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Patho: Chronic and Degenerative Neurological Disorders

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Term
Definition
how common are headache   30 million a year, women are more common  
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seizure vs. epilepsy   seizure= whole body convulsion (10%) epilepsy= disorder of seizures (3%)  
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generative neurological diseases   diminish neurological impulse transmission  
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epilepsy   chronic disease characterized by recurrent seizure  
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seizure   sudden, abnormal, disorderly discharge of neurons within the brain that is characterized by a sudden transient alteration in brain function  
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who is affected by seizure and some causes   infants less than a year old, greater than 65 years, all genders and ethnic groups caused by head trauma, hypoglycemia, altzeimer's  
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generalized vs. focal seizure   focal only affects on area-- can be completely or partially aware generalized affects other areas- no awareness/always impaired (tonic/clonic)  
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stages of seizure   1. aura 2. ictal 3. post ictal 4. interictal (repeat)  
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why are EEGs not a reliable source for diagnosis   does not rule out seizures- 50% don't show; especially if not seizure activity  
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secondary headaches   another primary condition causes these- concussion, aneurysm, disease, medications, brain tumor  
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most common types of primary headaches   tension headaches and trigeminal autonomic cephalgia  
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tension type headache (TTH)   infrequent episodic (less than a day a month), frequent episodic (10 a month for three months), chronic TTH (15 days or more a month)  
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presenting symptoms of TTH   bilateral pain, does not worsen with activity  
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migraines   unilateral, certain odors trigger, n/v, severe pain, more in women, disabling  
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four phases of migraine headaches   1: prodrome- neural hyper-excitability in the brain (fatigue) 2: aura- cortical spreading depression occurs 3: pain- trigeminovascular complex activation accounting for the pain 4: postdrome- sensitization of the trigeminal vascular complex  
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serotonin and calcitonin gene related peptides   released in a migraine; known to be a potent vasodilators  
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Parkinson's disease   anyone can get it, 50/60s diagnosed, young onset is younger than 40 cells of substantial nigra produces dopamine  
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imbalance of what two neurotransmitters leads to parkinson   acetoycholine and dopamine; dopamine is low and Ach is high meaning uncontrolled stimulation  
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symptoms of parkinsons   orthostatic hypotension, constipathion, insomnia, night terrors TRAP  
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TRAP   T: tremor= abnormal spasms and muscle movements; non intentional at rest R: rigidity= tightness/stiffness in arms, legs, trunks A: bradykinesia/akinesia= slow movements P: postural instability= loss of reflex/balance, gait  
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neuropsychiatric concerns   depression, cognitive dysfunction, dementia, apathy, anxiety  
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Parkinson's diagnosis   TRAP criteria, imaging is not good, PET scan, medications response  
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Amyotrophic Lateral Sclerosis   progressive fatal/neurogenerative disease resulting in loss of upper and lower motor neuron's, ultimately leading to respiratory failure progressive muscle weakness and atrophy  
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risk factors for ALS   men, occupation, heavy metal, smoking, physical trauma, caucasian (40-60)  
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2 types of ALS   familial/inherited sporadic (80%)- mutation of gene  
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patho of ALS   UMN and LMN become sclerotic ventilator to assist with breathing can develop dementia only damage motor neurons NOT sensory neurons  
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symptoms of ALS   weakness upper and lower extremities, difficulty speaking/swallowing upper= muscle spasm, hyperreflexia lower= muscle cramps  
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diagnosing ALS   based on symptomology- no biomarkers or tests no cure  
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Huntington's disease   an inherited progressive neurogenerative disease (autosomal dominant)- each child has 50% chance of inheriting, higher survival than ALS (10-20 years)  
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patho of Huntington   Huntington protein accumulates in the cytoplasm of brain cells causing cellular deterioration  
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manifestations of HD   involuntary motor symptoms: chorea, dystonia, dyskinesia emotional and behavior symptoms: depression, mania, irritability cognitive: apathy, impaired decisions, slow- dementia/lack judgement  
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HD diagnosed   genetic testing in blood; biomarkers absent  
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Guillain Barre Syndrome   happens after an infection (viral or bacterial) antecedent infections: epstein barr, mycoplasma pneumonia, s. jejuni men most common, older people  
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patho of GBS   acute peripheral neuropathy- motor neurons affected autoimmune- antibodies attack myelin sheath impacting conduction of signals  
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presentation of GBS   progressive, symmetric ascending weakness that progresses for days and usually stops after 4 weeks more of an event rather than a disease it starts with paresthesia and travels up the limbs or nerves mild-severe (ventilation) recovery after 2 years  
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Myasthenia Gravis   descending weakness, attacks Ach, T and B cell mediated reduction in receptors of Ach in the neuromuscular junction  
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symptoms   decreased muscle force with receptive motion and improves with rest muscle fatigue fluctuates muscle weakness gets worse as day goes on  
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myasthenia crisis   exacerbation of symptoms; cannot breath on own tired + fatigued  
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diagnosing GBS   edrophonium testing; help them become stronger can also do EMG and serum Ach receptors  
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complications or causes of death GBS   aspiration and respiratory failure can be a complication  
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ocular presentation of GBS   eye drooping; 50% in 2 years to get generalized  
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generalized presentation of GBS   muscle weakness all over  
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multiple sclerosis (MS)   most common;, young adults, 2x woemen, cooler climates, further from equator  
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patho of MS   demyelinization resulting in inflammation and damage to myelin sheaths remissions and exacerbations T cells attack myelin sensory and motor neurons  
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symptoms of MS   numbness and tingling, painful motor movements, blurred vision, balance, fatigue, motor impairment optic nerves impacted--loss of vision, painful extra-ocular movement  
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diagnose MS   MRI will show myelinating lesions blood tests show IG and infection evoked potential -- record timing of response to stimuli (pain)  
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two forms of MS   remitting and relapsing (85%)- episodes several weeks to 3 months (every 1-3 years) PPMS without remission (15%)  
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disabilities with MS   paralysis (hemiparlysis), sexual dysfunction, urinary and fecal incontinence  
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complications of MS   50% ger depression, 45-65% memory and executive dysfunction 50% develop PPMS  
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ataxia   uncoordinated/imbalance  
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myoclonus   muscle tetany- twitching  
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tonic   toned muscle  
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clonic   rhythmic jerking movement  
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