10 Nervous System Flashcards
Definition of consciousness
State of awareness of oneself and the environment, and a set of responses to that environment
Two distinct components of consciousness
Arousal
Contents of thought
Arousal
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
Content of thought
All cognitive functions that embody awareness of self, environment, and affective states (emotions & moods, from limbic system, hypothalamus, and cerebral cortex)
Causes of altered LOC
Structural - Supratentorial lesions, infratentorial lesions, subdural, extracerebral, intracerebral
Metabolic
Psychogenic arousal alterations
Causes of altered LOC
Infection Vascular Neoplastic Congenital Degenerative Polygenic Metabolic Hypoxia, lytes, hypoglycem, drugs and toxins
Polygenic
When an inherited characteristic is controlled by two or more genes
Spectrum of altered LOC
Confusion Disorientation Lethargy Obtudnation Stupor Coma
Confusion - frontal lobe
Loss of ability to think rapidly and clearly. Impaired judgement
Disorentation - into cerebral cortex (past frontal lobe)
First step in loss of consciousness.
First disoriented to time then place then impaired memory and lastly recognition of self
Lethargy - limbic
Limited spontaneous movement or speech, easy to arouse with normal speech or touch. May not be oriented to time place person
Obtundation - RAS effected
Mild to moderate reduction in arousal with limited response to environment
Falls asleep unless stimulated
Questions answered with minimal response
Stupor - shutting down RAS
Condition of deep sleep or unresponsiveness, response is often withdrawal or grabbing at stimulus
Needs vigorous repeated stimulation for arousal
Coma
No verbal response to external environment
Stimuli such as deep pain or suctioning may have motor response
3 levels of coma
Light coma - purposeful movement with stimuli
Coma - non purposeful with stim
Deep coma - unresponsive
5 categories of neurologic function used to evaluate LOC
LOC Breathing patterns Pupillary changes ocular response motor response
Most critical index of nervous system function
LOC
Breathing patterns
Brainstem takes over regulation with decreased LOC by responding to changes in PaCO2 (abnormal) should be in cerebrum
Cheyne-stokes - hemispheric breathing pattern
Crescendo in rate and depth in response to CO2 and a diminished ventilatory stimulus, breathing stops until CO2 reaccumulates
Brainstem patterns of breathing
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”
Vomiting without nausea
Indicates neural mechanism, particularly associated with vestibular nuclei (pons)
floor of 4th ventricle
Brainstem compression secondary to ICP
Pupillary changes
Areas controlling pupil are adjacent to brainstem controlling arousal. Pupil changes are a valuable guide to evaluating level of brainstem function
Drugs effects on pupils
Atropine, scopolamine fix and dilate
Opiates pinpoint
Barbiturates can caused fixed
Ischemia and hypoxia often fix and dilate
Oculomotor response to neuro insult
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
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
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
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
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
Survivors of cerebral death
Remain in coma, or awake in vegetable state
Mccaince also says minimally conscious state
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
VS vs coma eyes
Spontaenous or to stimuli in VS
No opening on coma
VS vs coma awareness
Neither has any evidence of awareness, or communication
Seizure definition
Sudden, explosive, disorderly discharge of cerebral neurons, characterized by sudden, transient, alteration in brain function.
A syndrome, not a specific disease
Convulsion/epilepsy defintion
Clonic-tonic movement associated with some seizures
General term for primary condition causing seizures, no underlying/correctable cause
Aura
Gustatory, auditory, feeling of dizziness or numbness, ‘funny’ feeling
Prodroma
Early clinical manifestations such as headache, malaise, depression that may occur an hour / a few days before seizures
Tonic/clonic phase
State of muscle contraction where there is excessive muscle tone
Clonic phase is alternating contracting and relaxation of muscles
Causes of seizures
Cerebral lesions
biochemical
Cerebral trauma
epilepsy (birth injury, trauma)
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)
Infra - low waves
Theta
3-8 - sleep
Alpha
8-12 meditation
Beta
12-38hz awake
Delta waves
.5-3hz
Gamma
38-42hz
Partial seizures
Begin local, focal motor - jacksonian (marches)
Involves only unilateral neurons, usually from cortical brain tissue
Three types of partial seizures
Simple, complex, secondary generalized - refers to extent of foci
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
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
Secondary generalized partial seizure
Partial onset evolving to generalized tonic clonic
Generalized seizure
Both hemispheres, usually from subcortical or deeper brain focus - drop in LOC
Types of generalized seizre
Petit mal, minor motor, limited grand mal, grand mal, drop attacks
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
Tonic phase
<1 minute, clonic phase lasts 2-5 minutes, stupor or coma 5 minutes, postical
Absence seizures
Simple abrupt sensation of activity 5-10 seconds
Complex - brief tonic clonic
Lennox-Gastaut
1-5 years old
Cognitive and motor dysfunctions
Experience decrease cognitive and motor development
Juvenile Myoclonic epilepsy (JME) - possibly same as lennox but later in life
Adolescents and young adults
Possible chromosomal
No decline in cognition
Infantile spasms
Flexor spasms of extremities and head
4-8 months
Idiopathic or in response to CNS insult
West syndrome
Myoclonic seizures
Sudden, uncontrolled, one or more extremity, often in morning, momentary loss of consciousness followed by postictal
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
Seizure numbers
During seizure 250% more ATP
60% increase in cerebral O2 consumption
Bloodflow increased 250%
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
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
Concies
Less than 5 min loss of consciousness
no structural damage, but cognitive dysfunction
T-tau
Can have bradycardia and hypotension (30 seconds)
Brain contusion
Edema and bleeding
ICP can take 24 hours to manifest, 72 hours to peak
Slower recovery
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
Subdural hematoma
Between dura and arachnoid, acute or chronic
Acute subdural
Within hours -
ICP
Headache, drowsiness, restlessness, agitation, confusion, LOC
Epi vs sub
Epidural usually begins with LOC, subdural progresses
Chronic subdural
Days to weeks to accumulate
More common in oldies at drunks
Headache and dementia
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
Intracerebral hematoma
Associated with contusions - frontal/temporal
Compression, edema, ICP
Major inflamm
Decreasing LOC
Vomiting in head injury
Compressed lateral ventricles push fluid into 3rd then 4th ventricle, 4th ventricle pushes on vomit centre. No nausea precipitating
Bursa
Fluid filled sac which protects muscles and ligaments
Spinal Cord Injuries
Vertical compression can injure anywhere
Rotational forces damage supporting ligaments, fracture vertebrae, common at thoracic/lumbar
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
Causes of back pain
Idiopathic, tumours, disk prolapse, bursitis, abnormal bone pressures, inflammation, ligament sprains
Degenerative disk
Biochemical alterations of intervertebral disk tissue
Spondyloysis
Forward displacement of vertebra due to structural deficit
Spondylolisthesis
Vertebra slide forward
Spinal stenosis
Nerve roots become entrapped
Lumbar disk herniation
Protusion of nucleus pulposis (compresses nerve root)
Normal ICP
5-15mmHg
Increased ICP causes
Increased content (tumor)
edema
Excess CSF
Hemorrhage
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
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
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
Stage 4 of ICP
Brain herniation, further blood supply compromise
Cerebral blood flow eventually ceases
Loss of vital functions
Clinical manifestations of ICP
Decreased LOC headache N/V Vital signs (Up BP, wide PP, bradycard) Papilledema Sluggish then fixed and dilated pupils
Papilledema
Increased ICP compresses optic nerve
Cerebral edema causes
Trauma Tumor Infection Ischemia/infarct hemorrhage hypoxia
Harmful effects of cerebral edema
from distortion of vessels, displacement of brain tissue and herniation
4 types of cerebral edema
Vasogenic (increased cap perm)
Cytotoxic
Ischemic (following infarction)
Interstital (with hydrocephalus)
