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Neuropathology
 

Neuropathology

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  • Afferent pathways – move sensory impulses towards CNS Efferent pathways – innervate effector organs such as skeleltal muscle, cardiac and smooth muscle as wel as glands – transmits impulses away from CNS Somatic NS – motor and sensory pathways regulating voluntary motor control of skeletal muscle Autonomic NS – motor and sensory components and regulates body’s internal environment through involuntary control of organ systems
  • Neurons – vary in size, shape and processes; contain cell body (AKA soma – in groups called ganglia or plexuses), dendrites (extensions carrying nerve impulses toward cell body) and axons (projections that carry impules away from cell body) Typical neurons have one axon covered in myelin (insulating substance) Schwann cells forms and maintains the myelin – myelin acts as an insulator allowing ions to flow between segments thereby increasing velocity Neuroglia are classifications of cell supporting the neurons of the CNS Nerve injury leads to swelling, hypertrophy of the neurofilaments, myelin shealth shrinks and disintigrates and axon degenerates and disappears Nerve regeneration depneds on location of the injury, type of injury, iflammatory response and scarring; the closer to the cell body, the greater the chance the nerve cell will die; a crushing injury allows recovery than a cutting injury Synapses – region between adjacent neurons – impulses are carried across by chemical and electrical conduction Chemical conduction uses neurotransmitters More than 30 neurotransmitters – norepinephrine, acetylcholine, dopamine, serotonin, histamine and various amino acids Neurotransmitters are responsible for regulation of sleep, mood, dreams, maintenance of arousal, perception and integration of pain, emotional experiences
  • Cranium
  • Acute – alerts a person to a condition or experience that is immediately harmful; acute pain is sudden in onset and is relieved when chemical mediators which produced the pain are gone; mobilizes the person to take action Chronic – cause is unknown and if known, the pain does not response to usual treatment; develops slowly, insidiously; individuals adapt and try to modify the pain; leads to hopelessness and depression, disability and unemployment
  • Neuralgias – result from infection or disease which damages a peripheral nerve – diabetic neuropathy Hyperesthesias – increased sensitivity and decreased pain threshold to touch and painful stimuli Phantom limb pain – pain felt in an amputated limb after the stump is completely healed; occurs if the neuronal pathway from the amputated limb is stimulated at any point along the pathway Cancer pain – pain attributed to the advance of the disease, associated with the treatment of the disease, pain attributed to comorbidities
  • Level of consciousness – confusion, disorientation, lethargic, obtunded, stuporous, coma – light (purposeful movement with stimulation), coma (nonpurposeful movement with stimulation only), deep (unresponsiveness to stimuli) Pattern of breathing – Cheyne-Stokes respirations – smooth increase (crescendo) in rate and depth of breathing which peaks and is followed by a gradual smooth decrease (decrescendo) in the rate and depth of breathing to the point of apnea Pupillary changes  used to guide to eval the presence and level of brain stem dysfunction b/c brain stem areas control pupils also control level of arousal; must consider drugs pt is taking in evaluation See figure 15-1 page 442 Oculomotor responses  resting, spontaneous and reflexive eye movements under changes with different levels of brain dysfunction – see table 15-5 page 443 – figure 15-3 pages 443 and 444 Motor responses  help evaluate level of brain dysfunction as well as determine the side of brain that is maximally damaged. Purposeful – defensive or withdrawal movement of limbs to noxious stimuli  requires an intact corticospinal systems. Inappropriate or not purposeful  generalized motor movement, posturing, grimacing or groaning. Not present  unresponsive  severe dysfunction of corticospinal system
  • Aura – partial seizure experienced as a peculiar sensation preceding onset of generalized seizure – gustatory, visual or auditory experience, dizziness, numbness Prodroma – early clinical manifestations such as headache, malaise, depression occurring hours to days before the seizure Tonic – muscle contraction with excessive muscle tone Clonic – alterhnating contraction and relaxation of muscles Postictal state – period immediately following seizure activity – in generalized seizures people are confused, disoriented, complaining of headache, muscle aches and fatigue; may need to sleep after seizure, no memory of the seizure
  • Generalized seizures Account for 30% of seizures Involve neurons bilaterally Not always with a focal onset Originate from a subcortical or deeper brain focus Consciousness is impaired or lost Partial seizures Unilateral neuron involvement Have a focal onset and originate from cortical brain tissue Consciousness is maintain if kept to one hemisphere May become generalized  loss of consciousness (secondary generalization) Status epilepticus subsequent seizures before a person has time to regain consciousness Lasts more than 30 minutes Occurs from abrupt discontinuation of anti-seizure medications or inadequate treatment of seizure disorder Medical emergency due to cerebral hypoxia
  • Classification is based upon etiology – trauma, tumors, vascular disorders, infections Degeneration of nerve tissue from genetics, inflammation, biochemical alterations; atherosclerosis  multiple infarcts; trauma, lesions in the frontal and temporal regions of brain; compression or increased intracranial pressures
  • Neurofib tangle – protein on the neurons becomes distorted and twisted Senile plaques – groups of nerve cells degenerate and coalesce around an amyloid core; plaques disrupt nerve transmission Dx of AD is made from a CT scan, history and physical exam Disease develops over 5 years Treatment – use of Aricept in early AD; pts are taught compensation techniques to help memory, maintain cognitive functions which are not impaired, maintain general health and nutrition
  • Extra dural hematomas – epidural is another name for them. Occur in all age groups and account for 1-2% of all major head injuries. Most common in persons 20-40 yrs old. Injuries to menigeal vein or dural sinus leads to bleed. Sx include loss of consciousness at time of injury; become lucid for a few hours to a few days; as blood accumulates  headache, vomiting, drowsiness, confusion, seizure and hemiparesis with subsequent loss of consciousness; dx with MRI or CT scan; tx is surgical evacuation and ligation of bleeding vessel Subdural hematoma – found in 10-20% of persons with TBI; acute form develops rapidly usually w/in 48 hrs; subacute subdural hematomas develop over a few days after initial injury; chronic subdural hematomas most commonly in elderly and chronic alcoholics and occur over days to wks to months; tearing of the bridging veins in acute, torn cortical veins or venous sinuses also the source; the accumulation of blood acts as an expanding mass and increase intracranial pressure; sx of acute SDH include headache, drowsiness, restlessness, agitation, slowed cognition and confusion; as bleed progresses may develop visual changes, loss of consciousness and pupillary dilation; sx of Chronic SDH include chronic headache and tenderness over the hematoma. Tx is surgical evacuation of clot; chronic SDH may require a craniotomy to evacuate the blood and cut away the meninges around the clot.
  • Thrombi formed in vessels supply the brain; most commonly due to atherosclerosis and inflammatory disease process that damage the vessel walls. TIA sx – depend on vessel affected; transient loss of vision, visual changes, speech/cognition changes, transient weakness, hemiparesis, facial drooping; treatment is life long anticoagulation with either anti-platelet medication, ASA or warfarin Sx of stroke
  • Migraine triggers – stress, hunger, weather changes, seasonal changes, sunlight, noise, jet lag, foods such as red wine and aged cheeses, chocolate, hormonal changes, oral contraceptives Migraine auras – smells, lights, visual changes Migraine w/o aura - Lasts 4-72 hours Unilateral throbbing pain – moderate to severe and aggravated by activity Nausea, vomiting, photophobia, diarrhea
  • Bacterial – secondary to infection in bloodstream or extension of infected area to subarachnoid space; mortality is 25%; children and adolescents are primarily affected – highly contagious Aseptic or viral – inflammation limited to meninges; seasonal with summer and autumn most common times of year;
  • Primary – loss of neurons in substantia nigra Secondary – anything other than primary cause – virus, trauma, infection, drugs, toxins “designer drugs” - “Ecstasy”
  • Degeneration of normal myelin sheaths
  • Relapsing-remitting – acute exacerbations with recovery and lasting disabilty; between attacks there is no disease progression Primary progressive – steady progression of disease; only occasional minor recoveries (Plateaus); this course is fairly uncommon Secondary progressive – pattern of clear cut relapses and recoveries; becomes steadily progressive over time with continued worsening of disease Progressive-relapsing – rare type that is a steady progressive form but with acute exacerbations

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