Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CBRC > CNS Disorders > Flashcards

CNS Disorders Flashcards

1
Q

Types of CNS Disorder

A
  • These are disorders within the brain and spinal cord
    • Traumatic Brain Injury (TBI)
    • Strokes
    • Infections – Meningitis, Encephalitis
    • Seizures
    • Tumors
    • Spinal Cord Injuries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Layers of Meninges of the Brain

A

Dura Mater (outer layer)

Arachnoid

Pai Mater (inner layer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Respiratory Center in the Brain Stem

A
  • Inspiratory Area (Medulla)
    • Stimulates the muscles of inspiration and eventually the pneumotaxiccenter
  • Expiratory Area (Medulla)
    • Inhibits the inspiratory center (mostly during high RR, and Vt.)
  • Apneustic Area (Pons)
    • Stimulates the inspiratory center
  • Pneumotaxic Area (Pons)
    • Inhibits apneusticand inspiratory center and allows exhalation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Central Neurogenic Hyperventilation

A

May be the result of compression of the mid-brain from edema or trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Central Neurogenic Apnea

A

Total loss of all respiratory drive

Destruction of the entire respiratory drive center

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Biot’s Breathing

A
  • Characterized by short episodes of rapid uniformly deep inspiration followed by periods of 10 to 30 seconds of apnea
  • Caused by damage to, or pressure on, the medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Apneustic Breathing

A
  • Prolonged insp. gasping
  • Pons damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Central Reflex Hyperpnea

A

Continuous deep breathing

Pons damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Central Reflex Hypopnea

A

•Head trauma, brain hypoxia, narcotic suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cheyne-Stokes Breathing

A
  • Cycles of gradual increase in rate and volume followed by gradual decrease, then a period of apnea before it repeats
  • Associated with decreased cardiac output (heart failure), central sleep apnea, and damage to respiratory centers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Kussmaul’s Breathing

A

Rapid and deep breaths associated with metabolic (often diabetic keto-acidosis),not neurogenic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cerebral Blood Flow and CO2

A

Mediated through formation of H+

­CO2 dilates brain vessels = CBF

Ventilation strategies include low-normal PaCO2 to ¯CBF and ¯ICP

Temporarily we may hyperventilate more than this but the disadvantage is decreased oxygen delivery to the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cerebral Blood Flow and ICP

A

Normal ICP is 10-15 mmHg

Small fluctuations normal; variability > 10 mmHg a bad sign

At 15-20 mmHg capillary bed is compressed and microcirculation is compromised; > 20 mmHg is intracranial hypertension

At 30-35 mmHg venous drainage is impeded and edema develops in uninjured tissue

CPP = MAP – ICP

ICP increase of 1 mmHg= Decrease CBF by 0.5-0.7 mL

PaCO2 decrease of 1 mmHg=3% decreased in CBF

PaCO2¯of 1 mm Hg = 3% ¯in CBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Traumatic Brain Injury

A

–Damage to the brain caused by external mechanical force

–Can be classed by severity, location (e.g. subdural hematoma), mechanism (closed vs. open)

TBI is a major cause of death and disability world wide!

Disabilities extend from the physical to include impact on cognitive, social, emotional and behaviouralfunctions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Traumatic Brain Injury

Major Causes

A
  • MVC/motorbikes
  • Sports related
  • Falls
  • Violence/abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TBI- Mild Injury

A
  • Glasgow Coma Scale 13-15, loss of consciousness up to 15 minutes
  • Usually recover
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

TBI- Moderate Injury

A
  • GCS 9-12, LOC up to 6 hours, may deteriorate because of rising ICP
  • CT scan useful but may not need hemodynamic or respiratory support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TBI- Severe Injury

A
  • GCS 3-8, LOC over 6 hours, CT scan to identify extent of damage
  • Respiratory and circulatory support usually needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Combative Patient

A

Combative patients may need to be heavily sedated to acquire a CT scan, necessitating intubation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

TBI- Mild Injury

Signs and Symptons

A

Headache, nausea and vomitting, lack of motor coordination, dizziness, clumsiness, visual disturbances, changes in sleep patterns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

TBI- More Severe Injury

Signs and Symptons

A
  • Loss of consciousness
  • Dilation of one or both pupils; blown pupils
  • Respiratory depression
    • Cushing’s triad: slow heart rate, high blood pressure and respiratory depression a sign of high ICP
  • Paralysis/weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cushing’s Traid

A

Cushing’s triad: slow heart rate, high blood pressure and respiratory depression a sign of high ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

TBI and Posturing

A
  • Damage to the cerebrum may cause decorticate posturing.
    • Arms, wrists and fingers will be flexed (bent in on themselves) and adducted (turned inward)
    • Legs will be rigid and straight (extended), feet rotated inward
  • Damage to the brain stemmay cause decerebrate posturing
    • Arms are extended and rotated inward
    • Legs and feet are rigid and hyper-extended
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Epidural Hemotoma

A

–Accumulation of blood between the skull and the outer duralayer. Usually from impact type trauma.

–May be rupture of the meningeal artery. Victim may fair well at first and then deteriorate rapidly as fluid accumulates.

–Treatment is immediate cerebral drainage (burr hole).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Sub Dural Hematoma

A
  • Accumulation of blood between theduraand arachnoid layers
  • Usually acceleration/ deceleration injury that caused rupture of cerebral veins
  • Typed by onset of symptoms:
    • Acute: within 48 hours of injury
    • Sub-acute: 3 to 20 days
    • Chronic: 20 or more days post injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Intracerebral Hematoma

A

–Blood in the parenchyma of the brain, could be from any of the previous types of traumas

–Ventricles fill with blood and enlarge, displacing other tissues

–Immediately life threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

TBI

Penetrating Injuries

A

–E.g. knives, bullets, projectiles

–Obviously life-threatening

–Vascular tearing as projectile enters the skull

–Small caliber bullets tend to ricochet around inside the skull and leave no exit wound

–Foreign matter introduced to brain tissue, possible infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Concussions

A

–Mild, diffuse injury to the brain; effects can last for years

–Typically due to acceleration/deceleration type injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Concussion Initial Symptons

A

Temporary loss of normal function (confusion, disorientation, amnesia),

Loss of consciousness

30
Q

Concussion Post Event Symptons

A

Headache, irritability, lack of concentration, visual disturbances

31
Q

Pathophysiology of Primary Injury of TBI

A

•The tissue damage that occurs at the moment of injury

32
Q

Pathophysiology of Secondary Injury of TBI

A

Complex processes may result:

  • Inflammation
    • Damage from inflammatory mediators
    • Cellular dysfunction
  • Cerebral edema
  • Increased ICP
  • Impaired cerebral perfusion and resulting ischemia and hypoxia
  • Brain death/herniation

Also may see complications such as arrhythmias and neurogenic pulmonary edema

33
Q

TBI

Diagnostic Interventions-Complete Neurological Exam

A

Diagnostic imaging

CT: quick and accurate; serial CTs

MRI: more detail; more info on long term outcome

Angiography

34
Q

TBI

Diagnostic Interventions-ICU Setting

A
  • ICP monitoring
    • Fluid filled vssolid-state systems
    • EVD capabilities for therapeutic management
  • SjvO2
  • Licox
  • EEG
35
Q

Management- Acute Phase

Manage the Primary Injury

A
  • Transport to a neurotreatment center!
  • Manage the primary injury
  • Supportive management
    • Airway, ventilation, circulation
    • Surgery
    • Remove masses/hematomas
    • Foreign objects/debris
    • Debridement of damage tissue
    • Perform craniotomy
36
Q

Management Acute Phase

Manage Secondary Injury

A
  • Therapeutic hypothermia
  • Controlling ICP
    • Patient positioning
    • Sedation/analgesia, +/- paralytics
    • Therapeutic hyperventilation
      • Consider vent strategy and ABG goals
    • Extra-ventricular Drain (EVP)
  • Maintain CPP through ensuring adequate/high MAP
    • Fluids and vasopressors if BP too low
  • Manage the cerebral edema
    • Mannitol
    • Lasix
    • Hypotonic saline
37
Q

TBI Management: Chronic Phase

A
  • Some patients remain in a vegetative state
  • Risk of complications (infection, DVT, pressure sores, pneumonia)
    • Rehabilitation!
      • This may last months to years
  • Includes:
    • Physiotherapy
    • Speech and language therapy
    • Cognitive rehabilitation therapy
    • Occupational therapy
    • Mental health support
    • Therapists, psychologists, psychiatrists
38
Q

Stroke

A

–A rupture or blockage of a blood vessel in the brain, depriving parts of the brain of blood supply

–The area of ischemia can become permanently damaged, creating an area of infarct

–Long term effects of stroke depend on the region and size of the area of infarct

–Results in loss of consciousness, paralysis or other symptoms depending on the site and severity of the injury

39
Q

Ischemic Stroke

A
  • Thrombotic strokes
    • Caused by a blood clot that forms in an artery directly leading to the brain
  • Embolic strokes
    • Occur when a clot develops somewhere else in the body and travels through the blood stream to the brain
  • TIA (Transient Ischemic Attack)
    • Caused by a temporary interruption of blood flow to the brain; symptoms are similar to an ischemic stroke except they go away within a few minutes or hours
40
Q

Hemorrhagic Strokes

A

Occur when an artery inside the brain - precipitated by smaller artery bleeds, hypertension and/or a sudden stress

41
Q

Predisposing Factors of Stroke

A

Common cause of death in persons over 65 years of age

Predisposing conditions include:

  • Genetics
  • Hypertension
  • Diabetes
  • High cholesterol
  • Smoking
  • Cardiac disease
  • Oral contraceptives
42
Q

Sincinnati PreHospital Stroke Scale

A
  • Facial Droop
    • One side of the face does not move as well as the other side
  • Arm Drift
    • When holding both arm straight out one arm will begin it drift down
  • Abnormal speech
    • slured words, using wrong words, unable to speak
43
Q

Meningitis

A
  • Infection of the membranes that surround the brain and spinal cord
  • Meningitis is an inflammation the membranes covering the brain and spinal cord:
    • Dura mater
    • Arachnoid
    • Piamater
44
Q

Encephalitis

A

•Inflammation of the brain itself, usually caused by infection

45
Q

Myelitis

A

•Infection of the spinal cord

46
Q

Meningitis vs. Encephalitis

A

These can occur concurrently: e.g. encephalomyelitis

47
Q

Encephalitis Etiology

A
  • Any pathogen can invade brain tissue and begin an inflammatory response
  • Pathogens:
    • Most often viral (people, food/drink, vectors like mosquitos or ticks…e.g. West Nile)
    • Many of the current vaccines protect against this (e.g. MMR)
    • Herpes simplex virus is the most common cause.
48
Q

Encephalitis Pathophysiology

A
  • Inflammation
  • Swelling (cerebral edema)
    • Can caused increased ICP, abnormal reflexes
  • May see:
    • Destruction of nerve cells
    • Intracerebralhemorrhage
    • Brain damage
49
Q

Encephalitis Initial Symptons

A

Initial symptoms are mild

Low-grade fever

Headache, malaise

Clumsiness, unsteadiness, rigidity

Confusion, lethargy, drowsiness

Nausea/vomiting

50
Q

Encephalitis As the Disease Progresses

A

Progressing to more serious as condition worsens

Loss of consciousness, respiratory depression

Muscle weakness/paralysis

Seizures

51
Q

Encephalitis Diagnosis

A

–MRI or CT of head

–Lumbar puncture and CSF exam/culture

–Serology tests to detect virus

52
Q

Encephalitis Management

A
  • Supportive care
  • Possibly antivirals
    • Acyclovir/Zoviraxand foscarnet/Foscavirfor Herpes
  • Antibiotics if bacterial etiology
  • Corticosteroids for swelling (possibly)
53
Q

Meningitis Pathogens

A
  • Viruses, parasites, fungal…
  • Bacterial meningitis is rare but deadly
    • Pneumococcal, meningiococcalpathogens most common
    • Vaccines available
54
Q

Meningitis Symptons

A

Similar to encephalitis but often characterized by

  • Sudden fever (bacterial)
  • Severe headache
  • Stiff neck/stiff back
55
Q

Meningitis Diagnosis

A

–Lumbar puncture and examination/culture of CSF

56
Q

Seizures

A
  • Are a symptom of an underlying brain problem
  • Result from sudden, abnormal electrical activity in the brain
    • Often, but not always, associated with convulsions
    • Note: Though often used interchangeably, seizures ≠ convulsions!
57
Q

Focal Seizure

A

•Happen in just one part of the brain

58
Q

Generalized Seizure

A

Happen on both sides of the brain

Can be:

  • Grand Mal (generalized tonic-clonic)
  • Absence (brief loss of concsiousness)
  • Myoclonic (sporadic/isolated jerking movements)
  • Clonic(repetitive jerking movements)
  • Tonic (muscle stiffness, rigidity)
  • Atonic (loss of muscle tone
59
Q

Seizure Etiology

A

NUMEROUS! Some causes include:≠

Those of CNS origin

  • Infectious (encephalitis, meningitis)
  • Head injuries
  • Stroke
  • Epilepsy

Those of systemic origin

  • Electrolyte imbalances (Na+ particularly)
  • Hypoglycemia
  • High fever
  • Kidney or liver failure
  • Illicit drugs
  • Withdrawal (ETOH, Benzos, analgesics…)
60
Q

Seizure Symptons

A

Occur suddenly! May include: Convulsions

Or less obvious:

  • Blank stare
  • Eye movements
  • Grunting, snorting
  • Sudden falling
  • Teeth clenching
  • Mood changes
  • Tasting a bitter, metallic flavour
  • Can last few seconds or up to 15 minutes

Most stop by themselves

61
Q

Seizure Warning Signs

A
  • Fear/anxiety
  • Nausea
  • Vertigo
  • Visual symptoms (bright spots, wavy lines…)
62
Q

Seizure Management

A

–Protect the person from injury during the seizure

–Determine the underlying cause

63
Q

Seizures are a Medical Emergency When

A

Seizures are prolonged (more than 5 min)

  • Treat with Benzodiazepenesas first line, possibly propofolor barbituates
  • Anti-epileptic drugs if recurring
  • EEG monitoring done to monitor background activity

The patient doesn’t wake up

64
Q

Seizure Supportive Care

A

•Airway management, ventilation

65
Q

Brain Tumors

A

There are several types of brain tumors. They are generally named for their site or tissue of origin (E.g. Oligodendrogliomas, astrocytomas, medullablastomas, meningiomas…)

Any tumor will have local effects on the surrounding tissue

If the tumor affects the respiratory center, apneas or dysfunction will result. Blood vessel patency can be compromised

Depending on the size of the growth, ICP will rise causing possible compression of brain tissue and subsequent pathology and manifestations

66
Q

Spinal Tumors

A
  • Will cause local tissue dysfunction
  • Blood vessel compromise and CSF blockage may compound dysfunction
  • Any nerve root distal to the tumor will be effected negatively, therefore
    • Tumors in the cervical spine can cause complete loss of breathing function
    • Tumors in the thoracic spine may effect inter-costal function etc.
67
Q

Tumors Clinical Manifestation

A

Slow growing lesions may be compensated for by the relative shrinking of cerebral ventricles

Clinical manifestations depend on the size and location of the lesion

Possible symptoms include:Headache, nausea and vomiting, mental changes, papilledema, visual disturbances, alterations in sensory and motor function and seizures

68
Q

Spinal Cord Injury

A

Any injury to the nerves of the spinal cord that is caused by trauma instead of disease

69
Q

Incomplete Spinal Cord Injury

A

Damage or dysfunction due to mechanical injury or edema to a part of the cord

70
Q

Complete Spinal Cord Injury

A

Total sensory, motor and autonomic dysfunction distal to the injury

Paraplegia is the result of thoracic/lumbar injury

Quadriplegia is the result of cervical injury

71
Q

Spinal Cord Injury and Spinal Nerves

A

Nerves involved in accessory muscles (sternocleidomastoid, scalene) exit the spine, C1 to C5

Severe damage or severance at C4 or higher will lead to profound respiratory deficit.

Phrenic nerve branches exit the spinal column at C3, C4, and C5

Inter-costal nerves exit the spine from T1 to T 12

Abdominal nerves used in forced exhalation exit the spine, T7 to L1

CBRC (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions