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Pathology > 10 Nervous System > Flashcards

10 Nervous System Flashcards

1
Q

Definition of consciousness

A

State of awareness of oneself and the environment, and a set of responses to that environment

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2
Q

Two distinct components of consciousness

A

Arousal

Contents of thought

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3
Q

Arousal

A

State of awareness mediated by reticular activating system which produces arousal to cerebral hemispheres
RAS and brainstem can maintain vegetative state WITHOUT cerebral function
Cerebral functions cannot occur without RAS

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4
Q

Content of thought

A

All cognitive functions that embody awareness of self, environment, and affective states (emotions & moods, from limbic system, hypothalamus, and cerebral cortex)

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5
Q

Causes of altered LOC

A

Structural - Supratentorial lesions, infratentorial lesions, subdural, extracerebral, intracerebral
Metabolic
Psychogenic arousal alterations

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6
Q

Causes of altered LOC

A 
Infection
Vascular
Neoplastic
Congenital
Degenerative
Polygenic
Metabolic
Hypoxia, lytes, hypoglycem, drugs and toxins
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7
Q

Polygenic

A

When an inherited characteristic is controlled by two or more genes

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8
Q

Spectrum of altered LOC

A 
Confusion
Disorientation
Lethargy
Obtudnation
Stupor
Coma
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9
Q

Confusion - frontal lobe

A

Loss of ability to think rapidly and clearly. Impaired judgement

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10
Q

Disorentation - into cerebral cortex (past frontal lobe)

A

First step in loss of consciousness.

First disoriented to time then place then impaired memory and lastly recognition of self

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11
Q

Lethargy - limbic

A

Limited spontaneous movement or speech, easy to arouse with normal speech or touch. May not be oriented to time place person

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12
Q

Obtundation - RAS effected

A

Mild to moderate reduction in arousal with limited response to environment
Falls asleep unless stimulated
Questions answered with minimal response

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13
Q

Stupor - shutting down RAS

A

Condition of deep sleep or unresponsiveness, response is often withdrawal or grabbing at stimulus
Needs vigorous repeated stimulation for arousal

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14
Q

Coma

A

No verbal response to external environment

Stimuli such as deep pain or suctioning may have motor response

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15
Q

3 levels of coma

A

Light coma - purposeful movement with stimuli
Coma - non purposeful with stim
Deep coma - unresponsive

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16
Q

5 categories of neurologic function used to evaluate LOC

A 
LOC
Breathing patterns
Pupillary changes
ocular response
motor response
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17
Q

Most critical index of nervous system function

A

LOC

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18
Q

Breathing patterns

A

Brainstem takes over regulation with decreased LOC by responding to changes in PaCO2 (abnormal) should be in cerebrum

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19
Q

Cheyne-stokes - hemispheric breathing pattern

A

Crescendo in rate and depth in response to CO2 and a diminished ventilatory stimulus, breathing stops until CO2 reaccumulates

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20
Q

Brainstem patterns of breathing

A

Neurogenic hyperventilation - central neurogenic
Apneusis (pause at full inspiration) - pons shutting down
Cluster - irregular - medulla shutting down
Ataxic - slow, random depth, irregular
Gasping - slow “all or none”

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21
Q

Vomiting without nausea

A

Indicates neural mechanism, particularly associated with vestibular nuclei (pons)
floor of 4th ventricle
Brainstem compression secondary to ICP

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22
Q

Pupillary changes

A

Areas controlling pupil are adjacent to brainstem controlling arousal. Pupil changes are a valuable guide to evaluating level of brainstem function

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23
Q

Drugs effects on pupils

A

Atropine, scopolamine fix and dilate
Opiates pinpoint
Barbiturates can caused fixed
Ischemia and hypoxia often fix and dilate

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24
Q

Oculomotor response to neuro insult

A

Destructive or compressed brainstem can cause skewed deviation, dysconjugate gaze (one eye out) converging (one eye in) dolls eye (eyes stay put as head turns), nystagmus

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25
Q

Posturing

A

Decorticate rigidity - cortical damage mostly upper extremity flexion with / without extensor in leg response
Decerebrate posturing - severe hemispheric damage extensor response in upper and lower ext

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26
Q

Cerebral death (instead of brain death)

A

irreversible coma
death of cerebral hemispheres exclusive of brainstem and cerebellum
Brain can maintain homeostasis, pt not able to respond to environment in significant way

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27
Q

Brain death

A

Extensive, irreversible damage. No potential for recovery, body can’t maintain homeostasis
Destruction of cerebellum and brainstem
No discernible evidence of cerebral hemisphere function & the brainstems vital centers

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28
Q

Clinical criteria for brain death

A

Unresponsive coma
PCO2 greater than 60 mmHg without breathing efforts (apnea)
Absent cephalic reflexes, pupils fixed and dilated
Flat EEG
Persistence of these for 30-60 min and for 6 hour after coma onset

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29
Q

Survivors of cerebral death

A

Remain in coma, or awake in vegetable state

Mccaince also says minimally conscious state

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30
Q

Vegetable state (VS)

A

Wakeful unconscious state
Lack of cognitive function but not necessarily a reduced level of arousal
Sleep / wake cycles are present
Maintains brainstem reflexes

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31
Q

VS vs coma eyes

A

Spontaenous or to stimuli in VS

No opening on coma

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32
Q

VS vs coma awareness

A

Neither has any evidence of awareness, or communication

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33
Q

Seizure definition

A

Sudden, explosive, disorderly discharge of cerebral neurons, characterized by sudden, transient, alteration in brain function.
A syndrome, not a specific disease

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34
Q

Convulsion/epilepsy defintion

A

Clonic-tonic movement associated with some seizures

General term for primary condition causing seizures, no underlying/correctable cause

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35
Q

Aura

A

Gustatory, auditory, feeling of dizziness or numbness, ‘funny’ feeling

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36
Q

Prodroma

A

Early clinical manifestations such as headache, malaise, depression that may occur an hour / a few days before seizures

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37
Q

Tonic/clonic phase

A

State of muscle contraction where there is excessive muscle tone
Clonic phase is alternating contracting and relaxation of muscles

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38
Q

Causes of seizures

A

Cerebral lesions
biochemical
Cerebral trauma
epilepsy (birth injury, trauma)

39
Q

Precipitating factors of seizure

A

Hypoglycemia, fatigue, emotional or physical stress, febrile illness, large amounts of water, constipation, use of stimulants, withdrawal from depressants, hyperventilation, environmental stimuli (blinking lights, loud noises)

40
Q

Infra - low waves

A
41
Q

Theta

A

3-8 - sleep

42
Q

Alpha

A

8-12 meditation

43
Q

Beta

A

12-38hz awake

44
Q

Delta waves

A

.5-3hz

45
Q

Gamma

A

38-42hz

46
Q

Partial seizures

A

Begin local, focal motor - jacksonian (marches)

Involves only unilateral neurons, usually from cortical brain tissue

47
Q

Three types of partial seizures

A

Simple, complex, secondary generalized - refers to extent of foci

48
Q

Partial simple seziure

A

No impairment of consciousness
Slow, repetitive jerking of body part which increases strength/rate, hand turning or movement of eyes and/or possible pins and needles phenomenon

49
Q

Complex partial seizure

A

Some impairment of consciousness
Can originate as simple
Can interact with purposeful although inappropriate movements
E.g - automation, lip smacking, chewing, panting, picking

50
Q

Secondary generalized partial seizure

A

Partial onset evolving to generalized tonic clonic

51
Q

Generalized seizure

A

Both hemispheres, usually from subcortical or deeper brain focus - drop in LOC

52
Q

Types of generalized seizre

A

Petit mal, minor motor, limited grand mal, grand mal, drop attacks

53
Q

Tonic clonic

A

May have prodromal, sudden loss of consciousness
Generalized tonic muscle contractions, apnea with cyanosis, pupils dilated and unresponsive
Tonic phase is increase in tone
Clonic is jerking motions

54
Q

Tonic phase

A

<1 minute, clonic phase lasts 2-5 minutes, stupor or coma 5 minutes, postical

55
Q

Absence seizures

A

Simple abrupt sensation of activity 5-10 seconds

Complex - brief tonic clonic

56
Q

Lennox-Gastaut

A

1-5 years old
Cognitive and motor dysfunctions
Experience decrease cognitive and motor development

57
Q

Juvenile Myoclonic epilepsy (JME) - possibly same as lennox but later in life

A

Adolescents and young adults
Possible chromosomal
No decline in cognition

58
Q

Infantile spasms

A

Flexor spasms of extremities and head
4-8 months
Idiopathic or in response to CNS insult
West syndrome

59
Q

Myoclonic seizures

A

Sudden, uncontrolled, one or more extremity, often in morning, momentary loss of consciousness followed by postictal

60
Q

Epileptic patho

A

Group of neurons with loss of afferent stimulation
Neuronal cell plasma membranes are more permeable –> hypersensitive and possibly in a partially depolarized state (chronically)
Firing becomes greater until threshold hit
Discharge spreads to normal neurons
Brainstem and subcortical area causes tonic phase and LOC
Movement through basal ganglia and cortex causes clonic phase
Continues until epileptogenic neurons become exhausted

61
Q

Seizure numbers

A

During seizure 250% more ATP
60% increase in cerebral O2 consumption
Bloodflow increased 250%

62
Q

Patho of severe seziures

A

ATP deficiency occurs along with phosphocreatine and glucose causing secondary hypoxia, acidosis, lactic acid accumulation.
All 3 may result in progressive brain tissue injury and destruction

63
Q

Basilar skull fracture

A

75% involve temporal bone, battle signs/racoon eyes. Often aggressive as damage is near limbic system or irritable if unconscious
extends to base of skull
Often arise as extensions of a linear fracture of cranial vault

64
Q

Concies

A

Less than 5 min loss of consciousness
no structural damage, but cognitive dysfunction
T-tau
Can have bradycardia and hypotension (30 seconds)

65
Q

Brain contusion

A

Edema and bleeding
ICP can take 24 hours to manifest, 72 hours to peak
Slower recovery

66
Q

Epidural hematoma

A

85% arterial
Between skull and dura mater
Brief LOC, lucid period (few hours to days if venous)
As hematoma builds, headaches (increasing severity) vomiting, drowsiness, confusion, seizure, hemiparesis

67
Q

Subdural hematoma

A

Between dura and arachnoid, acute or chronic

68
Q

Acute subdural

A

Within hours -
ICP
Headache, drowsiness, restlessness, agitation, confusion, LOC

69
Q

Epi vs sub

A

Epidural usually begins with LOC, subdural progresses

70
Q

Chronic subdural

A

Days to weeks to accumulate
More common in oldies at drunks
Headache and dementia

71
Q

Subarachnoid hematoma

A

Trauma, aneurysm, hypertension
Not a space occupying like sub and epi, but rather inflamm response for blood contacting neural tissue
ICP
N/V visual disturbances, nuchal rigidity
Often near circle of willis

72
Q

Intracerebral hematoma

A

Associated with contusions - frontal/temporal
Compression, edema, ICP
Major inflamm
Decreasing LOC

73
Q

Vomiting in head injury

A

Compressed lateral ventricles push fluid into 3rd then 4th ventricle, 4th ventricle pushes on vomit centre. No nausea precipitating

74
Q

Bursa

A

Fluid filled sac which protects muscles and ligaments

75
Q

Spinal Cord Injuries

A

Vertical compression can injure anywhere

Rotational forces damage supporting ligaments, fracture vertebrae, common at thoracic/lumbar

76
Q

Types of SCI

A 
Cord concussion, contusion or compression - swelling and ischemia, temp loss of function
Laceration - may be permanent
Transection - permanent/complete loss 
Hemorrhage - usually no major loss
Damage/loss blood supply - ischemia
77
Q

Causes of back pain

A

Idiopathic, tumours, disk prolapse, bursitis, abnormal bone pressures, inflammation, ligament sprains

78
Q

Degenerative disk

A

Biochemical alterations of intervertebral disk tissue

79
Q

Spondyloysis

A

Forward displacement of vertebra due to structural deficit

80
Q

Spondylolisthesis

A

Vertebra slide forward

81
Q

Spinal stenosis

A

Nerve roots become entrapped

82
Q

Lumbar disk herniation

A

Protusion of nucleus pulposis (compresses nerve root)

83
Q

Normal ICP

A

5-15mmHg

84
Q

Increased ICP causes

A

Increased content (tumor)
edema
Excess CSF
Hemorrhage

85
Q

Stage 1 of ICP

A

Altered cerebral blood volume
Vasoconstriction and external compression of venous system
May compensate with no ICP change
Subtle S&S, transient, slight confusion, drowsiness, pupil changes

86
Q

Stage 2 of ICP

A

Intracranial HTN
Overcomes compensatory mechanism
Neural O2 compromised
Systemic vasoconstriction, increased BP to overcome ICP
Decreased LOC, Cheyne stokes, sluggish/dilated pupils/ bradycardia

87
Q

Stage 3 of ICP

A

Loss of cerebral blood flow autoregulation
CO2 retention causes vasodilation
BP drops but blood volume increases (further ICP)
Severe hypoxia, acidosis

88
Q

Stage 4 of ICP

A

Brain herniation, further blood supply compromise
Cerebral blood flow eventually ceases
Loss of vital functions

89
Q

Clinical manifestations of ICP

A 
Decreased LOC
headache
N/V
Vital signs (Up BP, wide PP, bradycard)
Papilledema
Sluggish then fixed and dilated pupils
90
Q

Papilledema

A

Increased ICP compresses optic nerve

91
Q

Cerebral edema causes

A 
Trauma
Tumor
Infection
Ischemia/infarct
hemorrhage
hypoxia
92
Q

Harmful effects of cerebral edema

A

from distortion of vessels, displacement of brain tissue and herniation

93
Q

4 types of cerebral edema

A

Vasogenic (increased cap perm)
Cytotoxic
Ischemic (following infarction)
Interstital (with hydrocephalus)

Pathology (24 decks)

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