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					   CNS TRAUMA;
                   CNS Injury
• Increased intracranial pressure (i.c.p.)
  – Due to
     •   Tumor growth
     •   Edema
     •   Excess csf
     •   Hemorrhage
  Pathophysiology of CNS Trauma

• Example: trauma of head  breakdown of the
  blood-brain barrier 
• CSF most readily displaced content
     • As much as possible reabsorbed
     •  Relieves building fluid pressures
     • Where does it go?
• Alteration of cerebral blood volume
  – Controlled by incr’d venous return from brain
  – Also to decr’d fluid pressures in brain
• If fluid displacement doesn’t relieve pressures,
  fluid continues to accumulate, and
• Edema  increased tissue pressure
  – As fluids expand, pressures build
• Compensations of fluid displacement (csf and
  blood) may be overwhelmed
  – I.c.p. continues to incr, cranial content continues
    expanding. Next:
• Systemic b.p. changes
  – Arterial vasoconstriction to decr fluid toward brain
     • BUT: Now another problem:
     • This condition 
• Oxygenation of brain tissue compromised
  – Remember: ischemia  hypoxia
• Brain tissues hypoxic; hypercapnia, acidosis
   deterioration of brain cells
• Brain tissue shifts (herniates) from
  compartment of higher pressure to
  compartment(s) of lower pressure (Fig.14-9)
• Blood supply to herniated tissue now further
  – Now pressing against arterial vasculature 
    further ischemia, hypoxia to brain tissues
• Increased pressure builds in adjoining
  compartment(s)  further pressure on blood
  vessels leading to healthy tissue
  – Now have generated ischemia, hypoxia of
    adjoining region(s), so
  – Formerly healthy tissue begins to degenerate
• Finally, small hemorrhages begin; blood
  supply ceases
                    Head Injury
• Highest risk populations
  –   Young people 15-24 years old
  –   Children 6 months – 2 years
  –   Children 5-8 years
  –   Elderly
  –   Also, males at higher risk than females by 2:1
• Most likely causes of head injury
  –   Transportation accidents
  –   Falls
  –   Sports related events
  –   Crime
• Penetrating trauma
  – Causes focal injuries
• Blunt trauma common
  – Head strikes hard surface or is struck
  – Dura intact, so no brain tissue is exposed
  – Focal or diffuse injury
• Mild concussion, cerebral concussion most common
• About 75-90% of all head injuries
  – Not severe
  – Survival rate increased due to
     • Reduced severity
     • Improved management at accident scenes
• Contusion = impact hemorrhage, possibly
  – Coup (strike) – impact against object at front or
    back of head (Fig.15-1)
     • Causes direct brain trauma, shearing forces through
     •  Tearing of subdural veins and trauma
  – Contrecoup (rebound) – impact within skull from
    injury to back of head, so
     • Brain hits opposite side of skull
     •  Shearing forces
• Epidural hematomas – often caused by
  temporal fracture
  – Source of bleeding often artery
  –  Herniation (shift) of temporal lobe
• Subdural hematomas (Fig.15-2)
  –   Acute – develop rapidly after trauma
  –   Usually at top of head
  –   Often due to vein tearing
  –   Expanding mass  incr’d i.c.p.  herniation of
      brain tissue
• Clinical (contusion)
  –   Loss consciousness, reflexes
  –   Transient cessation of breathing
  –   Brief bradycardia
  –   Decr’d blood pressure
• Treatment
  – Contusions
       • Control i.c.p.
          – Drugs to relieve fluid pressures
              » Some alter Na+ concentration in brain fluids
       • Manage symptoms
  – Hematomas
       • Surgically ligate, remove bleeding vessels
         Cerebrovascular Disease
• Due to blood vessel pathology
  –   Lesions on walls of vessels
  –   Occlusions of vessel lumen
  –   Vessel rupture
  –   Alteration of vessel permeability
• Two types of brain abnormalities
  – Ischemia (with or without brain infarct)
  – Hemorrhage
          Cerebrovascular accident
               (CVA; stroke)
• Incidence
  –   Third leading cause of death in the U.S.
  –   Highest risk in the population > 65 years old
  –   BUT about 1/3 of patients are < 65 years old
  –   Evidence of familial patterns
  –   More often in
       • Females
       • Blacks
         Three types of CVA based on
• Thrombotic –from arterial occlusions
  – Thrombi in arteries to the brain
  – Risk factors – same as for thrombus formation in other vessels as
    well as:
     •   Oral contraceptive use
     •   Dehydration
     •   Sickle cell disease
     •   Chronic hypoxia
  – Development of disease
     •   Often arteriosclerosis and inflammation of vessels 
     •   Arterial wall damage
     •   Over time, plaques form 
     •   Clots in cerebral circulation
– Thrombotic strokes further subdivided  clinical types:
   • Transient Ischemic Attacks (TIAs)
      – Due to thrombotic particles  intermittent blockage of cerebral
        circulation or  vessel spasm
      – No residual dysfunction
      – Any neurological deficits cleared within 24 hrs
      – BUT often precedes completed stroke
   • Stroke-in-Evolution (Progressive Stroke)
      – May evolve over minutes/hours
      – Gradual progression of neurological deficit (over days)
   • Completed Stroke
      – Maximal destruction of neurological tissues
      –  Neurological defects
   • All cause decr’d blood supply to brain
      – Ischemia  hypoxia  necrosis, swelling of brain tissue  neuron
• Embolic – second type of CVA
  – Fragments of thrombus from outside brain (ex: heart, aorta,
    common carotid) travel
  – Obstruction often at bifurcations, points of narrowing of
  – Causes ischemia
     • Lumen of brain vasculature entirely plugged and embolus remains in place
     • OR embolus may break again  fragments travel to other brain areas
  – Associated conditions
     • Risk factors are same as for thrombus formation, arteriosclerosis elsewhere
       in body, as well as
         – Patients with atrial defibrillation
         – Patients with myocardial infarct
         – Patients with disorders of cardiac circulation
  – Also leads to loss of blood supply to brain, and ischemic/hypoxic
• Hemorrhagic CVA – third type of CVA
  – May be due to:
     • Hypertensive hemorrhage
        –   If incr’d blood pressure over several years
        –   Occurs within brain tissue
        –   Mass of blood forms  incr’d volume in cranium
        –   Blood mass displaces, compresses adjacent brain tissue
        –   Rupture or seepage can occur
     • Ruptured aneurisms (Fig.15-12)
     • Bleeding disorders
  – Pathophysiology not fully understood
     • Mass of blood causes compression  ischemia of surrounding
       brain tissue
     • Get incr’d i.c.p.  edema, other sequential steps
     • Resolves through reabsorption of blood from cranial cavity
• Clinical
  – Thrombotic/embolic
     • Maximal cerebral edema in 72 hours of obstruction
     • Commonly subsides within 2 weeks
     • Ischemic stroke survived by most, unless massive cerebral
     • Symptoms depend on site of obstruction
        – Different arteries supply different brain regions, which control different
          body functions
        – BUT massive brainstem infarct  death
        – Why? What functions are controlled by the brainstem?
  – Hemorrhagic – also depends on location, size of bleeding
     • Aneurism can symptoms from excruciating headache  
        unconsciousness
• Treatment
  –   Stabilize vital signs
  –   Detect/correct any cardiac arrhythmias
  –   Proper positioning
  –   Platelet anti-aggregants
  –   Surgery to ligate aneurisms, improve blood flow
  –   Preventive – hypertension is a most important risk
      factor, so
       •   Decrease salt intake
       •   Increase exercise
       •   NO SMOKING
       •   No oral contraceptives
        Degenerative Disorders
• Alzheimer’s Disease – intellectual dysfunction
  – Incidence – common
  – Probable causes
     • Both familial and non-inherited forms
     • Evidence for several, varied causes, including
        – Aluminum toxicity
        – Autoimmune dysfunction
        – Prions
  – Involvement of CNS neurons
– Aggregation of amyloid glycoprotein develops
   • Proteins in neurons become distorted, twisted 
     “neurofibrillary tangle” (Fig.15-14,15)
   • Groups of nerve cells degenerate, coalesce around
     amyloid core
      – Now “plaque”
   • Disrupt transmission of nerve impulses
      – Number of plaques corresponds with amount dysfunction
   • Memory loss may be due to decr’d ACh
      – ACh needed for recent memory
– Clinical
   • Progressive forgetfulness  disorientation, confusion
   • Behavioral changes
      – Anxiety, depression, hostility
   • Motor changes possible, depending on site(s) of
– Treatment
   • Maintain general health
   • Maintain any unaffected cognitive function
• Parkinson’s Disease – a movement disorder
  – Incidence: 130/100,000 population
     • Onset commonly after age 40; peak age of onset is early
     • About same male:female ratio
     • Apparently not familial
  – Probable cause(s) –unknown, but several theories
     •   Vascular disorder
     •   Viral infection
     •   Metabolic disorder
     •   May be age predisposes neurons to damage by toxins,
– Involvement of dopaminergic neurons  degeneration
  of basal ganglia (Fig.15-16)
  • Degeneration dopaminergic neurons  loss of neurons that
    produce dopamine as well as loss of receptors for dopamine
  •  Imbalance of dopaminergic to cholinergic activity
     – Dopamine mostly inhibitory, ACh mostly excitatory for motor
     – As dopaminergic neurons decr, inhibitory effects are lost
     –  Relatively more ACh neurons (excitatory)
     –  Patient dev’s movement disorders -- muscles are more active
– Clinical
   • Syndrome of abnormal movement = Parkinson’s
     syndrome (Fig.15-17)
      – Tremor at rest
      – Regidity
      – Akinesia – decr’d voluntary movement or incr’d time nec to
        perform voluntary movement
      – Dementia possible later
– Treatment
   • Need to incr brain dopamine
      – Dopamine can’t cross blood-brain barrier
   • Give L-dopa -- precursor to dopamine
      – Crosses blood brain barrier
      – In brain tissue, converted to usable dopamine
   • BUT L-dopa has many side-effects
• Multiple Sclerosis – demyelinating disease
  – Myelin = lipid covering over axons
     • Needed for proper action potentials and nerve
       conduction in correct path along axon
  – Previously healthy myelin degenerates (Fig.15-18)
     • Patients do not form successful action potentials 
       movement disorders
  – Incidence
     •   30-80/100,000 population
     •   Common time of onset 20-40 years old
     •   Mostly female, White
     •   Most prevalent -- those who live away from equator
     •   Some familial patterns but no clear genetic pattern
– Probable cause(s) – unknown; several theories exist
   • Exposure to environmental agent in childhood
   • Most MS patients have a specific histocompatibility Ag in
        – Increasing Ag concentration correlates with incr’d susceptibility
        – Believe Ag may alter immune response toward viruses
– Involvement of only CNS neurons (NOT PNS)
– Causes degeneration of previously normal myelin
   •   Axons seem well-preserved
   •   BUT impulses do not pass smoothly
   •   Demyelinization  plaque formation along axon
   •   Also gliosis  glial scarring
   •   Lesions form; diffuse, small, widespread
– Clinical
   • Symptoms remit following inflammatory edema near
      –   Sensory/visual problems
      –   Limb weakness
      –   Cerebellar signs
      –   Bladder dysfunction
      –   Mood disorders
– Treatment
   • Prednisone, glucocorticoids to decr inflam’n with acute
   • Manage symptoms
   • Supportive rehabilititative management
• Myasthenia gravis – disorder of the neuromuscular
   – “Grave muscle weakness”
   – Probable cause – autoimmune dysfunction
      • Assoc’d with development of other autoimmune diseases
   – At neuromuscular junctions, get defect in transmission of
     impulse to a muscle cell
   – Causes decr’d binding of ACh at its postsynaptic receptors
     on muscle cells
      • Ab’s prod’d by patient’s body against its own postsynaptic
          – Ab’s bind ACh receptors on muscle cells at synapse
          – Receptor therefore blocked from binding ACh from impinging neuron
          – So neuron’s signal is not received by the muscle cell
      • Finally receptors destroyed
          – Diminished transmission of impulses across neuromuscular junction
          – No muscle depolarization
– Clinical – “insidious onset”
   • Fatigue, recurrent upper respiratory infections
   • Muscles of eyes, face, mouth, throat, neck first affected 
       – Facial droop
       – Difficulty swallowing
       – Choking, drooling
   • Respiratory muscles weaken  impaired ventilation   respiratory arrest
– Treatment
   • Anticholinesterases
       – Cholinesterase -- enzyme present in synapse; breaks down ACh
           » Needed as body’s mechanism to stop ACh signal after time, once
               transmission is complete
       – Anticholinesterases stop the activity of cholinesterase enzyme
       –  Less ACh broken down
       –  More ACh available to bind to any remaining healthy receptors on muscle
       – BUT these agents have side effects
   • Steroids
   • Immunosuppressants to decrease Ab synthesis

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