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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
Posturing
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
26
Cerebral death (instead of brain death)
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
27
Brain death
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
28
Clinical criteria for brain death
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
29
Survivors of cerebral death
Remain in coma, or awake in vegetable state | Mccaince also says minimally conscious state
30
Vegetable state (VS)
Wakeful unconscious state Lack of cognitive function but not necessarily a reduced level of arousal Sleep / wake cycles are present Maintains brainstem reflexes
31
VS vs coma eyes
Spontaenous or to stimuli in VS | No opening on coma
32
VS vs coma awareness
Neither has any evidence of awareness, or communication
33
Seizure definition
Sudden, explosive, disorderly discharge of cerebral neurons, characterized by sudden, transient, alteration in brain function. A syndrome, not a specific disease
34
Convulsion/epilepsy defintion
Clonic-tonic movement associated with some seizures | General term for primary condition causing seizures, no underlying/correctable cause
35
Aura
Gustatory, auditory, feeling of dizziness or numbness, 'funny' feeling
36
Prodroma
Early clinical manifestations such as headache, malaise, depression that may occur an hour / a few days before seizures
37
Tonic/clonic phase
State of muscle contraction where there is excessive muscle tone Clonic phase is alternating contracting and relaxation of muscles
38
Causes of seizures
Cerebral lesions biochemical Cerebral trauma epilepsy (birth injury, trauma)
39
Precipitating factors of seizure
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
Infra - low waves
41
Theta
3-8 - sleep
42
Alpha
8-12 meditation
43
Beta
12-38hz awake
44
Delta waves
.5-3hz
45
Gamma
38-42hz
46
Partial seizures
Begin local, focal motor - jacksonian (marches) | Involves only unilateral neurons, usually from cortical brain tissue
47
Three types of partial seizures
Simple, complex, secondary generalized - refers to extent of foci
48
Partial simple seziure
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
Complex partial seizure
Some impairment of consciousness Can originate as simple Can interact with purposeful although inappropriate movements E.g - automation, lip smacking, chewing, panting, picking
50
Secondary generalized partial seizure
Partial onset evolving to generalized tonic clonic
51
Generalized seizure
Both hemispheres, usually from subcortical or deeper brain focus - drop in LOC
52
Types of generalized seizre
Petit mal, minor motor, limited grand mal, grand mal, drop attacks
53
Tonic clonic
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
Tonic phase
<1 minute, clonic phase lasts 2-5 minutes, stupor or coma 5 minutes, postical
55
Absence seizures
Simple abrupt sensation of activity 5-10 seconds | Complex - brief tonic clonic
56
Lennox-Gastaut
1-5 years old Cognitive and motor dysfunctions Experience decrease cognitive and motor development
57
Juvenile Myoclonic epilepsy (JME) - possibly same as lennox but later in life
Adolescents and young adults Possible chromosomal No decline in cognition
58
Infantile spasms
Flexor spasms of extremities and head 4-8 months Idiopathic or in response to CNS insult West syndrome
59
Myoclonic seizures
Sudden, uncontrolled, one or more extremity, often in morning, momentary loss of consciousness followed by postictal
60
Epileptic patho
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
Seizure numbers
During seizure 250% more ATP 60% increase in cerebral O2 consumption Bloodflow increased 250%
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Patho of severe seziures
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
Basilar skull fracture
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
Concies
Less than 5 min loss of consciousness no structural damage, but cognitive dysfunction T-tau Can have bradycardia and hypotension (30 seconds)
65
Brain contusion
Edema and bleeding ICP can take 24 hours to manifest, 72 hours to peak Slower recovery
66
Epidural hematoma
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
Subdural hematoma
Between dura and arachnoid, acute or chronic
68
Acute subdural
Within hours - ICP Headache, drowsiness, restlessness, agitation, confusion, LOC
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Epi vs sub
Epidural usually begins with LOC, subdural progresses
70
Chronic subdural
Days to weeks to accumulate More common in oldies at drunks Headache and dementia
71
Subarachnoid hematoma
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
Intracerebral hematoma
Associated with contusions - frontal/temporal Compression, edema, ICP Major inflamm Decreasing LOC
73
Vomiting in head injury
Compressed lateral ventricles push fluid into 3rd then 4th ventricle, 4th ventricle pushes on vomit centre. No nausea precipitating
74
Bursa
Fluid filled sac which protects muscles and ligaments
75
Spinal Cord Injuries
Vertical compression can injure anywhere | Rotational forces damage supporting ligaments, fracture vertebrae, common at thoracic/lumbar
76
Types of SCI
``` 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
Causes of back pain
Idiopathic, tumours, disk prolapse, bursitis, abnormal bone pressures, inflammation, ligament sprains
78
Degenerative disk
Biochemical alterations of intervertebral disk tissue
79
Spondyloysis
Forward displacement of vertebra due to structural deficit
80
Spondylolisthesis
Vertebra slide forward
81
Spinal stenosis
Nerve roots become entrapped
82
Lumbar disk herniation
Protusion of nucleus pulposis (compresses nerve root)
83
Normal ICP
5-15mmHg
84
Increased ICP causes
Increased content (tumor) edema Excess CSF Hemorrhage
85
Stage 1 of ICP
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
Stage 2 of ICP
Intracranial HTN Overcomes compensatory mechanism Neural O2 compromised Systemic vasoconstriction, increased BP to overcome ICP Decreased LOC, Cheyne stokes, sluggish/dilated pupils/ bradycardia
87
Stage 3 of ICP
Loss of cerebral blood flow autoregulation CO2 retention causes vasodilation BP drops but blood volume increases (further ICP) Severe hypoxia, acidosis
88
Stage 4 of ICP
Brain herniation, further blood supply compromise Cerebral blood flow eventually ceases Loss of vital functions
89
Clinical manifestations of ICP
``` Decreased LOC headache N/V Vital signs (Up BP, wide PP, bradycard) Papilledema Sluggish then fixed and dilated pupils ```
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Papilledema
Increased ICP compresses optic nerve
91
Cerebral edema causes
``` Trauma Tumor Infection Ischemia/infarct hemorrhage hypoxia ```
92
Harmful effects of cerebral edema
from distortion of vessels, displacement of brain tissue and herniation
93
4 types of cerebral edema
Vasogenic (increased cap perm) Cytotoxic Ischemic (following infarction) Interstital (with hydrocephalus)

Pathology (24 decks)

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