-Interaction between sensory, affective, evaluative system

-Not jus simple sensory

-How we see it, or how we feel that day

-Lateral spinomaic tract has to do with pain

-Nerve endings that sense painful stimuli

         -C Fibers

         -A Delta Fibers

         -Spinothalamic tract

-Small

-Unmeylinated

-Dull achy pain

-Myelinated

-Large

-Stubbing toe, get that immediate pain -Tells us to get out of there -Reflex arc is involved with this (when pull hand away from hot plat is a reflex arc)

-Afferent track carrying signals further

-Specifiicity

-Gate Control Theory

-Neuromatrix Theory

-

-Intensity of pain correlated with amount of tissue damage

-Simple theory

-Amount of tissue damage is directly correlated with how much pain

-Cerebral cortex can only process so much stimulus at once

-Only allows so much stiumulus before clses the gate

-Ex: When you hit your arm a pain signal goes to your cortex, if you run your arm after that sensation also goes to your cortex.  With there now being to signals head to the cortex and it can only accept so much stimuli, there is less emphasis on the pain sensation.

        -Introduce another stimulous to less pain

-Most Global Theory

-Bascially says there are too many things to influence the pain to understand

-Pain with physical cause

-Fracture your leg

-Some talkeda bout in inflammation

     -they cause pain to be percieved

-Seratonin and endorphines: make you feel good

     -Released through exercise

-Opiates: Morphine

-Pain without physical cause

-Feels real

-Protective

-Self limiting (short duration)

-A Delta Fibers are involved in acute pain

-Acute pain matches the healing process

Superficial injury

-Skeletal muscle pain

-Pain which presents at site differing from origin

-Ex: Heart Attack (feel pain in your arm)

-Ex: Gallbladder (Feel the pain in your shoulder)

-Persistant pain from 3-6 months

-Persists after healing occured

-Chronic Pain

-Hypersensitivity to painful stimulus

-Ex: Fibro myalsia

Dysfunction of the CNS

-Strokes

-Most difficult pain to treat of any known

-Lowest Intensity stiumuls percieved as painful

-Varies Person to person

-Perceptual Dominance: If have area with more pain, your going to focus on that area

Amount of time or intensity of pain a person can endure before exhibiting symptoms

-How well or how much pain can you take before start crying or making faces

1) Hyperthermia

2) Hypothermia

-May be theraputic or accidental

-Associated with stroke or brain injury

-Can cause nerve damage or protein death

-Heat Exhaustion: Person is very sweaty and red

-Heat Stroke: Stop sweating and become coool and clamy

     -Have confusion, CNS is affected

     -Worse then heat exhaustion

-Decrease in body temperature

-Seen more often theraputic then accidental

-Can cause depression of CNS and respiratory system

-If get really bad can cause vasconstriction (whiting of fingers), then chemical (red and numbness), and then cogulation (frostbite)

There are two types

    1) Dyssomnia

    2) Parasomnias

1) Insomnia: Diffiuculty sleeping

2) Sleep Apnea: Stop breathing during the night

3) Hypersominia: Primary & Secondary

           -(excessive sleep)

1) Somnambulism: Sleep Walking

2) Night terrors

3) Resless leg syndrom

-Arousal or alertness, consciousness

      -Reticular activating system

      -Clinically assessed by levels of consciousness scale- table 14-3

-Respiratory:

-Normals breathing regulated by forebrain, with injury lower centers regulate and respond to CO2 levels

 -Irregular breathing- Cheyne strokes repsriations (know there is some sory of injury to the brain)

-Pupillary changes (figure 14-2)

-Oculomotor responses: (double visions etc)

-Motor Responses- Purposeful vs. Reflex Driven

-Complex, Reflex-driven motor responses (vomiting, yawning, hiccups)

-Posturing: Decorticate/decerbrate

      -Tell us where injury is (usually in cerebral cortex)

-Brain Death

-Cerebral Death (Irreversible coma)

 -Persistent Vegetative State:

-Minimally conscious state

-Locked-in syndrome

-No possible recover

-Inability to maintain homeostasis

-Includes brain stem and cerebellum

Cerebral Death

-Irreversible coma

-Death of cerebral hemispheres

-Intact brainstem and cerebellum

Persistent vegetative State

-Complete unawareness of self or environment

-Loss of cognitive function

-Sleep/wake cycles present

-Normal cognitive function

-Complete paralysis except eye movement

-Occurs with certain kind of stroke (verebral Basal Stroke)

-Selective Attention Deficits

-Memory Disorders

-Executive function deficits (whats safety)

-Causes include cerebral lesions, cerebral trauma, biochemical imbalances, and epilepsy

-Triggers

   -Flashing lights

   -Drugs and alcohol

   -Temperature

-Multifactorical

-Epileptogenic focus: Group of neurons which depolarize spontaneously or with inappropreaite trigger

-Cortical excitation Spreads: Spreads and patient undergoes a stroke

-Tonic Phase: Exciation of subcortical, thalamic, and brain stem areas

-Clonic Phase: Alternating conraction/relazations occcur due to the inhibitory neurons of the basal ganglia, cortex, and anterior thalamus reacting to the excitation

-Seizures are exhausting -60% more oxygen consumed

Aural: Flushed face, sweat or Prodroma

Agnosia: Defect in recognition

   -May be tactile, visual, or auditory

   -Most commonly associated with stroke

   -Inability to recgonize things (not their touch, sight or hearing)

-Impairment of comprhension or production of language

-Receptive (Wernicke's)

-Expressive aphasia (Broca's)

    -Hard to understnad language

*Mixed Aphasia: Have both agnosia and dysphasia

-Occur as a result of drug intoxication, metebolic imbalances, or nervous system disease

-Onset is abrupt

-Initial sympotms include decreased concentration, reslessness, irritability, insomnia

-Later sympotoms include delusions, hallucinations, OCD behaviors

-Indiviual has greatly altered perception

-Appears distressed

-Dilated pupils

-Rapid Pulse

-Temperature increase

-Sweating

-Highest Level of Acute confusion

-Progressive failure of cerebral function

-Not cuased by imparied level of consciousness

-Cognitive deficits present (oreinations, memory, language, executive function)

    -Executive woudl be having them count backwards from 100 by 7

-3 forms

1) Early onset

2) Early Onset Familial

3) Late Onset (Most common)

-Pathophysiology theoires include: Loss of acetyltransferase choline neurotransmitter and mutation in amyloid protein coding

   -Builds up protein and causes plawues in the brain

-Looks at the cererbral spinal fluid and how it effects the brain

-Incrased Intracranial Pressure: When pressue exceeds ability to compensate, vascular supply to neurons is compromised

     -May be caused by tumor, edema, CSF volume or hemorrhage

-Initial symptoms include confusion, restlessness, drowsiness, pupillary or respiratory changes

-If ICP increase further symptoms include decreased altertness, significant respiratory chanes, small and sluggish pupils, vomitting

-Swelling of brain that causes pressure build up

-Occurs after trauma, infection, hypoxia etc.

-Increased fluid in the ventricles

-Communicating or non-communicating

-Excessive fluid in ventricles

-May be acute or chronic

     -Acute presents in similar manor to increased ICP

-Chronic: Normal-Pressue hydrocephalus

-Unsteady

-Wide based gait

-History of falls

-Incontinence

-Dementia

-Hypotonia: Low muscle tone

    -Can be associated with downsyndrome

-Hypertonia: Spasticity, dystonia, rigidity

    -Increased muscle tone

-Categorizes many of the disorders

-Two categories

1) Upper Motor Neuron Lesions

2) Lower Motor Neuron Lesions

-Central Nerous System

-Diseases

  -Cerebral Pasly

  -CVA (stroke)

  -Spinal Cord Injury

  -Parkinson Disease

  -Multiple Sclerosis

-Associated with Hypertonicity

-Peripheral Nervous System

Diseases

 -Polymyelitis

 -Myasthenia Gravis

 -Guliian-Barre Syndrome

 -Progressive spinal muscular atrophy

-Associated with Hypotonicity

-No cognitive impact

-Table 14-19

-Huntington disease

-Movements are bigger and less controlled

-Very think becasue their muscles are always working since they are continually moving

-Slow Moving

Diseases

-Parkinson

-Akinesia or Bradykinesia

-Posture

-Gait

-Expression

-Tramatic Brain Injury (TBI)

-Closed Vs. Open:

  -Closed is more common

      -Nothing opened the skull

  -Open: Gunshot wound, it opens the skull

-Focal vs. Diffuse

 -Focal is localized

 -Diffuse: Moer brain is involved

Focal Brain Injury Clinical Manifestations

-Two differnet categories

1) Contusion

2) Hematoma

-Causes brief loss of consciousness

-Loss of reflexes

-Suppressed cardiovascular function

-Increased cerebrospinal fluid pressure

-Accumulation of blood

-Extradural and subdural hematomas present with inital loss of consciousness

-After preiod of lucidity, the accumulation hematomy causes headache, vomiting, drowsiness, seizure, hemiparesis

-If discovered can be treated

   -Example: Her friends dad falling off the ladder

-Following concussion, all cells fire simultaneously

-Glutamate is released triggering potassium release

-Calcium rushes into cells impairing mitochondria

-Associated with shaking forces or rapid deceleration

-Physical, and long term consequences

Physical consequences

-Cognitive Deficits

-Behavioral Defiicits

-Caused by hyperextension, hyperflexion, axial compression, or excessive rotation

-Certain areas of spine more prone to injury: C1-C2, C4-C7, and T10-L2

-Primary and secondary tissue injury

-Spinal Shock - Loss of reflexes and function below level of leasions

-Immediately after injury

-Loss of reflex adn muscle tone below level of injury

-Ends when start to have return of reflexes

-May occur after spinal shock resolves

 -Sympathetic nervous system kicks in

-Can occur anytime and multiple times after injury

-Likely to occur with injuries T6 or above ( so hgher )

-Signs and symptoms include marked hypertensions, headache, blurred vision, flushing of face and neck, bradycardia

-Could get stroke from high blood pressure

-Causes damage to CNS

-Degnerative Joint disease

-Degenerative Disk Disease

-Spondylosis

-Spondyloisthesis

-Spinal Stenosis

-Causes compression of spinal cord

-Signs and sympotoms depend on the levels of injury

-Herniated intervertebral disk

-Most common in lumbosacral verebraie (l5-S1 and L4-L5), may also be present at C5-6 and C6-7

-Cervical goes to arms

-Lumbar goes to legs

Risk Factors

-Risk Factors

-Hypertension

-Smoking

-Diabetes

-Thrombocythemia

-Lipoprotein

-Increased homocysteine

-Atrial Fibrillation

-Chlamydia

-Thromotic: clot or blockage

-Transient Ischemic Attacks

-Embolic

-Hemorrhagic

-Lacunar

-Result form atherosclerosis and arteritis

-Thrombus formation impedes cerebral circulation

-Comes from brain

-Temporary

-No residual deficits after 24 hours

-Predictive of future TIA or Stroke (80% in 1 year)

-Starts somewhere else and travels to the brain

-Thrombus travels from somewhere else outside the brain into the brain

-Atrial fibrillation, myocardial infarction, atrial septal defect, aortic stenosis

-Fat emboli

-Air Emboli

Hemorrhagic Stroke

Caused by hypertensions, aneurysm, malignancy, trauma, drug use

-Blood is cytotoxic to CNS

-More severe because blood is toxi, will kill everything in that area

-small

-Common in basal ganglia and pons

-Associated with small vessel disease

-Smoking

-Diabetes

Initial Cerebral edema peaks in 72 hours and lasts approximately 2 weeks

-Presentation dependent on area of infarct or hemorrhage

-Meningities: Bacterial, viral, fungal

-Predisposing factor of upper respiratory bacterial infection

-BActeria become blood borne

-Passes blood-brain barrier

-Toxins induce inflammatory reaction of meninges

-Fever

-Rash

-Headache

-Photophobia:  light sensitive

-Nuchal Rigidity: Becomes stiff (looking down will really hurt

-Progression to neurologic symptoms: changes in alertness

-Men more at risk

-Localized collections of pus

-Resk factors include: open trauma or surgery, middle ear or sinus infection, metastatic spread

Clinical Manifestations of CNS Abscess

-Dependent on area of abscess

-Extradural may have drainage from nasal passages or ear

Encephalitis

-Usually viral origin

-Acute febrile illness

-West Nile virus, herpes simplex I

-All involve the meninges

-Fever

-Delirium

-Confusion

-Loss of consciouness

-Seizures

-Paresis/Paralysis

-Increased ICP

-Autoimmune, demylinating disorder or central nervous system

-Female more common

-Ages 20-50

-Caucasiona in northern latitudes

         -Vitamin D Levels

-Remitting-relapsing

-Primary Progressive: most rapily deterior mas

-Secondary Progressive: Slower straight decline

-Progressive relapsing

-Generally have spinal, cerebellar, and cognitive effects

-Optic neuritis: Double vision

-Lhermitte Sign: Lightening Sensation

-Cognativly very with it

-Motor dygression

-Degeneration of upper and lower motor neurons

-Lou Gehrigs Disease

-Males most likely

-Peak occurence in early 50s

-Genetic Causes - lack enzyme which destroys free radicals, glutamate toxicity occurs

-Non-inflammatory

-Progressive Weakness

-No sensory, cognitive, or autonomic deficits

-Average life expectancy is 2-3 years