PANCE Review Neurology – Flashcards
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Tension HA S/S
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-Bilateral, non-throbbing, Band like "dull," "pressure," "head fullness", "head feels large," or, more descriptively, "like a tight cap", "band-like," or a "heavy weight on my head or shoulders." -Without photophobia, phonophobia, nausea, or vomiting.
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What is the common HA:
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Tension HA
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Tension HA Tx
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1st NSAIDS 2nd Relaxation exercises
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Triggers for Tension HA
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Stress, fatigue
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Migraine S/S
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Unilateral, throbbing, photophobia, N/V Migraine patients often retreat to quiet, dark rooms and prefer to lie quietly.
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Migraine triggers:
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including chocolate, red wine, hard cheeses, monosodium glutamate, hormonal changes, exertion, fatigue, and stress.
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Migraine often precede by
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aura (involving visual changes, field cuts, or flashing lights affecting one's visual hemifield.)
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Migraine often is associated with other diseases, such as
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seizure disorders, essential tremor, Tourette's syndrome, depression, anxiety, and stroke.
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The triad of headache, nausea, and vomiting in the morning are concerning for a brain tumor in the
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posterior fossa
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Migraine Tx
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Mild to moderate migraine headache (1) Abortive therapy may include aspirin, acetaminophen, NSAIDs, or isometheptene. A variety of products may be combined with caffeine, which has an adjunctive effect. (2) Subsequent measures for migraine might include serotonin-receptor agonists, such as the triptans (e.g., sumatriptan, zolmitriptan, rizatriptan, naratriptan, almotriptan, frovatriptan, eletriptan). Various forms of the ergotamines also are useful. Triptans, Reglan (Metocloppramide: SE --> Tardive Dyskinea), *Verapamil for Basilar migraine*
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Migraine HA prophylaxis
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BB, Tricyclic, Progestin if menses related.
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Cluster HA S/S
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-Severe, unilateral, periorbital headaches, Lacrimation, eye injection, rhinorrhea, -unilateral pain of cluster headache often is accompanied by ipsilateral lacrimation, conjunctival injection, nasal congestion, and myosis and ptosis
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Headaches Diagnosis Test
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CT scan or MRI
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Prophylactic therapy for cluster headaches includes:
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valproate, cyproheptadine, lithium, *calcium channel blockers*, and oral corticosteroids.
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Cluster HA Tx
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-Administration of *100% oxygen, injectable forms of ergotamines or sumatriptan*, and analgesics (e.g., intranasal butorphanol).
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Cluster HA assoc.
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Horner's Syndrome (ptosis, miosis, anhydrosis) and Alcohol
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Complex regional pain syndrome (CRPS) is a disorder of a body region, usually of the extremities, that is characterized by
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pain, swelling, limited range of motion, vasomotor instability, skin changes, and patchy bone demineralization. It frequently begins following an injury, surgery, or vascular event such as a stroke.
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Three stages may occur during the course of CRPS
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It is a systemic disease affecting both the central and peripheral nervous system
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Complex Regional Pain Syndrome S/S
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Severe Pain, burning inupper or the lower extremities; involvement of both upper and lower limbs in the same patient is unusual. "Pain out of proportion"
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Complex Regional Pain Syndrome risk factor:
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immobilization, trauma, female
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Complex Regional Pain Syndrome Dx
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Radionuclide uptake on Bone scintigraphy
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Complex Regional Pain Syndrome Treatment
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Stage 1: 1st Neurotin Stage 2: Add steroid Stage 3: Pain management -Temporary sympathetic nerve block -Smoking cessation ?Anticonvulsants ?Bisphosphonates ?Oral glucocorticoids ?Nasal calcitonin
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Peripheral Neuropathy S/S
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Slow onset for DM (sensory), but fast onset for Guillain (Motor): Sensory Loss, Burning, Weakness
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Peripheral Neuropathy Dx
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Electromyography/ Nerve conduction study
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Peripheral Neuropathy for DM Tx
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Tight blood sugar control Med: Gabapentin, if obese give Topiramate
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Diabetic Neuropathy
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is primarily a symmetrical sensory polyneuropathy, initially affecting the distal lower extremities.
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Diabetic polyneuropathy is generally considered *predominantly axonal-sensory*
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Is extremely complex and likely relates to inflammatory, metabolic, and ischemic effects
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The earliest signs of diabetic polyneuropathy probably reflect the gradual loss of integrity of both large myelinated and small myelinated and unmyelinated nerve fibers:
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?Loss of vibratory sensation and altered proprioception reflect large-fiber loss ?Impairment of pain, light touch and temperature is secondary to loss of small fibers
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Treatment of diabetic peripheral neuropathy ?Glycemic control ?Foot care ?Treatment of pain
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-Pregabalin has been found to significantly decrease mean pain score -On a daily basis, patients need to inspect their feet for the presence of dry or cracking skin, fissures, plantar callus formation, and signs of early infection between the toes and around the toe nails. Regular foot examinations by the physician to detect early neuropathy are also an essential component of the treatment of diabetic patients.
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Treatments that are beneficial for painful diabetic neuropathy include:
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a number of antidepressants (eg, amitriptyline, duloxetine, venlafaxine), anticonvulsants (eg, pregabalin, sodium valproate), and capsaicin cream
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Complications — Diabetic polyneuropathy is
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frequently insidious in onset and can lead to formation of foot ulcers and muscle and joint disease.
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The most common forms of hereditary neuropathy
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*Charcot-Marie-Tooth* types 1A, 1B, and X-linked, are all predominantly demyelinating in nature, although substantial coexistent axonal loss is usually also identified.
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Charcot-Marie-Tooth is
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also known as hereditary* motor and sensory neuropathy* (HMSN), encompasses the majority of hereditary peripheral neuropathies
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The most common features of Charcot-Marie-Tooth are weakness and atrophy of the lower leg and foot. High-arched feet and hammertoes (pes cavus) are common but not pathogneumonic.
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Most patients present with difficulties walking, twisting of the ankles, and slapping of the feet. Features are normally symmetric, although asymmetries may occasionally occur. The majority of patients remain ambulatory, although they may need braces and other assistive devices. Severe cases also exist. Children with delayed motor milestones, who never ran or ambulated, have a severe early-onset phenotype of CMT1, CMT2, and CMT4 called Dejerine-Sottas syndrome.
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Diagnostic Factors for Charcot-Marie-Tooth
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-family history of neuropathy, pes cavus, or abnormal gait -walking difficulties -pes cavus (hammertoe) -*steppage gait* -diffuse deep tendon hyporeflexia or areflexia -reduced muscle strength -reduced sensation -transient sensory symptoms -transient motor symptoms
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Charcot-Marie-Tooth treatment
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Low-impact exercises, such as cycling and swimming, as well as *physical therapy* sessions, increase energy, as well as reducing fatigue and pain
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*Initial diagnostic procedure for patients with suspected polyneuropathy *
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Electrodiagnostic testing with electromyography and/or nerve conduction studies (EMG/NCS)
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Restless Leg Syndrome is
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is a disorder characterized by voluntary leg movements prompted by an urge to move which is often associated with unpleasant paresthesias.
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Restless Leg Syndrome
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The urge to move is worse at rest and at night and relieved by movement. Accompanied by *dysesthesias described as creeping, crawling, tingling, cramping, or aching of the extremities.*
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Restless Leg Syndrome Risk factors:
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-Family history consistent with autosomal dominant inheritance -Conditions associated with iron deficiency -End-stage renal disease (hemodialysis patients); associated factors that have been posited to play a role include anemia, iron deficiency, elevated serum calcium, and alterations in central nervous system dopamine. -DM, Multiple sclerosis, Parkinson's Disease pt
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Restless Leg Syndrome Treatment:
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-Iron replacement -Dopamine Agonist: pramipexole or ropinirole
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Bell's Palsy S/S
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Unilateral facial paralysis: -Inability close eye -unable to Wrinkle the forehead -Mouth drawn the non affected side -Loss of taste 2/3 anterior of the tongue -hyperacusis (hearing sensitivity)
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Bell Palsy's with left affected
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On physical exam, the left eye is more open than the right, the left *nasolabial fold is absent, and the left corner of her mouth droops.* On the left side, she cannot voluntarily raise her eyebrow, close her eyelid, elevate her mouth into a smile, snarl, or pucker her lips.
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Bell's Palsy+ Zoster
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Ramsay Hunt Syndrome
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Bell's Palsy Tx
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Predinose, Acyclovir (if +herpes)
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Bell's Palsy others causes
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Lyme disease
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Transient ischemic attack (TIA) is a
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Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.
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Majority of TIAs resolve within the
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first hour, and diagnostic imaging allows recognition that some events with rapid clinical resolution are associated with permanent cerebral infarction
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Etiology of TIA
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-atherosclerosis, lipohyalinosis, inflammation, amyloid deposition, arterial dissection, developmental malformation, aneurysmal dilation, or venous thrombosis. -embolism of thrombus -Inadequate cerebral blood flow due to decreased perfusion pressure or increased blood viscosity. -rupture of a vessel in the subarachnoid space or intracerebral tissue.
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A transient ischemic attack (TIA) should be considered a syndrome. These syndromes are conveniently divided into three pathophysiologic mechanisms:
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?Large artery low-flow TIA (true TIA) ?Embolic TIA, which may be artery-to-artery, or due to a cardioaortic or unknown source ?Lacunar or small penetrating vessel TIA
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Large artery low-flow TIA (true TIA) Low-flow TIAs usually are short-lived (minutes) and often recurrent.
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Due to hemodynamically significant stenotic lesions at the origin of the internal carotid artery, at the siphon portion of the internal carotid artery where collateral flow to the circle of Willis is inadequate, or in the middle cerebral artery stem. Symptoms due to ischemia from these lesions often include hand, arm, leg, face, tongue, or cheek numbness or weakness together
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Embolic TIAs in the anterior circulation: Embolic TIAs typically last hours rather than minutes as in low-flow TIAs.
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may be large enough to occlude the middle cerebral artery stem, producing a contralateral hemiplegia
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TIA Clinical features
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a. If the TIA is related to a disturbance in carotid circulation, patients may demonstrate contralateral hand-arm weakness with sensory loss, ipsilateral visual symptoms or aphasia, or amaurosis fugax. Carotid bruit may be present, but with a high-grade stenosis (95%), it may be absent. b. Those experiencing vertebrovascular TIA may demonstrate diplopia, ataxia, vertigo, dysarthria, cranial nerve palsies, lower extremity weakness, dimness or blurring of vision, perioral numbness, or drop attacks.
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TIA S/S
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Has weakness , visual loss, numbness but resolves
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TIA Dx
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-Brain imaging with CT or MRI -Noninvasive options for evaluation of large vessel occlusive disease include magnetic resonance angiography (MRA), computed tomography angiography (CTA), carotid duplex ultrasonography (CDUS), and transcranial Doppler ultrasonography (TCD)
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TIA tx
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-ASA, clopidogrel (Plavix) -*Cardiogenic TIA* requires anticoagulation, initially with *intravenous (IV) heparin for those who are admitted to the hospital and with warfarin for long-term therapy.*
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TIA with BP ;185/100 treat with:
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Labetalol
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Ischemia — There are three main subtypes of brain ischemia:
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?Thrombosis ?Embolism ?Systemic hypoperfusion
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What is a major risk factor for ischemic stroke?
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Chronic hypertension Others: hypercholesterolemia, diabetes, oral contraceptives, cigarette smoking, heavy alcohol use, AIDS, and elevated blood homocysteine levels.
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Stroke Clinical features a. Signs and symptoms of stroke begin abruptly and, by definition, last longer than 24 hours. They correlate with the area of the brain that is supplied by the affected vessel, especially with ischemic events.
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b. In most cases, hemiparesis or hemisensory deficit is revealed on history and physical examination. One can localize the lesion to one side, contralateral to these deficits.
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Anterior Circulation Stroke:
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associated with hemispheric signs and symptoms (aphasia, apraxia, hemiparesis, hemisensory losses, visual field defects: Homonymous Hemianopia).
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Posterior Circulation Stroke:
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which supplies the brain stem, cerebellum, thalamus, and portions of the temporal and occipital lobes, commonly are associated with evidence of brain stem dysfunction (coma, drop attacks, vertigo, nausea, vomiting, ataxia).
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Ischemic Stroke Anterior involves
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Frontal and middle cerebral arteries
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Ischemic Stroke S/S
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Hemiparesis
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tPA contraindition
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1. BP ; 185/100 2. Recent MI the last 3 months 3. Major surgery 14 days ago 4. Increase PTT 5. Platelet 1.7 7. Glucose ;50 8. Active bleed 9. Head trauma the last 3 months 10. Hx of intracranial Hemorrhage
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Ischemic Stroke Posterior Cerebellar Function "VANISH'D
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Vertigo Ataxia Nystagmus Intention tremor Slurred speech Heel-shin test Dysdiadochokinesia
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Lacunar Stroke Syndrome
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?Pure motor hemiparesis ?Pure sensory stroke ?Ataxic hemiparesis
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Lacunar Stroke often occur with pt with
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HTN and Diabetes
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Pure motor hemiparesis
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It is characterized by weakness involving the face, arm, and leg on one side of the body in the absence of "cortical" signs (aphasia, agnosia, neglect, apraxia, or hemianopsia) or sensory deficit.
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Pure sensory stroke
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defined as numbness of the face, arm, and leg on one side of the body in the absence of motor deficit or "cortical" signs.
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Ataxic hemiparesis
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Develop ipsilateral weakness and limb ataxia that is out of proportion to the motor deficit. Some patients may exhibit dysarthria, nystagmus, and gait deviation towards the affected side.
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What is the Cerebral Aneurysm?
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is an acquired focal abnormal dilation of the wall of an artery in the brain. Intracranial aneurysms are most commonly located at branching points of the major arteries at the base of the brain, which course through the subarachnoid space.
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Types of cerebral aneurysm
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*Saccular* -Often termed a *berry aneurysm*, as it resembles a berry hanging from a vine -Rounded outpouching attached by a neck or stem to a brain artery. *Fusiform* -Also called atherosclerotic aneurysm -Forms as media damage leads to arterial stretching and elongation -Intraluminal clots may form.
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Cerebral Aneurysm most common
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Berry Aneurysm
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Ruptured saccular (berry) aneurysm accounts for approximately 75% of nontraumatic cases of:
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subarachnoid hemorrhage (SAH) and has a mortality rate of 50%
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Cerebral Aneurysm Presentation
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HA, nuchal rigidity (New neck stiffness that includes pain on stretching the neck meninges with maneuvers.)
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Cerebral Aneurysm assoc with
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Polycystic kidney Disease, Coarctation of the aorta, Endocarditis, Ehlers-Danlos
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Cerebral Aneurysm Dx
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CT(referred initial diagnostic study)/MRI
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Cerebral Aneurysm Tx
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Coiling. Clipping
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Cerebral Aneurysm if rupture can lead to:
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Subarachoid Hemorrhage
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Subarachnoid hemorrhage S/S:
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Acute onset Tunderclap HA, "Worst HA of my life" PE: Nuchal rigidity, impaired mental state Other signs of meningeal irritation, including *photophobia, nausea/vomiting*, and meningeal stretch signs, may also be seen.
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HA, nuchal rigidity (Cerebral Aneurysm) + photophobia, nausea/vomiting (bleeding) =
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Subarachnoid hemorrhage
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Subarachnoid hemorrhage Dx on CT
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-Look for Hyperdense area on CT. -Hyperdense areas in the basal cisterns, major fissures, and sulci
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Subarachnoid hemorrhage Tx
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Clip or coil aneurysms
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How you reverse Heparin treatment?
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Protamine Sulfate "He Pro me"
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Subarachnoid hemorrhage: What should be performed if CT is unrevealing?
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Lumbar Puncture
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How you reverse Warfarin treatment?
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Vitamin K & fresh frozen plasma (FFP) "War with Kings"
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Brain Tumor Met
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1st Breast 2nd Lung 3rd GI 4th Kidney "Be loved or Get Knocked up"
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Brain Tumor Dx
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MRI
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Primary Brain Tumor Frontal lobe
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personality or intellectual change
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Primary Brain Tumor Temporal Lobe
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lip smacking, olfactory or gustatory
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Primary Brain Tumor Parietal Lobe
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sensory seizure or sensory loss
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Primary Brain Tumor Brain stem
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cranial nerve palsy
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Primary Brain Tumor Pituitary Tumor
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Endocrine symptoms
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Primary Brain Tumor Occipital Lobe
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Visual defect or hallucination
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Primary Brain Tumor Tx
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Surgery or radiotherapy
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Epidural hematoma caused by
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Someone getting hit in the head
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Epidural hematoma
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Transient loss of consciousness so-called "lucid interval"
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Epidural hematoma other signs to look for:
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hematoma expansion leads to elevated intracranial pressure and clinical signs, such as an ipsilateral dilated pupil, hemiparesis.
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Epidural hematoma artery involved
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Middle meningeal artery "MMA fighter"
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Epidural hematoma CT brain
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Convex, biconvex, lens shape
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Epidural hematoma Tx
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Urgent surgery
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Elderly pt with multiple fall over the past 6 months or year..think!
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Subdural Hematoma
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Subdural hematoma is
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a collection of blood between the dural and arachnoid coverings of the brain. As the volume of the hematoma increases, the intracranial pressure may rise and cause herniation.
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___________ is the most common cause of Subdural hematoma, with the majority of cases related to motor vehicle accidents, falls, and assaults.
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Head trauma
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Subdural hematoma risk factors:
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-Patients with significant cerebral atrophy are at high risk for SDH. -Recent trauma, elderly, those with a history of chronic alcohol abuse, and those with previous traumatic brain injury, coagulopathy, anticoagulant use.
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Subdural Hematoma Dx:
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CT brain -Concave, crescent shaped
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The categories of acute, subacute, and chronic SDH are arbitrarily defined by time from onset:
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?Acute SDH presents one to two days after onset ?Subacute SDH presents 3 to 14 days after onset ?Chronic SDH presents 15 or more days after onset
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Acute subdural hematoma PE
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symptoms of elevated intracranial pressure including headache, vomiting, anisocoria, dysphagia, cranial nerve palsies, nuchal rigidity, and ataxia.
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Chronic subdural hematoma PE
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The insidious onset of headaches, light-headedness, cognitive impairment, apathy, somnolence, and occasionally seizures, may occur as a consequence of chronic SDH, and symptoms may not become evident until weeks after the initial injury. Global deficits such as disturbances of consciousness are more common than focal deficits after SDH.
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Subdural Hematoma S/S
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HA, N/V, nuchal rigidity, anisocoria, dysphagia
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Subdural Hematoma Tx
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*Burr holes* or craniotomy -Once the diagnosis has been established, *burr holes* over the hematoma are indicated to evacuate the clot.
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Subdural Hematoma increase intracranial pressure. What is treatment?
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Hyperventilation, *Mannitol*
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Seizure Partial Seizure: Simple and complex
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Simple: Consciousness is not impaired Complex: Consciousness is impaired (Over 30 sec)
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Seizure Generalized: Absence, Tonic-Clonic
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Absence: Staring <15 sec Tonic: Body very stiff and rigid Clonic: Convulsions and limb jerking
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Seizure eval:
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Glucose Level, Electrolytes, ABG, CBC, Urine toxic, Drug
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Partial Seizure two type: -Complex partial seizure -Simple partial seizure
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-A complex partial seizure (CPS) implies that consciousness is impaired -Simple partial seizures (SPS) are not associated with altered consciousness.
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Complex partial seizure
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they often seem to stare into space and either remain motionless or engage in repetitive behaviors, called automatisms, such as facial grimacing, gesturing, chewing, lip smacking, snapping fingers, repeating words or phrases, walking, running, or undressing. Patients may become hostile or aggressive if physically restrained during complex partial seizures.
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-Simple partial seizures
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-Beginning of the seizure are referred to as the warning or aura. -The symptoms of simple partial seizures vary from one patient to another and depend entirely on where the seizure originates in the brain, that is, the part of the cortex that is disrupted at the onset of the seizure. A seizure that begins in the occipital cortex may result in flashing lights, while a seizure that affects the motor cortex will result in rhythmic jerking movements of the face, arm, or leg on the side of the body opposite to the involved cortex (Jacksonian seizure).
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Partial Seizure focal location in the brain affected often
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temporal lobe
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Generalized Seizure: start midbrain or brainstem, spread to both cortices
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Subtypes of generalized seizures are: -tonic-clonic seizures (grand mal) -absence seizures (petit mal) -myoclonic seizures.
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What is the frequent complication of alcohol withdrawal?
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Generalized Seizure
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Tonic-Clonic Seizure Presentation
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-It begins with an abrupt loss of consciousness, often in association with a scream or shriek. -*All of the muscles of the arms and legs as well as the chest and back then become stiff*. The patient may begin to appear cyanotic during this *tonic phase* -After approximately one minute, the *muscles begin to jerk and twitch for an additional one to two minutes. During this clonic phase* the tongue can be bitten, and frothy and bloody sputum may be seen coming out of the mouth.
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Absence seizures (petit mal)
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Absence seizures (also called petit mal) usually occur during childhood and typically last between 5 and 10 seconds. They frequently occur in clusters and may take place dozens or even hundreds of times a day. *Absence seizures cause sudden staring with impaired consciousness*
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Absence Sz tx
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Ethosuximide, Valproic Acid
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Partial Sz Tx
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Carbamazepine, 2nd line Valproic Acid
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Generalized Sz Tx
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Valproic Acid
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Phenytoin can be used for
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Partial and Generalized, but not Absence Sz
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The most common medical neurologic emergency in childhood, ____________ is a serious and often life-threatening medical emergency
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status epilepticus (SE) Lasts for a sufficient length of time (30 minutes or longer in most studies) or is repeated frequently enough that the individual does not regain consciousness between seizures
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Status epilepticus emergency due to
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permanent brain damage secondary to hyperthermia, circulatory collapse, or excitotoxic neuronal damage
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Status Epilepticus
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Sz longer than 5-10 min.
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Status Epilepticus Tx
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-Maintain ABCs; consider rapid intubation for airway protection. -Administer thiamine, followed by glucose and naloxone to presumptively treat potential etiologies. -Give an IV benzodiazepine (lorazepam or diazepam) plus a loading dose of fosphenytoin.
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Status Epilepticus Caused by
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Decrease in K+, Na+, hypoglycemia
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Neurogenic Syncope is due to
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reflex response Triggered by stress: Venipuncture, prolonged standing, heat, fear of injury, painful or noxious stimuli
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Neurogenic Syncope Dx
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Check orthostatic , Glucose Tilt table test Holter monitor
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Neurogenic Syncope Tx
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Avoid situation causing the trigger Pt education Proper Hydration
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Concussion is
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is a closed head injury due to a direct blow to the head or deceleration of the head from an impulsive force that results in a change in mental status.
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Diagnosis of concussion should be considered if 1 or more of the following are reported or observed:
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-Confusion or disorientation -Amnesia near the time of the injury (retro- or anterograde) -Loss of consciousness for up to 30 minutes -Neurologic or neuropsychological problems -Score 13 or higher on the Glasgow Coma Scale (GCS).
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Concussion Symtoms and Sign
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-The hallmark symptoms of concussion are confusion and amnesia, sometimes with, but often without, preceding loss of consciousness. - Early symptoms of concussion (within minutes to hours) include headache, dizziness (vertigo or imbalance), lack of awareness of surroundings, and nausea and vomiting
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How many min after injury can you do the Glasgow Coma Scale?
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30min after injury
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Tremors: Resting
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Parkinson's disease Tremor at rest goes away with movement Tx: Dopamine agonist
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Cantu Guidelines Grade 2
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+LOC 30mins but <1 week Anything less than that should be grade 1 Anything greater should be grade 3
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Tremors: Action 2 kinds
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Physiologic: Due to caffeine, catecholamines, nicotine, anxiety. Tx with removal of offending agents Essential: Genetic Tx: Propranolol and primidone
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Tremors: intention
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Tremor increase in severity as the hand moves closer to its target. Tx: no treatment
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Parkinson's Treatment
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age 65: Levodopa, carbidopa Pt <65 taking Levodopa, this can cause dyskinesia
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Parkinson's Disease S/S:
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shuffling stepping gait, cogwheel rigidity, pill-rolling, lack of facial expression.
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Huntington' s disease
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is an inherited, autosomal dominant disorder that occurs throughout the world in all ethnic groups.
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Huntington' s disease S/S
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a. The disease is characterized by progressive *chorea* and dementia; it is usually fatal within 15 to 20 years. b. The earliest mental changes often are behavioral, with irritability, moodiness, and antisocial behavior that generally progress to an obvious dementia. c. The earliest physical signs may be a mere restlessness or fidgetiness, but, eventually, *severe choreiform* movements and dystonic posturing occur.
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Huntington' s disease Dx
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CT demonstrates cerebral atrophy as well as atrophy of the caudate nucleus. MRI and PET scans have shown decreased glucose metabolism in an anatomically normal caudate nucleus.
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Huntington' s disease Tx:
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*Chorea: Tetrabenazine* Chore+psychosis: Olanzapine, risperidone, haloperidol Symptomatic treatment for the disease may include phenothiazines to control dyskinesia, and haloperidol or clozapine to control any behavioral disturbances.
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Extrapyramidal syndrome is usually due to the intake of
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Haldol
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Extrapyramidal syndrome
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movement disorders such as akathisia, dystonia, and parkinsonism, caused by antipsychotic drug therapy
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What is akathisia?
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-The state of restlessness characterized by an urgent need for movement, usually as a side effect of medication.
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What akathisia can be prevented by giving?
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Benzodiazepine medicationf
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Extrapyramidal syndrome tx
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Diphenhydramine (Benadryl)
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Tardive Dyskinesia
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A side effect of long-term use of traditional antipsychotic drugs causing the person to have uncontrollable facial tics, grimaces, and other involuntary movements of the lips, jaw, and tongue.
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Guillain-Barre is an
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autoimmune neuropathies, are *predominantly demyelinating*, and a variety of clinical and experimental data have implicated both humoral factors and cell-mediated immune phenomena, which damage myelin and/or the myelin-producing Schwann cells.
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Guillain-Barre PE
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Acute asymmetric ascending inflammatory neuropathy; Weakness begins in lower and ascends; respiratory failure can occur in sever cases; *reflexes invariably decreased or absents*; 2/3 of patient have respiratory or GI illness 1-3 weeks prior to onset; Albuminocytologic dissociation
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Guillain-Barre
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Weakness of the legs to total paralysis of all four limbs, facial muscles, and eyes.
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Initial diagnosis of Guillain-Barré syndrome (GBS) is based upon the clinical presentation.
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Cerebrospinal fluid analysis — In patients with GBS, lumbar puncture often reveals an *elevated CSF protein with a normal CSF white blood cell count. This finding, known as albuminocytologic dissociation*
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Guillain-Barre can be cause by what...
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Campylobacter jejuni, CMV, HIV, or by recent immunization
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Guillain-Barre Dx
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1st initial :Lumbar puncture Increase CSF protein, with normal WBC -Electromyography
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Guillain-Barre Tx
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-1st Line IV Immune globulin -Plasma exchange (remove circulating antibodies) *Avoid Steroids*
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Myasthenia Gravis
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autoimmune attack of acetycholine receptors in neuromuscular junction
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Myasthenia Gravis Word breakdown
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My=Muscle A= Without Sthenos= Strength
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Myasthenia Gravis Symptoms
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Proximal to distal weakness Eyes: bilateral Ptosis usually 1st The weakness is limited to the eyelids and extraocular muscles
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Myasthenia Gravis
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DTR are intact, no sensory abnormalities, normal pupillary light relfex
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Myasthenia Gravis Dx:
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Best initial test: Acetylcholine receptor antibody. *More reliable laboratory methods that aid in the confirmation are serologic tests for autoantibodies and electrophysiologic studies* (muscle fiber contraction on repetitive nerve stimulation) Edrophonium/Tensilon Test (Acetylcholinesterase inhibitor)
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Myasthenia Gravis: Chest radiographs (CT or MRI should be obtained to rule out a coexisting _________.
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Thymoma
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Myasthenia Gravis associated with
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High incidence of thymus abnormalities
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Myasthenia Gravis tx
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Pyridostigmine (cholinesterase inhibitor) Thymectomy if < 60 y.o.
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Myasthenia Gravis Alternative treatment
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-Corticosteroids, immunosuppressive agents. -If steroid fail- Azathioprine usually added. -IV immunoglobulin, and plasmapheresis are effective in patients with refractory disease.
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Myasthenia Gravis can cause by medication:
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Magnesium Sulfate, pencillamine, *aminoglycoside*, interferon-Alpha
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Myasthenia Gravis S/S
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ptosis, weak chewing, fatigue, weakness with everday activities (brushing hair, etc)
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Multiple Sclerosis
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Distal to proximal weakness or or visual changes often over many years due to demyelination and inflammation on CNS not peripheral).
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Patients with MS typically follow either a relapsing-remitting pattern of episodes or a primary progressive course.
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A secondary progressive form also is seen, in which the relapsing-remitting pattern changes to one of progressive degeneration.
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Multiple Sclerosis Dx
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-diagnosis cannot be based exclusively on laboratory findings. *MRI with gadolinium is very effective for visualizing white matter lesions in the CNS.* 2nd: *Oligoclonal bands and elevated CSF IgG and IgG synthesis rates are present in 80% of MS cases*
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Multiple Sclerosis MRI hints
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White matter changes/ T2 hyperintensity
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Multiple Sclerosis Lab
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mild lymphocytosis or slight protein elevation, elevated immunoglobulin G index, oligoclonal bands, and increased myelin basic protein
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Multiple Sclerosis S/S
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Optic neuritis & vision changes often 1st
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Multiple Sclerosis Tx
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Acute: Glucocorticoids Long-term: Interferon Beta
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The cerebral palsy (CP) syndromes are
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characterized by abnormalities of motor activity and posture.
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Cerebral Palsy 3 Types Movement disorder classification
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Spastic Dyskinetic Ataxic
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Cerebral Palsy: Spastic
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Spastic CP is an upper motor neuron syndrome. S/S: spastic hyperreflexia, extensor plantar, response, and clonus May be: Diplegia, asymmetric, Hemiplegia, Quadriplegia
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Cerebral Palsy: Dyskinetic
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Involuntary, recurring, and occasionally stereotyped movements with a varying muscle tone. Subgroups include: Dystonia: characterized by involuntary, sustained contractions resulting in twisting and abnormal postures. Chorea: rapid, involuntary, jerky, and fragmented motions; tone is usually decreased but fluctuating. Athetosis: slower, constantly changing, writhing, or contorting movements.
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Cerebral Palsy: Ataxic
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Loss of muscular coordination with abnormal force and rhythm, and impairment of accuracy. Commonly presents with gait and trunk ataxia, poor balance, past pointing, terminal intention tremor, scanning speech, nystagmus and other abnormal eye movements, and hypotonia.
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Cerebral Palsy due to
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The multifactorial etiology was illustrated in a series of 213 children diagnosed with CP in Australia. Major CP-associated pathologies other than acute intrapartum *hypoxia were identified in 98 percent of cases*
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Cerebral Palsy Diagnostic test:
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MRI periventricular leukomalacia, congenital malformation, stroke or hemorrhage, cystic lesions
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Cerebral Palsy Treatment:
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Treatment is supportive, with the goal of attaining maximum function and potential in physical, occupational, and speech ability
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Meningitis aseptic meningitis:
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-Viral or other cause -Most common cause is enterovirus (Coxsackie A and B viruses, Echoviruses, and Polioviruses) - Additional etiologies include other infections, (mycobacteria, fungi, spirochetes), parameningeal infections, medications, and malignancy
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Meningitis Bacteria
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S. Pneumonia N. Meningitis (Look for rash)
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Meningitis aseptic Presentation
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headache, nausea and vomiting, photophobia, neck stiffness (nuchal rigidity), fever
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Meningitis Daignostic
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Examination of the cerebrospinal fluid (CSF) is crucial for establishing the diagnosis of bacterial meningitis, identifying the causative organism, and performing in vitro susceptibility testing . Indications for CT scan before LP — Every patient with suspected meningitis should have CSF obtained unless lumbar puncture (LP) is contraindicated.
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What is the rational for dosing dexamethasone prior to or along with the first dose of antibiotics for empiric treatment of bacterial meningitis?
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Dexamethasone when given with or prior to the first dose of antibiotic reduces the risk of *Hearing losss* in children with meningitis, especially in the cases of Influenza B, TB, meningitis.
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Meningitis Bacteria Tx
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Dexamethasone (used to minimize adema within the CNS) Ceftriaxone, Macrolides, Penicillin
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In adults with bacterial meningitis, dexamethasone reduces both morbidity and mortality especially in the case of
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Strept Pneumo
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Meningitis Bacteria look for increase in intracranial pressure
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Do fundascopic exam to r/o papillaedma
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Most common Meningitis Bacteria in the 1st month of life
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Group B strep and E.Coli
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In the adult with rash, which of the following is the most likely organism to cause bacterial meningitis?
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N. Meningitis
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What is the treatment for viral meningitis?
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-Acetaminophen for pain -IV Fluid -Empiric antibiotics Until viral is confirmed -Acyclovir if suspicion of HSV
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In the adult neutropenic (immunocompromised) patient, which of the following is the most likely organism to cause bacterial meningitis?
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Listeria
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What is Encephalitis?
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is a pathologic state of brain parenchymal dysfunction demonstrated by an altered state of consciousness and/or signs of neurologic dysfunction (e.g., seizures, personality changes, cranial nerve palsies, speech problems, and motor and sensory deficits).
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Encephalitis organisms:
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HSV and arboviruses are the most common causes of encephalitis. Rarer etiologies include CMV, toxoplasmosis, West Nile virus, VZV, Borrelia, Rickettsia, Legionella, enterovirus, Mycoplasma, and cerebral malaria. Children and the elderly are the most vulnerable
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Encephalitis presentation
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-markedly altered consciousness, seizures, personality changes, or other focal neurologic signs. -Lethargy, confusion, coma, and focal neurologic deficits (cranial nerve deficits, accentuated DTRs) may also be present.
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Encephalitis Diagnostic Test
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initial diagnostic step in the patient with suspected viral encephalitis is analysis of the CSF; lumbar puncture
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Encephalitis treatment
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-HSV encephalitis: Requires immediate IV acyclovir. -CMV encephalitis: Treat with IV ganciclovir +/? foscarnet. -Give doxycycline for suspected Rocky Mountain spotted fever, Lyme disease, or ehrlichiosis.
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Rabies S/S
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Hydrophobia, aerophobia, pharyngeal spasms, and hyperactivity
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Rabies Tx
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Rabies Immunoglobulin
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Encephalopathy: vomiting, confusion, Sz, coma in child after exposure to
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Saliccylates (ASA), Pept-Bismol Condition called *Reye's Syndrome*
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What is Reye's Syndrome?
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Reye's Syndrome, or fatty liver encephalopathy, has been associated with ASA use in children with viral infections, including influenza.
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Reye's Syndrome treatment
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-Ondansetron may be given to decrease vomiting. -Seizure: phenytoin
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Dementia with Lewy Bodies:
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-Visual hallucinations -Progressive dementia -Spontaneous motor features of Parkinsonism
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Alzheimer's Disease
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-Age >60 -MMSE -Memory loss
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Alzheimer's Disease Treatment
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Donepezil, rivastigmine, and galantamine.