain

A
  • widespread pain that is not otherwise explainable and evidence of sensory deficit
  • peripheral nerve damage
  • small area peripheral nerve damage: nerve entrapment, tumors, neuralgias lead to pressure on nerve, chemical or physical injury to neuron
  • large area peripheral nerve damage: DM, chronic EtOH, hypothyroidism, renal insufficiency all caused by chronic ischemia and inflammation
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16
Q

Explain Neuralgia

What are the two types of neuralgia mentioned

A
  • severe, brief, often repetitive pain
  • occurs along spinal or cranial nerve
  1. trigeminal neuralgia - most common and most severe (CN 5)
  2. postherpetic neuralgia - nerve damage due to herpes virus
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17
Q

Name the types of headaches

A
  • migraines
  • tension-type
  • cluster headache
  • chronic daily headache
  • temporomandibular joint syndrome
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18
Q

Explain the characteristics of migraine headaches

A
  • migraine with or without aura
  • Cranial Nerve 5 activation (trigeminal)
  • vasodilation of meningeal blood vessels
  • increased blood flow creates pressure in the brain
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19
Q

Explain the characteristics of tension type headaches

A
  • most common
  • dull, aching, diffuse, nondescript headaches
  • “hatband”
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20
Q

Explain the characteristics of cluster headaches

A
  • more often in men

- episodes of headaches

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21
Q

Explain the characteristics of chronic daily headache

A
  • 15 days or more a month for 3 months
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22
Q

Explain the characteristics of temporomandibular joint syndrome

A
  • common cause of headache related to bruxism (teeth grinding), joint issues, poor bite
  • occurs at night
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23
Q

What is bruxism

A

teeth grinding

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24
Q

What are the assessment elements for motor units

A
  • body position
  • involuntary movements
  • muscle characteristics (strength, size, tone)
  • spinal reflexes (clonus)
  • coordination
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25
Q

Explain the types of muscle strength

A
  • paralysis = loss of movement
  • paresis = weakness
  • plegia = stroke or paralysis
  • mono = one limb
  • hemi = both limbs on one side
  • di- or para- = both upper limbs or both lower limbs
  • quadri- or tetra-= all four limbs
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26
Q

Explain fasciculations

A

muscles that twitch (eye muscle twitching)

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27
Q

Explain the different types of tone

A
  • hypotonia (normal): higher tone than normal; upper motor neurons control this
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28
Q

What is one of the most common muscle fiber disorder

A

muscular dystrophy

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29
Q

Explain muscular dystrophy and the most common type

A
  • genetic disorders (Duchenne’s)
  1. progressive deterioration of skeletal muscle
    - hypertrophy, atrophy, and necrosis
    - fat and connective tissue replaces muscle tissue (pseudohypertrophy)
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30
Q

What does pseudohypertrophy

A

the muscle fibers look bulked up but its not actually muscle fiber, its fat and connective tissue that has replaced muscle tissue

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31
Q

Name the drug and toxin induced disorders of the neuromuscular junction and explain why they make sense

A
  1. botulism: block ACh release which makes no muscle contractions and leaves the muscles paralyzed (botulism)
  2. curare: block/prevent depolarizations (poison)
  3. organophosphates: pesticides that are outlaws; typically used for bioweapons
  4. physostigmine or neostigmine: inhibits ACh; these would be given to someone with paralyzed gut because it will allow for peristalsis
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32
Q

Explain myasthenia gravis and what structure is effects

A
  • autoimmune disease that effects neuromuscular junctions
  • decrease in ACh receptors
  • myasthenia crisis (compromised ventilation, occurs during physical or emotional stress
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33
Q

What is the job of ACh E

A

it breaks down ACh

34
Q

What are the two types of injuries related to lower motor neuron disorders (LMN related to muscles)

A
  • mononeuropathies: compression such as carpal tunnel syndrome
  • polyneuropathies: demyelination and immune disorder (Guillain Barre syndrome which includes ascending paralysis and acute, influenzas like illness before the onset of symptoms)
35
Q

What are the 3 lower motor neuron disorders

A
  • injury
  • back pain
  • herniated disc
36
Q

What are the key functions of the cerebellum

A
  • to maintain equilibrium and posture
  • coordinated movement of the hands and fingers
  • coordinate sequential body and limb movements
37
Q

Name and explain the different pathways within the cerebellum

What would be affected if each pathway was injured

A
  1. vestibulocerebellar pathway: ear to cerebellum; this would cause truncal ataxia (can’t maintain trunk) and nystagmus (seeing someone’s eye pulsate/quiver)
  2. spinocerebellar pathway: spine to cerebellum; would cause dysmetria (over and under reaching when performing tests like touch my nose then touch my finger)
  3. cerebrocerebellar pathway: dystaxia or ataxia; this is when the sobriety walk would be useful because alcohol messes with this pathway
38
Q

What is the main function of the cerebellum

A

controls smooth and coordinated movements

39
Q

What are the basal ganglia dysfunction characteristics that you would see

A
  • tremors
  • tics (tourettes)
  • hypokinetic disorders
  • hyperkinetic disorders
40
Q

What are examples of the hyperkinetic disorders that occur with basal ganglia dysfunction

A
  • chorea: jerky movements
  • athetosis: continuous twisting movements
  • ballismus: violent flinging movements
  • dystonia: rigidity
41
Q

Explain Parkinson’s. Where is the damage? What is the presentation of it?

A

Definition: degenerative disorder; dorsal part of substantia nigra uses dopamine as a neurotransmitter so now you no longer have the dopamine to smooth your movements

Presentation:

  • tremor, rigidity, akinesia/bradykinesia, and postural changes
  • excessive sweating, sebaceous gland secretion, salivation
  • severe dementia (20% of the time)
42
Q

What are the upper motor neuron disorders

A
  • amyotrophic lateral sclerosis (Lou Gehrig’s)

- multiple sclerosis

43
Q

Explain amyotrophic lateral sclerosis. What are the effects of the motor neurons that it damages

A
  • damages both upper and lower motor neurons
  • UMN = weakness, lack of motor control with loss of control over spinal reflexes, stiffness, and spasticity
  • LMN damage = irritation which lead to fasciculations (eye twitching), decreased neuron firing, weakness, denervation atrophy, and hyporeflexia
  • no cognitive changes
44
Q

Explain multiple sclerosis

A
  • immune mediated
  • inflammation and destruction of mostly the CNS myelin (UMN)
  • decreased conduction velocity, conduction block
45
Q

What are the consequences of plaques forming when discussing upper motor neuron disorders

A
  • optic nerve
  • various nerve tracts (speech, swallowing, muscle strength, gait, coordination, balance)
  • conjugate gaze function
  • position, vibratory sensation
  • cognitive ability will eventually be affected
46
Q

Explain acute spinal cord injury. What can cause it? What are the effects of the primary neurologic injury

A
  • damage to the neural elements of the spinal cord
  • compression, rotational, flexion/extension injuries can cause it
  • primary neurologic shock: irreversible; complete transection leads to spinal shock which will cause flaccid paralysis, loss of DTRs, loss of sensation, loss of bowel and bladder function, loss of systemic sympathetic vasomotor tone
  • you’ll have to wait until the inflammation goes down to see the damage
47
Q

What is a secondary injury to the spinal cord? What are the possible causes of secondary injury to the spinal cord

A
  • neurons and white matter in the area of initial damage are affected

Possible causes:

  • damage to blood vessels supplying the area
  • decreased vasomotor tone decreasing blood supply
  • local release of substances that cause vasospasm
  • release of digestive enzymes from damaged cells
48
Q

Explain the characteristics of a complete spinal cord injury to upper and lower motor neurons and where in the spinal cord they would occur

A
  1. To upper motor neurons: (T12 and above)
    - spinal reflexes still work
    - no longer modulated by the brain (brain can’t control reflex arc)
    - hypertonia, spastic paralysis (the reflex arc is still intact so muscle fibers will respond)
  2. To lower motor neurons: (T12 and below)
    - cell in spinal reflex arcs damaged
    - flaccid paralysis
49
Q

Explain the movements that you will be able to perform if no damage is done to C5, C6, C7 and C8 with a spinal cord injury

Explain the respiratory muscle function functions that could occur with a spinal cord injury and the nerves involved

A
  1. Motor and somatosensory function
    C5 - deltoid and biceps function is spared (you can move arms
    C6 - wrist dorsiflexion by the wrist extensors is functional, allowing tenodesis
    C7 and C8 - full elbow flexion, wrist plantar flexion, and some finger; finger flexion added
  2. respiratory muscle function
    - C3 to C5: innervate the diaphragm (concerned about their breathing)
    - T1 to T7: innervate the intercostals, coughing and deep breathing
    - T6 to T12: abdominal muscles used for expiration
50
Q

Explain the chronic complications of a spinal cord injury, where they occur

A
  1. autonomic dysreflexia (most significant): T6 or above
  2. Vasovagal response: leads to severe bradycardia, potentially asystole (rapid position changes or deep suctioning)
  3. postural hypotension: T4 to T6 injury levels; interruption to sympathetic outflow to blood vessels in extremities
  4. immobility issues: DVT and skin issues
  5. Temperature regulation
51
Q

What are the common pathways to brain injury

A
  • the effects of ischemia
  • excitatory amino acid injury (Glutamate)
  • cerebral edema
  • injury due to increased intracranial pressure
52
Q

What are the conditions causing brain injury

A
  • trauma
  • tumors
  • stroke
  • metabolic derangements (hypoglycemia and lack of O2 are metabolic needs of the brain; those are 2 examples but not all inclusive)
  • degenerative disorders
53
Q

Define brain death and vegetative state

A

Brain death:

  • irreversible loss of function of the brain
  • apneic despite high CO2; no response to pain
  • absent brain stem reflexes

Vegetative state:

  • loss of all cognitive functions and awareness of self and surroundings
  • reflex and vegetative functions remain, including sleep-wake
  • spontaneous eye opening without concurrent awareness
  • brain stem is intact
54
Q

The brain is __% by weight, receives _____% of CO, using ____% of O2

A

2%, 15%, 20%

55
Q

Name and explain the two mechanisms of brain injury

A

Cerebral Edema

  • Vasogenic: extracellular fluid; there is impaired blood brain barrier; hemorrhage, brain injury, and infectious processes; inflammatory response which affects surrounding tissue and leaks into interstitium
  • Cytotoxic: intracellular fluid; hypoosmotic states or severe ischemia (NA-K failure); brain cells swell leading to confusion

Excitotoxic brain injury
- typical causes = stroke; hypoglycemic injury; trauma; chronic degenerative disorders such as Huntington disease and Alzheimer dementia

56
Q

When brain herniation occurs, what are the different mechanisms that the brain will use to ‘fix’ the situation

A
  1. first it’ll move around CSF to make room by squeezing out all CSF until it is at it’s minimum requirements
  2. if the pressure is still too high, the blood will be let go until the brain is at the bare minimum for blood as well
  3. Last to go is the brain; the self regulatory mechanisms fall and everything vasodilates which causes the brain to leak out
57
Q

What are the causes of hydrocephalus

A
  • an interference in cerebrospinal fluid flow either by decreased reabsorption, increased fluid production, or obstruction in the ventricular system
58
Q

Name and explain the types of hydrocephalus

A

Noncommunicating (intraventricular):

  • caused by an obstruction
  • entrance is broken (choroid plexus is broken)

Communicating (extraventricular):

  • caused by impaired absorption
  • the ‘exit’ (arachnoid villi) is broken
  • normal pressure hydrocephalus: occurs during middle age; wet, wacky, and wobbly

Acute:
- caused by head injury

59
Q

When discussing intracranial pressure, what is cerebral perfusion pressure? What is normal? How do we calculate it?

A

it is the pressure perfusing the brain; normal is about 70 to 100 mm Hg (its the minimum amount needed to perfuse the brain)

CPP = MABP - ICP

60
Q

What is one of the earliest and most reliable signs of increased ICP

A

a decrease in the level of consciousness

61
Q

What does an altered level of consciousness imply with a brain injury? What two sections is ALOC divided into?

What are the other manifestations of a brain injury related to altered LOC

A
  • implies diffuse brain injury

Two sections:

  • Arousal / wakefulness: RAS and both cerebral hemispheres
  • content / cognition: functioning cerebral cortex

Manifestations:

  • earliest sign = change in LOC
  • early changes = confusion, disorientation, blunted responses
  • confusion leads to lethargy leads to obtundation leads to stupor leads to coma
62
Q

What are the manifestations of brain injury

A
  • pupillary reflexes and eye movements (dolls eyes and blown pupils)
  • abnormal flexion (decorticate) and extension posturing (decerebrate)
  • respiratory response: early signs = yawning and sighing; moves to Cheyne-Stokes (something is wrong with the brainstem)
63
Q

What is a late sign of ICP

A

Cushing triad

64
Q

What are the components of Cushing Triad

A
  • irregular, decreased respirations (caused by impaired brainstem function)
  • bradycardia
  • systolic hypertension (widening pulse pressure) (systolic is high, diastolic stays low)
65
Q

What does traumatic brain injury lead to

A

contusions, hematomas, concussions, and diffuse axonal injury

66
Q

Primary and secondary traumatic brain injuries are due to what

A

Primary

  • focal lesions: contusions, hemorrhage (coup and contra-coup injuries)
  • diffuse injuries: concussion, diffuse axonal injury

Secondary injuries

  • brain swelling
  • infection
  • ischemia
67
Q

Explain the grading system of concussions

A

Grade I-II:
- attention and memory deficits but no loss of consciousness

Grade III:
- loss of consciousness of seconds to minutes

Grade IV:
- loss of consciousness <6 hours

68
Q

Explain the grading scale for diffuse axonal injury

A

Mild DAI:
- posttraumatic coma 6-24 hours

Moderate DAI:
- >24 hours

Severe DAI:
- brainstem signs that disappear after a few weeks (GCS 3-8; these look braindead but not

69
Q

Explain the three types of hematomas

A

Epidural:
- rapid bleeding; meningeal arteries (most serious because its an artery)

Subdural:

  • rupture of bridging veins
  • slower bleeding; gradual development over days or weeks
  • this is venous outflow so not as fast and furious
  • the brain shrinks because of hypernatremia which causes cells to shrink
  • elderly can tolerate longer because the brain naturally shrinks and the bridging veins are continuously rupturing

Subarachnoid:
- Blood in the CSF filled subarachnoid space

70
Q

Explain the different types of ischemic strokes

A 
Ischemic penumbra (halo): 
- tissue surround necrotic core, tissue integrity intact, but receives marginal blood flow/nutrients

Transient Ischemic Attacks (TIA):

  • transient deficit without time limits; best described as a zone of penumbra without central infarct
  • nothing died; practicing to have a stroke though
  • some part of the brain is denied blood flow but not enough to kill any part of the brain; the brain is stunned
Large Vessel (thrombotic): 
- often affect the cortex, causing aphasia or hemineglect, visual field defects, or transient monocular blindness

Small vessel (lacunar infarct):

  • tend to be purely motor, pure sensory
  • associated with dementia
  • aka vascular dementia
  • these are atherosclerotic plaques so people with heart disease are at risk

Embolic

71
Q

Explain Hemorrhagic stroke. Explain the sources, complications and causes

A
  • most frequently fatal stroke type

Causes:

  • advancing age and hypertension
  • trauma, tumors, blood coagulation disorders, drugs

Sources:

  • subarachnoid hemorrhage aneurysm (SAH)
  • AVM - arteries feed directly into veins through a vascular tangle of malformed vessels (vessels created inappropriately; its a knot of weak vessels that can rupture and cause stroke so they are clipped and removed)

Complications:
- vasospasms, compression of brain contents

72
Q

What are the different types of brain tumors

A
  • primary intracranial tumors of neuroepithelial tissue
  • primary intracranial tumors originating in the cranium: meninges, primary CNS lymphoma, pituitary gland tumors
  • metastatic tumors
73
Q

What are the presentations of brain tumors

A
  1. Focal disturbances
    - dysfunction of particular brain areas
    - seizures, hallucinations, weakness or palsies in specific areas, sensory deficits
    - dependent on where the damage is
  2. Generalized disturbances:
    - increased intracranial pressure: headache, vomiting, visual problems
74
Q

Name and explain the different types of seizures

A
  • abnormal, excessive nerve firing
  • provoked seizures: fever, metabolic imbalances, brain injury (tumors, drug abuse, vascular lesions)
  • unprovoked (epileptic) seizures: cause unknown
75
Q

What can seizures lead to if not resolved? What are the consequences of that condition?

A
  • medical emergency
  • seizures that do not stop spontaneously or occur in succession without recovery (the body who can’t keep up with metabolic demand)

Consequences:

  • adenosine triphosphate (ATP) is increased by 250%
  • cerebral oxygen consumption is increased by 60%
  • cerebral blood flow also increases by approximately 250%
  • a deficiency in ATP and glucose leads to hypoxia and acidosis which leads to progressive brain tissue injury
76
Q

Explain delirium

A
  • is an acute state of brain dysfunction
  • onset is usually abrupt
  • autonomic nervous system is overactive
  • is common in critical care units, post surgically, or during withdrawal from CNS depressants (e.g. alcohol or narcotics)
  • reversible
  • elderly, post surgery patients experience this
77
Q

Explain dementia

A
  • is the progressive failure of many cerebral functions
  • onset is usually gradual
  • progressive dementias produce nerve cell degeneration and brain atrophy
  • age is the greatest risk factor
  • not reversible
78
Q

Explain the pathophysiology of Alzheimer disease

A
  • decreased Ach
  • cortical atrophy, ventricular enlargement
  • neuritic plaques
  • neurofibrillary tangle
  • formal diagnosis of this is post mortem
79
Q

Explain the stages of Alzheimer Disease

A

Initial:
- short term memory loss

Moderate:

  • global cognitive impairment
  • language, spatial relationships, problem solving, depression, confusion, disorientation, lack of insight, inability to carry on daily activities

Severe:
- loss of ability to respond to environment; require total care, bedridden

80
Q

Name the other types of dementias mentioned in the PowerPoint

A
  • vascular - ischemic, hemorrhagic
  • frontotemporal - atrophy
  • Wernicke-Korsakoff syndrome – vitamin B1 deficiency
  • Huntington disease - autosomal dominant inheritance
81
Q

Explain Huntington disease

A
  1. hereditary disorder characterized by chronic progressive chorea, psychological changes, and dementia
  2. produces localized death of brain cells
    - severe degeneration of the basal ganglia and frontal cerebral cortex
    - depletion of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter
  3. abnormal movements that occur without conscious effort, emotional lability, and dementia
  4. Treatment:
    - no known treatment; dopamine receptor-blocking agents

Patho (10 decks)

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