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Neuro 2 Midterm
Neuro 2 Midterm presentations
| Question | Answer |
|---|---|
| What disease is the most common form of endolymphatic hydrops? | Menier's Disease - Endolymphatic hydrops: a disorder relating to the membranous inner ear - consequence of over-accumulation of endolymph in the perilymphatic space - and lack of absorption of endolymph in endolymphatic duct and sac |
| Which disease involves the disruption of the homeostasis in the inner ear fluid? | Menier's disease - deficits related to changes in volume and pressure |
| Which disease is Dx'ed with a PMHx of 2 or more definitive episodes of spontaneous rotational vertigo lasting at least 20 minutes (with nausea and vomiting)? | Menier's disease - other Dx tests include: Low-frequency sensorineural hearing loss documented by audiometry; Tinnitus or aural fullness in the affected ear; Exclusion of other causes for the symptoms |
| Which disease has a clinical manifestation of Recurrent, abrupt episodes of vertigo (may last 30 minutes to 24 hours), Postural imbalance and Varying degrees of nausea and vomiting? | Menier's disease - other manifestations include: Fluctuating, sensorineural hearing loss, Sensation of fullness in the ears, tinnitus, drop attacks and progressively worsening symptoms with each acute attack |
| What are some medical management options for Menier's disease? | Diuretics, diet modifcations, histamine, antiemetics, sedatives, antidepressants, psychiatric tx, rest in bed during an attack, surgery on Endolymphatic sac drainage with local steroids |
| What are some PT interventions for Menier's disease? | Work with behavior therapy for coping with disorder, reduce stress/phobias, relax, balance/proprioception training, pt education |
| Which disease has the prognosis of affecting 1 ear then spreading bilaterally 45% of the time, with fluctuating hearing loss that can eventually become irreversible? | Menier's disease - attacks increase in frequency within the first year and then decrease |
| Which disease is a disease of the brain, coverings of the brain and spinal cord where Upon contracting syphilis it invades the CNS almost immediately but may not involve it until later on if untreated? | Neurosyphilis - 5 different types: asymptomatic, meningeal, meningiovascular, general paresis and tabes dorsalis |
| Which disease can be caused by the bacteria, treponema pallidum, which uses man as its primary host and transmission is attained through acute infectious lesions ? | Neurosyphilis - T. Pallidum begins to invade other organisms, most commonly the heart and CNS causing many neurological signs and symptoms |
| What type of Neurosyphilis does not have any neuro s&s, but has CSF abnormalities such as positive CSF VDRL, pleocytosis, and/or elevated protein concentration? | Asymptomatic Neurosyphilis - Rates of ANS decreases as duration of syphilis infection increases - Those that had signs of syphilis and were diagnosed with ANS posed a higher risk if untreated of developing late neurological symptoms |
| What type of neurosyphilis has Diffuse inflammation of the meninges causing symptoms of meningitis such as headache, stiff neck, nausea and vomiting, cranial nerve palsies, photophobia and occasionally seizures? | Meningeal Neurosyphilis - Can occur within the first two weeks of contracting syphilis up to a few years after contracting the STD - may affect vision and hearing |
| What type of neurosyphilis can occur with in the first few weeks to several years after contracting syphilis, where Individuals will have the same symptoms as meningeal neurosyphilis however, these individuals carry the possibility of having a stroke? | Meningovascular Neurosyphilis - If spinal cord vessels involved, develop syphilitic meningiomyelitis or spinal vascular syphilis - inflammation of the inner lining of vessels in the CNS = thrombosis and infarction - esp middle cerebral arteries |
| What type of neurosyphilis can occur 3-30 years after contracting syphilis, with an insidious or sudden onset, leading to Atrophy of temporal/frontal lobe and sparing motor, occipital and sensory cortex leading to dilation of the lateral ventricles? | General Paresis Neurosyphilis - Early symptoms: irritability, forgetfulness, personality changes, HAs/changes in sleep habits; Late symptoms: emotional lability, impaired memory/judgment, disorientation, confusion, delusions and occasional seizures |
| What type of neurosyphilis has Psychiatric manifestations of depression, mania, delirium, and psychosis, dementia and Neurological symptoms: pupillary abnormalities, dysarthria, tremors of facial, lingual or hand muscles? | General Paresis Neurosyphilis |
| What type of neurosyphilis Can occur anywhere from 5-50 years after contracting syphilis and is Characterized by pain in the limbs or abdomen, failure of muscle coordination and bladder disturbances? | Tabes Dorsalis - has s&s of Ataxic gait, lightning pains, paresthesia, bladder dysfunction, failing vision, Pupillary abnormalities, diminished reflexes, ocular palsies, Charcot’s joints and Degeneration of posterior roots and column of spinal cord |
| Which 2 types of neurosyphilis are less common now due to prevention, screening and treatment ? | Tabes Dorsalis and General Paresis |
| What is a "confirmed" dx of syphilis according to the CDC? | any stage of syphilis and a reactive CSF VDRL |
| What is a "presumptive" dx of syphilis according to the CDC? | Presumptive is any stage of syphilis, a nonreactive CSF VDRL, CSF pleocytosis or elevated protein, and clinical signs and symptoms consistent with syphilis without an alternate diagnosis to account for these |
| What disease involves Two types of serological testing is necessary to make a diagnosis, including nonspecific lipoidal tests (RPR and VDRL) are chosen as screening tests and treponemal specific tests are used to confirm diagnosis? | Neurosyphilis - A positive response to treatment is seen as a 4 fold decline in nontreponemal titers; early stages: results expected 6-12 months after treatment is started; In late stage: results expected 12-14 months after treatment is started |
| What do the 2006 CDC treatment guidelines recommend that a CSF examination be performed in all patients with? | 1. Serological evidence of syphilis and neurological symptoms 2. When serological titers among asymptomatic patients don’t respond appropriately to treatment |
| What is the medical management for neurosyphilis? | PCN (IV or daily intramuscular injections for 10-14 days) w/ probenecid by mouth 4 times a day; or ceftriaxone |
| Which 2 types of neurosyphilis usually return to normal health with resolution of all neurological symptoms with treatment? | asymptomatic or meningeal |
| Which 3 types of neurosyphilis usually don’t return to normal health and still maintain some neurological symptoms but do get much better? | meningovascular, general paresis and tabes dorsalis |
| How is response to tx assessed with neurosyphilis? | based resolution of CSF abnormalities and CSF VDRL - Normalization of CSF WBC count occurs in the majority of non HIV patients within 6 months and CSF VDRL titers within 14 months after treatment |
| Which type of neurosyphilis should be considered as a differential diagnosis in individuals at a young age who have suffered a stroke, Especially in those patients with prodromal syndrome of headaches, cranial neuropathies or cognitive changes? | Meningovascular neurosyphilis - do lumbar puncture during stroke workup of younger pts with the absence of conventional risk factors |
| Why are HIV pts w/ syphilis more likely to develop neurosyphilis? | Cell mediated immunodeficiency and functional defects in macrophages and immunoglobulin producing B cells alter the course of the disease |
| What disease should be a differential dx for HIV pts with unexplained neurological symptoms? | Neurosyphilis - may be the first presentation of HIV and all patients diagnosed with neurosyphilis should be tested for HIV |
| What is the role of the PT in neurosyphilis pts? | Awareness of neuro s&s, treat stroke symptoms, refer out, address any lasting neurological symptoms that may affect balance, gait, ADL’s, coordination and muscle strength, and educate at risk pts |
| What are 3 functional measures for Vitamin B12 deficiency? | Peripheral neuropathy, Cognitive function, Disability |
| What are 3 combinations of Vitamin B12 deficiency? | 1. B12 deficient – higher total disability and cognitive impairments 2. B12 deficient + homocysteine rich - peripheral neuropathy, total disability, LE immobility 3. B12 deficient + MMA rich – higher peripheral neuropathy than B12 alone |
| What medication causes pts with Type 2 DM to have significantly lower B12 serum levels? | Metformin |
| Which vitamin was found deficient in first-time stroke survivors over the course of a year? | Vitamin D deficiency |
| What was the association found between Vit D deficiency and Type 2 DM? | High association between vitamin D deficiency and peripheral neuropathy |
| What are some medical management options for vitamin deficiencies? | dietary changes, supplementation, address underlying causes (GI disturbances or dec sun exposure) |
| What is the prognosis for vitamin deficiencies? | Early detection is key! Neurological symptoms of B12 deficiency may be irreversible Vitamin D repletion after stroke needs to be explored for effects on MS |
| What are some PT interventions for vitamin deficiencies? | Recognize S&S Recognize risk factors (Ie, metformin, etc.) Talk to physician |
| What type of vitamin deficiency Causes paresthesias or numbness of skin, coordination disorders as well as decreased NCV, unsteady gait and May be associated with progressive brain atrophy in elderly? | Vitamin B12 Deficiency - Increased Hcy levels associated with increased risk of dementia and Alzheimer’s |
| What is the Parasitic fungus, belongs to genus Claviceps, forms sclerotia on grains & grasses? | Ergot sclerotia- which causes Ergotism - Disease contracted by ingesting toxic levels of sclerotia. |
| What are the 2 types of ergotism? | Convulsive and Gangrenous |
| What do ergot alkaloids act upon? | the 5-HT serotonin subreceptors causing: 1.Peripheral vasoconstriction - Ischemia, 2. CNS damage affecting Posterior commissure, dorsal horn, posterior columns, cerebral cortex |
| What were the most recent outbreaks of ergotism? | France 1951 and Ethiopia 1977-78, 2001 |
| What are the modern causes of ergotism? | Caused by ergot-based drugs used to treat migraines |
| What are the Dx criteria for egotism? | MHx of grain ingestion, Sternbach's criteria: ergot exposure and at least 3 of: change in mental status, agitation, diaphoresis, diarrhea, fever, incoordination, clonus, hyperreflexia, shivering/tremors, absence of other etiologies or use of neuroleptics |
| What is the clinical manifestation of ergotism? | Initial Symptoms of GI distress, tactile formication; either convulsive or gangrenous presentation depending on amount of ergot ingested |
| Which type of ergotism as the following: pulseless limbs, blisters, distal skin color changes, dec blood flow, burning pain in extremities, and sensation loss? | Gangrenous ergotism - may develop dry gangrene and need amputation - high mortality |
| Which type of ergotism has distortion of trunk and limbs (muscle stiffness and abnormal postures), dec energy, hallucinations, delirium, mania, double vision, and profuse sweating? | Convulsive gangrene - mortality 10-20% |
| What are options for medical management of ergotism? | St. Anthony's Fire (lol), D/C ergot based meds, vasospastic drugs (caffeine, nicotine, beta blockers), use of vasodilators, balloon angioplasty, vascular surgery, hyperbaric chamber therapy |
| What are some PT interventions for ergotism? | educate on meds and traveling to regional danger zone, amputee care, improve function with residual paralysis, vision changes, ataxia and sensory loss |
| What disorder has Reduced blood flow to the extremities due to cold exposure or emotional triggers, is Episodic and spasmodic in nature, and Most commonly affects the fingers, toes, nose, and ears? | Raynaud's phenomenon - excessive vasospasm with imbalance in the constriction and dilation of vessels |
| What are the 2 types of raynaud's? | Primary idiopathic and Secondary - Occurs in association with other medical conditions generally rheumatic type conditions: Scleroderma (systemic sclerosis) and Systemic lupis |
| Which type of raynaud's is the most common, has an unknown cause and requires lifestyle changes? | Primary - The function of the endothelium in the blood vessel wall is changed |
| What type of raynaud's is linked to hematological disease (occlusive arterial disease), where the microvascular structure is irregular? | Secondary - Warning sign for underlying connective tissue disease (10-20% of patients with connective tissue disease have Raynaud’s) and pts can suffer from skin ulcers or gangrene |
| What are the 3 signs of the triphasic response to raynaud's? | 1. whitening of digits from vasoconstriction 2. black/blue cyanosis resulting in extreme coldness/pain 3. red flushing and burning sensation as blood travels back into tissue |
| What are some s&s for raynaud's? | Spasms, pain, numbness, throbbing, tingling - disappears within 1 hr, Thumb often spared with primary but involved in secondary Raynaud’s |
| Which type of raynaud's has normal nail bed capillaries but with functional abnormalities? | Primary |
| Which type of raynaud's has enlarge nail bed capillaries, presents with autoantibodies and structural abnormalities? | Secondary - due to the autoimmune component |
| What are some risk factors for raynaud's? | Family Hx, genetic link, operators of vibrating tools, meds (Beta-adreoceptor blocking drugs, amphetemines), Hypothyroidism, polycythaemia |
| What disorder has a diagnosis where MHx is important including: cold sensitivity, skin changes when cold (white, blue or black), digital ulcers, bilat s&s, family Hx and linked conditions? | Raynaud's |
| What are ways to dx raynaud's? | Blood tests for autoimmune diseases, rule out TOS (unilateral S&S), nailfold capillaroscopy (Differential between primary and secondary), and cold stress test (Performed if unsure about a diagnosis) |
| What is the medical management for raynaud's? | 1. Lifestyle changes (stop smoking, avoid cold) 2. Med (Calcium channel blockers: dilates vessels to allow for better blood flow, and Nitroglycerin or topical antibiotics for ulcers) 3. decrease stress (Regular exercise, Tai Chi, relaxation techniques) |
| What are some PT interventions for raynaud's? | Myofascial release - decrease length and intensity of primary raynaud's event; wound care for ulcers; educate on stress mngmt and lifestyle changes |
| What is the prognosis for raynaud's? | No cure, decrease freq/intensity of episodes, treat ulcers, avoid triggers |
| What disroder is a rapid involuntary movement of the eyes that can be pathological or non-pathological? | Nystagmus - If pathological, it is a symptom of an impairment from any system that affects eye movement - pathological can be congenital or acquired |
| What mechanism explains how nystagmus can be elicited in healthy individuals? | Optokinetic nystagmus – (The optokinetic reflex) is a normal reflex that allows the eye to watch objects in motion while the head remains stationary |
| What are 3 congenital causes for nystagmus? | Congenital blindness, albinism and INS (infantile nystagmus syndrome) - INS appears in first 6wks-3mo - can affect vision (corrective lenses help), most pts do not notice eye movements and compensate |
| What are some acquired causes of nystagmus? | BPPV, drugs, alcohol, inner ear infections of labyrinths, head injury, meniere's disease, stroke, thiamine or Vit B12 deficiency, or any other disease of the brain |
| What are the 3 directions of nystagmus and the 2 types? | Horizontal, vertical, rotational - Jerk or Pendular nystagmus |
| Which type of nystagmus comes from central disorders caused by lesions in the cerebellum, brain stem or cortex, where the oscillations of the eye are equal? | Pendular nystagmus |
| Which type of nystagmus comes from peripheral disorders, where The direction of pathological ocular movement is related to the semicircular canal that is being affected by the pathology? | Jerk Nystagmus - (most common) The oscillations alternate btwn fast movement one way and a slow movement the other way - latency is between 2-20 sec, duration is <60 sec. Is relieved by gaze fixation |
| What are ways to test for nystagmus? | Slowly perform figure 8, H pattern, or accommodation; fix pt gaze on single point 30 deg to left/right of center for 20 sec (no nystagmus should be noted); Dix-hallpike, Caloric reflex test |
| How do you document nystagmus? | list direction (vertical, horizontal, rotational), movement pattern (jerk/pendular) and direction of fast segment ( ie. horizontal jerk nystagmus to the right) |
| What meds or surgery options are there for nystagmus? | Meds: Baclofen, neurontin, levetiracetam, 3,4 diaminopyridine 4-aminopyridine, acetazolamid; Surgery: Recession of a rectus muscle insertion moved to a more posterior point on the eye (5-7 mm from insertion) |
| What are some problems associated with nystagmus? | dec depth perception, impaired balance/coordination, problems with binocular vision, "null point" head positions to dec S&S - Nystagmus can be aggravated by fatigue and stress |
| What are the PTs role for treating nystagmus? | mediate effects, refer out, balance/coordination training, stretching/strengthening or jt mobs to help with null points, reduce stress and increase endurance |
| What are some clinical implications of nystagmus? | no cure, may go away depending on underlying condition, cannot be used to dx a particular problem, identify during eval to help refer out, and document pt's hx and meds |
| Which condition involves the Patient loses the ability to perform previously learned movements on command, even though the command is understood and there is a willingness to perform the movement? | Apraxia - desire/capacity to move intact but cannot execute - Deficits most often seen in the limb contralateral to the affected hemisphere. |
| What are 5 causes of apraxia? | Stroke, neurodegenerative disease (corticobasal degeneration, progressive supranuclear palsy, parkinson's, alzheimer's, huntingtons), brain tumor, dementia, TBI |
| Damage to What part of the brain most commonly presents with apraxia? | L hemisphere, esp L parietal lobe - other areas include: The frontal and parietal lobes, basal ganglia, and white matter tracts [9] |
| What are the 3 main types of apraxia? | Limb kinetic, ideomotor, ideational |
| Which apraxia is an Inability to make precise or isolated movements with fingers, hand, arm, or leg, with Inaccurate or clumsy distal limb movements? | Limb-kinetic apraxia |
| Which apraxia is difficulty with the "how to," where the pt is unable to imitate another person’s gesture, to perform the appropriate action in response to a visually presented object, or to carry out a movement using the actual object? | ideomotor - can still perform action without thinking about it - affects timing, sequencing, amplitude, configuration and limb position in space |
| Which apraxia is difficulty with the "what to do," where the pt is unable to create a plan for a specific movement? | ideational |
| What are 4 other types of apraxia? | Dissociation (cannot gesture normally to command but can use tools/objects); Conceptual (cannot recall use of tools/objects); Bucco-facial (unable to move face on command); Speech (unable to plan or coordinate speech) |
| What system is affected with apraxia? | The praxis system: 1.brain regions that are involved in taking in processed sensory input 2. obtaining stored information about tools, gestures, and actions 3. translating these into a motor output |
| What are some differential dx's from apraxia? | Rule out comprehension deficit, muscle weakness, sensory impairment, tone abnormality, other movement disorder |
| How would you Dx apraxia? | present a tool and ask pt what it is or how to use it or ask pt to copy gesture |
| What factors affect prognosis of apraxia? | size of lesion, presence of associated disorders, health and attitude of pt and time of post-onset - pts with posterior lesions have poorer prog than anterior lesions |
| What are some implications for PT with apraxic pts? | become dependent with ADLs, useless limb can become clenched/painful fist, high risk of falls, nutritional deficits - refer out (esp OT) |
| What neuro condition is a recognition deficit affecting a single modality where cognitive abilities in other areas are preserved? | Agnosia - caused by stroke, dementia, neuro disorders, brain infection, head injruy (esp occipital or parietal) |
| What are 3 types of agnosia? | visual, auditory and tactile (cannot recognize objects by touch) |
| What are types of visual agnosias? | achromatopsia (color blindness-V4), color anomia (name colors -V4), akinetopsia (perceive visual motion V5/middle temporal gyrus), prosopagnosia (recognize faces-fusiform gyrus), pure object agnosia and simultagnosia (grasp multiple components of vision) |
| What are types of auditory agnosias? | agnosia for sounds, amusia, auditory verbal agnosia (word deafness) |
| How do pts with agnosia present? | Pt's are usually unaware of the extent of their sensory deficits - must make them aware |
| What are some treatments for visuoperceptual agnosias? | Eye movements, convergence, word reading, visuokinetic funcitoning, writing - teach pts use alternate modalities |
Created by:
rjchokito
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