neuro

Question 1

angiogram indications

Answer 1

• Evaluate blood vessels • Aneurysm • AV malformation

Question 2

plain film indications in nuero

Answer 2

• Evaluate for stenotic arteries in patients with TIA stroke

Question 3

• Nerve Conduction Studies (NCS) –

Answer 3

integrity of peripheral nerves: axons, myelin

Question 4

• Electromyography (EMG)

Answer 4

– electrical activity of muscle fibers

Question 5

EEG indications

Answer 5

− Seizure, seizure disorder − Altered level of consciousness, coma − Encephalopathy

Question 6

bacterial meningitis: etiology and pathophsyiology, RFs, clinical presetnation, lab findings, plan, sequelae of untx’d

Answer 6

Risk Factors • Exposure to meningitis • Travel to endemic areas- meningitis belt in Sub-Saharan Africa, important for travel exams • Respiratory tract infection • Injection drug use • Penetrating head trauma • Neurosurgery • Devices - shunt, cochlear implants Pathophysiology − Infections break down the blood-brain barrier and enter brain − Inflammation and irritation of meninges − Meningeal signs − Neurological complications − Cerebral edema Meningeal signs • Nuchal rigidity – stiff neck − Indicated by decreased neck flexion– inability to touch chin to chest or neck feels stiff when felt • Kernig’s sign- flex hip to 90° and patient doesn’t allow knee extension • Brudzinski’s sign- flex head and hip comes up sx Mild/moderate • Headache • Confusion • Irritability • Nausea • Vomiting sx severe Severe • Altered mental status • Cushing reflex- ↑BP and ↓ pulse • Papilledema- edematous look in the eye from ↑ cranial pressure • Cranial Nerve (CN) palsy • Herniation Systemic signs • Fever • Ill appearing • Pericarditis • Arthritis • Sepsis/septic shock • ARDS • N. meningitidis: Rash, Arthritis • Meningococcemia rash Physical Exam • Vital signs–temp • Meningeal signs − Nuchal rigidity – stiff neck − Often they can’t flex chin toward chest actively or passively. Document on exam or say “neck is supple” (normal) − Kernig’s (knee, can’t extend knee) − Brudzinski’s sign (when passively flex neck their hip will flex which is a reflex that takes pressure off spinal cord) • Neuro exam • Skin exam • Signs bacterial infection Labs • CBC, CMP, blood cultures (About 50% may be positive—not super helpful but if we can’t get a lumbar puncture its our best bet) • Lumbar puncture ASAP • Opening pressure elevated • Leukocytosis- can’t r/o with low WBC • Thrombocytopenia • PT/PTT- later stage • Electrolytes, BUN, creatinine, glucose tx: abx fatal if not tx’d

Question 7

bacterial meningitis presentation in infants

Answer 7

Infants: • Fever • Hypothermia • Lethargy • Respiratory distress • Jaundice • Poor feeding • Vomiting • Diarrhea • Seizures • Restlessness • Irritability • Bulging fontanel Neonates • Temperature instability • Neuro signs: Irritability, lethargy, poor tone, tremors, twitching, seizures, bulging/full fontanel, nuchal rigidity • Other: Poor feeding/vomiting, respiratory distress, apnea, diarrhea

Question 8

lumbar puncture side effects

Answer 8

• Post-LP headache • Infection • Bleeding • Cerebral herniation (since lowering pressure in spinal cord, risk that brain will herniate there) • Back pain • Minor neurological symptoms

Question 9

ddx of meningitis

Answer 9

Differential Diagnosis • Fever − Pneumonia − Influenza − URI − Viral infection − Gastroenteritis • Headache − Subarachnoid Hemorrhage- sudden, worst headache • Nuchal Rigidity − Musculoskeletal causes − Injury − Arthritis − Sleeping position

Question 10

aseptic meningitis patho, eti, clinical, dx, eval, tx

Answer 10

Pathophysiology • Mucosal surfaces of respiratory and GI tract • Viral replication in regional lymph nodes • Primary viremia – onset of illness and seeding of other organs • Second viremia - invasion CNS Symptoms • Viremia: − Signs of virus (viral exanthem) − Nonspecific viral symptoms − Fever, headache, malaise, myalgia, anorexia, nausea, vomiting • CNS invasion/meningeal inflammation: − Meningeal signs − Focal neurological deficits – less common Evaluation • Fever, headache, nausea, vomiting, photophobia, stiff neck Historical clues: • Travel history • Exposure to ticks and animals • TB risk factors • Sexual history (herpes, syphilis can cause it) • Exposure • Medications • Symptoms of specific viruses • Preceding illness Physical exam • Meningeal signs, neuro exam • Look for signs to suggest etiology • Rash, parotitis- mumps, genital lesions, thrush • Malignancy Diagnostic Tests • Labs – CBC, electrolytes, BUN, creatinine, glucose, blood cultures, PT/PTT Treatment • Still admit to hospital to follow them • Symptomatic treatment- can be outpatient − Analgesics, antipyretics, antiemetics − Fluids • Suspected viral − Antibiotics: elderly, immunocompromised, recently received abx (b/c at higher risk) − Observe: everyone else • Unclear viral or bacterial − Empiric antibiotics − Observe, repeat LP • Etiology confirmed- specific treatment as indicated

Question 11

encephalitis dx, patho, tx, eti

Answer 11

• Inflammation of brain parenchyma • Primary viral infection − Viral invasion of CNS − Culture from brain tissue • Postinfectious − Virus cannot be detected or recovered − As initial infection is resolving or subclinical illness Etiology • Most viruses predominantly cause either meningitis or encephalitis: • Arthropod-borne viruses- West Nile Virus • Herpes viruses- see below • St. Louis encephalitis • La Crosse virus • Varicella-zoster virus • Epstein-Barr virus History • 7 attributes of symptom • Encephalitis symptoms • Regional exposure and outbreaks • Geographic location- CO tick virus, etc. • Exposure history (insects and animals) • Sexual history • Recent travel Symptoms • Abnormalities in brain function • AMS – confused, agitated, obtunded • Seizures • Motor or sensory deficits • Altered behavior and personality • Speech or movement disorders • Focal deficits of meningitis: − Hemiparesis − Flaccid paralysis − Paresthesias − CNS deficits • Lack meningeal signs (photophobia, nuchal rigidity) • Fewer nonspecific signs and symptoms − Many times have fever, headache, nausea/vomiting • May have signs outside CNS of specific virus Physical Exam • No pathognomonic signs • Altered mental status • Focal neurological signs Signs of underlying illness • Rash • Mumps – parotitis • West Nile virus − Flaccid paralysis − Maculopapular rash − Tremors eyelids, tongue, lips, extremities • Rabies − Hydrophobia, aerophobia, pharyngeal spasm, hyperactivity • Varicella-zoster virus – grouped vesicles in a dermatome Tests • Consider PCR (HSV-1, HSV-2, and enteroviruses), bacterial culture, fungal culture, mycobacterial tests and serology for arbovirus • CSF: confirm inflammatory disease of CNS • May look like viral meningitis • CT to rule out space-occupying lesions or brain abscess • MRI can detect demyelination • EEG often abnormal • Brain Biopsy – last resort, if still unclear etiology tx: sxatic

Question 12

seizures: all possible causes

Answer 12

Etiology • Idiopathic • Degenerative: MS, presenile dementia- cause degradation of neurons or myelin sheaths • Infectious: meningitis, abscess, neurosyphilis • Metabolic: HYPOGLYCEMIA (easy to miss—if diabetic always check the blood sugar), hepatic failure, hyper-/hyponatremia- predisposing factor for electrolyte imbalance • Neoplastic: primary or metastatic tumors • Perinatal: infection, metabolic disorders (metabolites build up in brain)- newborns might be missing key enzymes • Toxic: theophylline, lidocaine (stabilizes neuronal membranes at therapeutic doses), TCAs, cocaine (and other street drugs) do a “tox screen” on anyone that prevents with a first time seizure • Head trauma: epidural/subdural hematomas, cerebral contusion • Vascular: stroke, Arterial Venous Malformation (AVM- clusters of dilated blood vessels susceptible to bleeds, AVMs in brain can cause seizures), subarachnoid hemorrhage (bleeds from aneurysm) • Eclampsia: pregnancy (preeclampsia↑BP, edema, and proteinuria- at risk for seizure → actual seizure=Eclampsia) (preeclampsia=toxemia of pregnancy) • Alcohol withdrawal- CNS depressant preventing seizure activity, withdrawal (usu 12-24 hr after last drink) removes that limitation

Question 13

what are the phases of grand mal seizures?

Answer 13

tonic, clonic, post ictal

Question 14

do petit mal seizures have post ictal phase?

Answer 14

no • Typically very brief (few seconds) • Abrupt LOC • Blank stare- eyelids may twitch • No response to voice • No falls, no involuntary movement, no incontinence- no tonic clonic behavior (Don’t lose muscle tone) • No post-ictal phase, attacks cease abruptly, patient unaware that

Question 15

what are simple partial seizures?

Answer 15

• No alteration of consciousness (totally alert) • Manifestations may be: 1. Motor − Tonic or clonic movements, often unilateral, often limited to one extremity 2. Sensory − Paresthesias/numbness (can’t feel this half of my body…i.e.) − Flashing lights − Olfactory/gustatory (taste) hallucinations

Question 16

what are myoclonic seizures?

Answer 16

• LOC associated with isolated jerking of one extremity • Unusual • Can have a post-istal phase after these as well • Still considered a generalized seizure because they have lost consciousness

Question 17

what criteria fit a generalized seizures?

Answer 17

• Near-simultaneous activation of entire cerebral cortex • Causes abrupt LOC

Question 18

what is a complex partial seizure?

Answer 18

• Involves AOC (alteration of consciousness) or mentation, lasting several minutes, no one set pattern, can present in a lot of ways • Usually bizarre symptoms with psychic features − Visceral symptoms (nausea, butterflies in stomach) − Hallucinations (visual, olfactory, auditory, olfactory) − Memory disturbances (déjà vu, jamais vu (should be familiar with something, like this classroom, but they aren’t) − Dream-like states − Automatisms: repetitive, purposeless movements (lip-smacking, playing with clothes) − Affective disorders (paranoia, depression, elation)

Question 19

what’s in the ddx for a seizure?

Answer 19

• Syncope: has premonitory feeling of “going to black out”, graying of vision, quick recovery of consciousness- may have sudden twitches from lack of oxygen to brain but lacks post-ictal phase • Narcolepsy: brief attacks of uncontrollable daytime sleepiness • Movement disorders (tics, jerks, tremors): consciousness preserved, movements involuntary but pt. can usually suppress it • Hyperventilation syndrome: gradual onset with SOB, anxiety, numbness of mouth/extremities (blood becomes alkaline), maybe LOC • Psychogenic seizures/Pseudo seizures

Question 20

when would CT, MRI, EEG be used in people with seizures?

Answer 20

CT if first time to look for structural lesions but not established seizures pts, MRI for first time seizures to look for more subtle changes, EEG in everyone with first time seizure

Question 21

what should all patients be warned about after having a seizure?

Answer 21

• No driving (until better handle on what’s going on—established criteria in consult with neurologist) • No operating dangerous machinery • No heights • No unsupervised swimming

Question 22

status epileptics definition and causes, action steps (tx in pharm)

Answer 22

Continuous seizure activity lasting >30 min. or Two or more seizures without return of consciousness in between Causes of Status Epilepticus • CNS infection • Trauma • Anoxia • Noncompliance or change in anticonvulsant meds • Stroke • Metabolic derangements- glucose is most important, hypo/hypernatremia tx • ABC’s − O2 by facemask, consider intubation − Large-bore IV • Check stat glucose! − Administer D50 if hypoglycemic • Anticonvulsant therapy • Labs − Glucose, Electrolytes, BUN/Cr − Tox screen − Anticonvulsant levels − Serum CK for rhabdomyolysis • CT head after seizures controlled • IV antibiotics/LP if meningitis suspected

Question 23

what is delirium?

Answer 23

• Transient, global disorder of cognition; also called ‘acute confusional state’ • Syndrome with multiple causes that result in a similar constellation of symptoms • Clinical hallmarks are decreased attention span and a waxing and waning type of confusion • Often unrecognized or misdiagnosed • Medical emergency associated with increased morbidity and mortality rates

Question 24

these sx represent what disorder? • Transient, usually reversible, global disorder of cognition and consciousness • Develops over a relatively short period (hours to days)- dementia takes longer to develop • Fluctuates over the course of a day • most sx late in the day with a change in light “sundowning” • Cognitive impairment generally represents a significant change from baseline

Answer 24

delirium

Question 25

possible causes in development of delirium

Answer 25

Common causes: • Toxins • Metabolic conditions • Infections • Endocrinologic conditions • Cerebrovascular disorders • Autoimmune disorders • Seizure-related disorders • Neoplastic disorders • Hospitalization • Terminal end-of-life delirium or D: Dementia E: Electrolyte disorders L: Lung, liver, heart (MI, HF), kidney, brain I: Infection R: Rx drugs I: Injury, pain, stress U: Unfamiliar environment M: Metabolic

Question 26

what is the most common reversible cause of delirium?

Answer 26

• Medications are the most common reversible cause of delirium (22-39%)

Question 27

what are risk factors for delirium?

Answer 27

Cognitive impairment (dementia, mental retardation) Sleep deprivation Immobilization Psychoactive medications Vision impairment Hearing impairment Dehydration

Question 28

what are the types of deliirum/

Answer 28

• Hyperactive: Restlessness, agitation, fearfulness (can be subtle); associated with drug intake, alcohol withdrawal, amphetamines, PCP, LSD • Hypoactive: Lethargy, stupor associated with hypercapnia, hepatic encephalopathy (most common in patients \> 65, easily missed or misdiagnosed as depression) scary b/c they can become dehydrated, immobilized • Mixed: Fluctuation between hyperactive and hypoactive; usually nocturnal agitation and daytime sedation

Question 29

how would you manage delirium?

Answer 29

r/o preexisting causes, do cognitive testing, H&P, review med lest, eval labs (i.e. syphilis), search for occult infection, can do other tests (like tox, ABG, lumbar puncture for meningitis). create supportive and familiar environment (− Well lit, large clock, familiar items, uninterrupted sleep, family nearby, frequent staff checks)

Question 30

what is dementia?

Answer 30

An acquired, sustained impairment in intellectual function with compromise in at least three of the following spheres of mental activity 1. Memory 2. Language 3. Visulospatial skills 4. Personality 5. Other instrumental cognitive abilities (abstraction, calculation, judgment) DSM-5 Diagnostic Criteria  Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains:  Learning and memory  Language
  Executive function 
 Complex attention  Perceptual-motor  Social cognition

Question 31

potential causes of dementia

Answer 31

Degenerative AD, Huntington’s, Parkinson’s Vascular Cerebrovascular dz, vasculitis\* Metabolic Uremia\*, liver failure\* Toxic EtOH\*, medications\*, heavy metals\* Vitamin deficiency B12\*, thiamine\* Structural disease or trauma Normal-pressure hydrocephalus\*, neoplasms\*, dementia pugilistica (multiple concussions—repetitive traumatic encephalopathies) Intracranial space-occupying lesions Subdural hematoma, tumor\* Anoxic Cardiac arrest, resp. failure\*, CO poisoning\* Infections CJD, HIV, neurosyphilis\*, postencephalitis Endocrine Hypothyroidism\*, ↓ Ca++\* Psychiatric Depression\*, schizophrenia\* \*Indicates reversible cause

Question 32

what are the reversible causes of dementia?

Answer 32

uremia, liver failure, ethos, medications, heavy metals, b12, thiamine, hydrocephalus, neoplasms, respiratory failure, CO poisoning, neurosphyilis, tour, hypothyroidism, calcium, depression, schizophrenia

Question 33

what parts of the brain are affected in cortical dementia (like AD)

Answer 33

Temporal cortex (medial) Parietal cortex Frontal lobe cortex

Question 34

what parts of the brain are affected in subcortical dementia (like parkinson)

Answer 34

Thalamus Striatum Midbrain Striatofrontal projections

Question 35

what is vascular dementia?

Answer 35

• Second most common cause of dementia • May result from multiple infarcts (multi-infarct dementia), strategically placed single infarcts, small vessel disease with subcortical ischemia, hypoperfusion, amyloid angiopathy, brain hemorrhage, and some inherited disorders of blood vessels • Tends to have an earlier age of onset, affects more men than women, and a shorter duration of survival after onset than AD • Patients often have risk factors such as HTN, DM, hyperlipidemia, and cigarette smoking • Cognitive dysfunction can develop abruptly, and patients may experience stepwise deterioration or have a history of TIAs • May be focal signs on neuro exam • Deficits include early incontinence, gait disturbances and flattening of affect

Question 36

what is levy body dementia/

Answer 36

• Eosinophilic inclusions (Lewy bodies) in subcortical neurons of patients with Parkinson’s disease • Accounts for 15-25% of all degenerative dementias • Shares clinical and pathologic features with AD- may be considered a variant of AD • Regarded by some as an AD variant • Clinical features: Dementia and at least 2 of the following: Fluctuations in cognition, visual hallucinations, and parkinsonian motor signs • Patients have slowed cognition and impaired attention, otherwise similar to AD • Consider it with bizarre, erratic behavior and no response to medications

Question 37

what is frontotermporal dementia/

Answer 37

• In 1906, Arnold Pick identified a progressive behavioral disorder associated with bilateral frontal lobe atrophy with intraneuronal inclusions (pick bodies) • Bilateral frontal lobe atrophy with intraneuronal inclusions (Pick bodies) • Frontotemporal dementia describes patients who have Pick’s disease with Pick bodies, or frontotemporal atrophy without Pick bodies, and frontotemporal atrophy with motor neuron disease • Frontal lobe- planning, inhibition, executive actions • Remain fluent with phonation but have progressive difficulty with naming and word comprehension. Preserve memory, spatial skills, and praxis but executive function, emotional regulation and conduct impaired.

Question 38

creutzfeldt jakob dz

Answer 38

• Prion disease in the family of transmissible spongiform encephalopathies • thru contaminated meat, not person to person • Affects about 1/1,000,000 per year • Typical onset of symptoms occurs about age 60 and 90% of patients die within 1 year • Early stages are characterized by failing memory, behavioral changes, lack of coordination and visual disturbances, myoclonus (muscle twitching) • With disease progression, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur

Question 39

patho pays of AD

Answer 39

abnormally processed amyloid precursor protein (beta-amyloid) (EXTRACELLULAR) accumulations of the cytoskeletal protein tau • Healthy neurons have microtubules that act like tracks, guiding nutrients & molecules to end of axon & back • Tau makes those tubules stable, but in AD tau is chemically changed (hyperphosphorylated) • Hyperphosphorylated tau pairs with other threads of tau & becomes tangled inside nerve cell bodies→ neurofibrillary tangles→ nerve cell death (INTRACELLULAR)

Question 40

genetic influences in AD

Answer 40

• Early Onset Familial AD − About 5% of all AD cases − Majority of patients with EOFAD have autosomal dominant AD − Three genes identified, all result in ↑ production of β amyloid: PS1(Presenilin 1), PS2, APP (amyloid precursor protein) • Late Onset Familial AD − 15-25% of all AD − Majority of LOFAD is of complex inheritance via “susceptibility gene” APOE (apolipoprotein E) • Sporadic APOE • Environmental factors, e.g. head trauma, affect both (? familial late onset \> familial early onset)

Question 41

how do you dx alzheimers?

Answer 41

history: onset, time course, meds, any other illnesses. tests: baseline cognitive testing (mini mental status exam, neuropsych testing, depression)

Question 42

what tests would be recommended to r/o other causes of alzheimers?

Answer 42

Recommended Rules Out Recommended Rules Out • CBC • Infection • LFTs • Liver failure, hepatic encephalopathy • Electrolytes r/o Ca¬2+ • Depression screening r/o Depression • Glucose r/o Hyperglycemia • Head CT/MRI r/o Subdural hematoma, trauma • Cr/BUN r/o Renal function If indicated: • Serum B12 levels r/o Vitamin deficiency VDRL/RPR- syphilis test r/o Neurosyphilis • TSH r/o Hypothyroidism • Lumbar puncture r/o Normal pressures

Question 43

what should be included in family education for pt with dementia?

Answer 43

• Education of patient and family/caregivers is very important (Recommendation from the California Workgroup on Guidelines for Alzheimer's Disease Management, 2008) • Discuss diagnosis, progression, treatment choices and goals of AD care with patient and family in a manner consistent with their values, preferences and the patient’s abilities • Refer to support organizations for educational materials on community resources, support groups, legal and financial issues, respite care, future care needs and options − Alzheimer’s Association www.alz.org − Family Caregiver Alliance www.caregiver.org − Clinic social services department • Discuss the patient’s need to make care choices at all stages of the disease through advance directives and identification of surrogates for medical and legal decision-making • Discuss the intensity of care and end of life care decisions with the patient and family • Be aware of caregiver stress

Question 44

what are ways to differnetiate delirium from dementia?

Answer 44

delirium is acute and fluctuating, and only lasts days to weeks. patients with delirium have altered consciousness whereas those with dementia have clear. pts with delirium will have altered attention but those with dementia will have pretty good attention.dementia is rarely reversible whereas delirium is, and delirium is usu caused by non brain causes whereas dementia is caused by brain dz

Question 45

what's your assessment? Ms. Smith is an 83-year-old woman who has Alzheimer's dementia and cannot care for herself. She is ambulatory in a special care unit, but requires assistance with activities of daily living. Her memory deficit has been very gradually progressive; she continues to generally recognize family members and enjoys meals and activities. Her past medical history includes s/p TAH-BSO, cholecystectomy, a basal cell carcinoma removed from the left arm, and presbycusis. She uses glasses and a hearing aid. She is on no regularly scheduled medications in the nursing home. The nursing staff from the nursing home report that over the past few days she has become more confused and she has not been taking part in activities. She has had increased episodes of incontinence over the past couple of days and is eating less than usual. Her family is concerned because she did not recognize them this morning when they came to visit

Answer 45

Assessment: Delirium from UTI- treat UTI, delirium will subside

Question 46

what's your assessment and plan? Mr. Jones is a 79-year-old man who was admitted to the hospital for an elective transurethral resection of the prostate (TURP) for moderate benign prostatic hypertrophy symptoms not responsive to medication therapy. Other stable medical problems include coronary artery disease, hypertension, and bilateral cataracts. Medications before admission were ASA 81 mg daily, diltiazem CD 180 mg daily, HCTZ 25 mg daily, and finasteride 5 mg daily. He is a retired businessman who lives alone. He quit smoking 10 years ago when he had an MI; he drinks wine with dinner. He is independent, still drives, and spends time with family and friends regularly. After an uneventful surgical procedure, he is put on standard post-up orders. On the evening of the second hospital day Mr. Jones begins to exhibit some fluctuation in level of alertness and has some confused content in his communications with his nurses and family members.

Answer 46

Delirium- unfamiliar environment, opioids for post-op pain management, potential catheter- consider changing analgesic to non-opioid medication, bring in familiarity, remove catheter¬

Question 47

parkinsons: eti, epi, pathpphys, features, dx, tx

Answer 47

epi: 1% affected over 60 pathophys: • Lesion occurs at substantia nigra • Hallmark: Lewy body- pink mark/collection of proteins (synuclein protein aggregation) on the substantia nigra cell is the hallmark of PD striatal dopamine depletion feautres: • Resting tremor- distinguishes PD from other diseases (pill rolling look) often most apparent when sitting still, can be somewhat suppressed if moving or muscle contracted (20-25%) • Bradykinesia • Rigidity (might have stiffness or cramping on one side +/- tremor) • Posture/balance changes (can be lopsided or worse on one side) arm doesn’t move when walk, stooped over • Insidious onset, often unilateral • Patient may complain of voice change (gets quieter), small handwriting, change in gait dx on h&P and rulin gout other cases of parkionsonsims non motor changes: • Sleep: REM behavior disorder (no paralysis during dreams but may yell, kick—bothers bed partner), restless legs, depression, wearing off of PD meds, nocturia, pain • Autonomic nervous system: constipation, bladder urgency, drooling, orthostatic hypotension, abnormal sweating • Skin: 2 to 6-fold increased melanoma risk in people with PD and 1.5-fold higher incidence of PD in people with melanoma tx: none, static with dopamine and exercise

Question 48

risk factors for parkinson

Answer 48

Environmental • Good: coffee, cigarettes, estrogen, exercise • Bad: rotenone, herbicides, welding, head injury Genetic • LRRK2 variants account for 8% of “familial” PD and some “sporadic” PD • At least 10 different genes implicated in PD • Parkin gene important in young-onset PD (

Question 49

how do you tell the difference between parkinson and these other movement disorders?• Disorders that begin with Parkinson’s-like symptoms but progress in other ways • Progressive supranuclear palsy- • Corticobasal degeneration- • Lewy body disease- • Shy-Drager syndrome- • Multiple systems atrophy-

Answer 49

• Disorders that begin with Parkinson’s-like symptoms but progress in other ways • Progressive supranuclear palsy-no tremor; unable to look up/down, rigidity of trunk, falling • Corticobasal degeneration-unilateral tremor, apraxia, “alien limb” • Lewy body disease-PD with simultaneous dementia, hallucinations • Shy-Drager syndrome-PD with severe autonomic dysfunction • Multiple systems atrophy-ataxia, neuropathy, other “systems”

Question 50

how should parkinson dz be managed/

Answer 50

early dz; wellness, education mid stage; lifestyle changes, ceasing some important activities, non motor sx, meds wear off end stage: safety, quality of life, needs assistance in daily life

Question 51

what are the most common COD in parkinson patients?

Answer 51

• The most common causes of death: pulmonary infection/aspiration, urinary tract infection, pulmonary embolism and complications of falls and fractures

Question 52

what is restless legs syndrome? mean age of onset, patho pays

Answer 52

Characterized by... 1. Desire to move in association with paresthesias/dysesthesias of the limbs 2. Motor restlessness Often confused with periodic limb movements of sleep=involuntary movements during sleep that bed partner will complain about. But restless legs is a creepy crawly feeling that makes you want to move your legs around. mean age of onset=27years majority are familial, can get secondary from other causes: • Renal failure • Iron deficiency • Neuropathy • Radiculopathy • Diabetes • Pregnancy • RA • Edema (stretching soft tissues) pahto phys • CNS abnormality (cerebral generators) • Dopaminergic dysfunction (of enzyme that makes it that uses iron as a cofactor…not degenerative of neurons that use it) • Disinhibition of the flexor reflex during sleep • Possible involvement of the endogenous opiate system

Question 53

essentia tremor: definition, classifications

Answer 53

Bilateral (PD usu one side), postural or kinetic tremor involving the hands and forearms • Tremor is persistent and visible or • Additional or isolated tremor of the head in the absence of abnormal posturing classifications: • Rest tremor- common in PD • Action tremor − Postural tremor − Kinetic tremor − Task- or position-specific tremor

Question 54

what do each of these signs with tremor mean? 1. Unilateral tremor, focal tremor, leg tremor, gait disturbance, rigidity, bradykinesia, rest tremor 2. Sudden or rapid onset 3. Current drug treatment that may cause or exacerbate tremor 4. Isolated head tremor with abnormal posture

Answer 54

1. Unilateral tremor, focal tremor, leg tremor, gait disturbance, rigidity, bradykinesia, rest tremor--parkinsons 2. Sudden or rapid onset 3. Current drug treatment that may cause or exacerbate tremor 4. Isolated head tremor with abnormal posture (head tilt or turning is probably dystonia from torticollis)

Question 55

what are some ways to "tx" or overcome essential tremor?

Answer 55

• No treatment—how bad is it? She discourages it in the older pop. • Psychological measures/lifestyle changes-wrist weights, biofeedback, bigger pens (hand in more relaxed position) Pharmacologic approaches: • Beta-blockers • Primidone (barbiturate) • Benzodiazepines (can be used prn) Surgery-thalamic stimulation

Question 56

dystonia

Answer 56

neurologic movement disorder characterized by sustained muscle contractions that frequently cause twisting or repetitive movements and abnormal, sometimes painful, postures or positions.”

Question 57

what is the difference between primary and secondary dystonia?

Answer 57

primary : its the only sign; secondary can be d/t parkinsonism, post traumatic, drugs

Question 58

what are some examples of focal dystonia?

Answer 58

• Blepharospasm- eyelids shut • Oromandibular dystonia • Meige syndrome • Cervical dystonia (spasmodic torticollis) • Laryngeal dystonia (spasmodic dysphonia; abductor or adductor types)- most common form in the US • Limb dystonia (task-specific dystonia - writer’s or musician’s cramp)

Question 59

what important things should be considered in the hx of someone suspected of having dystonia?

Answer 59

• Secondary dystonia may present months or years after the initial cerebral insult • Exposure to drugs: anti-dopaminergics (e.g., neuroleptics, anti-emetics, anti-vertiginous agents) • Toxins: manganese, methanol, cyanide, etc. • Trauma: birth asphyxia, peripheral trauma, etc.

Question 60

what is spasticity?

Answer 60

“Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.” It’s like a clasped knife if you try to move their limbs and then suddenly it gives. Whereas Parkinsons stiffness is called “lead pipe” and its stiff all the way through.

Question 61

what is ataxia and what is a good way to test for it?

Answer 61

• Dysmetria of eye movements, nystagmus (eyes wiggle when at extreme of lateral or medial) (sichatic eye movements—have them jump eyes from one of your fingers to the other their eye will overshoot and have to wiggle back) • Dysarthria (dysregulated speech: slurred or explosive) • Limb dysmetria (clumsy hitting a target), incoordination (can’t do movements smoothly) • Gait ataxia • Finger to nose test (quickly but accurately touch tip of finger), rub heel on opposite shin • Indicates cerebellar problem, esp if smack face when trying to hit nose

Question 62

what is hunting tons disease?

Answer 62

• Movement disorder − Chorea (same as dyskinesia), other involuntary movements − Later dystonia − Voluntary motor dyscontrol − Premotor planning affected • Cognitive disorder (dementia) • Emotional disorder − Includes depression, anxiety, obsession, paranoia

Question 63

what is the genetic basis of huntingon's dz?

Answer 63

automsomal dominant disorder with CAG repeat in huntington's gene

Question 64

huntington's dz: diagnostic eval, pathophys

Answer 64

dx: MRI Scans in HD • Shrinkage of the caudate nucleus is indicative of HD (near the central dark portion of the ventricles) genetic test path physDegenerating cells develop intranuclear inclusions of abnormal huntingtin protein

Question 65

how do you manage huntingnont's dz?

Answer 65

meds for sx, PT, OT, nutrition, social services, genetic counseling, care of families, psych/neuropsych assessment and counseling

Question 66

when infarcted, which area of brain will cause these sx? • This artery supplies area of brain for speaking • Most common • Large infarction with contralateral weakness/hemiplegia (face and arms \> legs) • Conjugate eye deviation toward the side of the infarct/lesion, hemianesthesia. Even if you say look over here, they won’t do it. • LEFT side: Brocas (expressive) aphasia –difficulty speaking, understanding OK and Wernickes (receptive) aphasia—fluent speech but not making sense--commonly seen together • Associated global aphasia if the dominant hemisphere and hemineglect with nondominant hemispheral lesions. • RIGHT side: Neglect. They might completely ignore one hand when both presented together, even if they can ID both on their own. Might not even

Answer 66

middle cerebral artery

Question 67

what's the difference between a stroke and a TIA?

Answer 67

tia

Question 68

RFS for stroke: modifiable and non modifiable

Answer 68

modifiable: HTN, etoh, afib, HLD, obesity, sedentary life style, smoking, DM, estrogen use, cardiac dz (like prostethic valves, cardiomyopathy, Pfo) nonmodifiable: age, race, family history, genetic hyper coagulable states

Question 69

differing pathophys of ischemic vs. hemorrhagic vs cerebral aneursm

Answer 69

ischemic strokes can be cause by a thrombus/embolus or dissection within that vessel; hemorrhagic are caused by bleeding out that causes loss of blood distally, aneurysm do not cause blood loss unless grow to big and bust

Question 70

clinical presentation of stroke vs. hemorrhagic stroke

Answer 70

stroke is usually painless with focal near deficits while hemorrhagic is usually painful

Question 71

what kind of stroke is caused by atherosclerosis?

Answer 71

large artery thromboembolic

Question 72

what type of stroke is caused by emboli from hear?

Answer 72

cardioembolic stroke

Question 73

what type of stroke is caused by untreated HTN?

Answer 73

small vessel lacunar

Question 74

what type of stroke presents with head/neck pain?

Answer 74

dissection of carotid or vertebral arteries

Question 75

ddx of stroke

Answer 75

• Hypertensive Encephalopathy • Epidural/subdural Hematoma (hemorrhagic stroke) • Demyelinating Disease (MS) • Drug Toxicity (lithium, dilantin, Etoh) • The bends • Conversion disorder • Tumor • Migraine • Seizure (Todds paralysis) • Hypoglycemia/Hyperglycemia Bell’s Palsy

Question 76

area of brain: contralateral weakness and sensory loss in R leg, +/- aphasia, impaired memory or emotional disturbances

Answer 76

Left anterior cerebral

Question 77

area of brain associate with amaourosis fugax

Answer 77

intenral carotid/retinal arteyr

Question 78

area of brain associated with stroke causing left half of page to disappear (field is cut)

Answer 78

posterior cerebral

Question 79

area of brain affected by stroke causing dysarthria (feel like drunk when talking), dysphagia, vertigo, gaze palsy

Answer 79

lateral medulla

Question 80

area of brain affected by stroke with sx of Ipsilateral Ataxia 
 • Vertigo 
 • Nausea and Vomiting 
 • Nystagmus 


Answer 80

cerebellum

Question 81

when is MRI indicated over CT for stroke?

Answer 81

CT initially to r/o bleed before giving tpa. mRI good later on, esp if been a while since sx started

Question 82

initial management of storke

Answer 82

CT to see if d/t hemorrhage, mRI for location, size, iv TPA, MRA or CTA of head and neck, EKG, echo, blood glucose, BP and lipids, hyper coagulable work up in young

Question 83

what are some common migraine precipitants?

Answer 83

Migraine Precipitants • Menstruation (pre or mid cycle) • Too little/too much sleep • Fasting • Physical activity • Stress • Tyramine-containing foods- Red wines, Hard cheeses, Herring • Phenylethlamine- chocolate • Nitrates- processed meats • Caffeine withdrawal or excess- vasoconstrictor • Medications- OCP’s- can cause or prevent migraines, antiHTNs- affect vasomotor tone

Question 84

common migraine characteristic

Answer 84

• Represents vast majority of migraines • Usually lasts 4-72 hrs • Characteristics: − Unilateral, Intensity: moderate to severe − Pulsating- intense vasoconstriction, followed by vasodilation − Aggravated by physical activity − Nausea/vomiting- very common − Photophobia/phonophobia • Patient should have at least 5 attacks before dx. madecommon migraine

Question 85

what's different in the "classic migraine" from common migraine? describe it.

Answer 85

Aura. Aura comes on gradually, usually lasts

Question 86

where can headaches and migraines occur in the head?

Answer 86

extracranially (muscle, BVs, periosteum), intracranially (BVs, venous sinuses, dura, falx cerebri) but NOT BRAIN PARENCHYMa

Question 87

prophylactic meds for migraine

Answer 87

• Beta-blockers- most common prophylactic treatment, decrease blood flow to the brain and vasodilation − Propranolol • Calcium-channel blockers- smooth muscle relaxation → vasodilation − Verapamil • SSRI’s- decrease frequency of migraines − Paroxetine (Paxil), Fluoxetine (Prozac) • Tricyclic antidepressants − Amitriptyline, Nortryptaline • Anti-seizure meds- stabilize neuronal membranes − Valproic acid (Depakote), − Gabapentin (Neurontin)

Question 88

abortive tx of migraines

Answer 88

OTC analgesics, ergots, anti-emetics, serontonin agonists, IV/IM NSaids, narcotics, steroids

Question 89

when do most migraines usu start in life?

Answer 89

adolescence or young adulthood

Question 90

what kind of HA? usu in males, usu stabbing (not throbbing), unilateral, trigeminal nerve involved (behind eye), +/- lacrimation, conjunctival injection, nasal congestion/rhinorrhea, ptosis, /miosis; usually a few in a row every few years

Answer 90

cluster headaches

Question 91

tx of cluster headaches

Answer 91

o2, same meds as migraine except no beta blockers

Question 92

what kind of hA?• Duration: 30 min.-7 days • Contraction of muscles for a long period of time − Pressing/tightness/band-like (usually non-pulsating) − Mild-moderate intensity − Unaffected by physical activity − Possibly associated with photo-/phonophobia − Usually without nausea/vomiting

Answer 92

tension headaches

Question 93

ddx of hA

Answer 93

Subarachnoid hemorrhage Meningitis Hypertensive headache Subdural hematoma Epidural hematoma Brain tumors/cerebral mets Migraine Cluster HA Tension HA Sinusitis Acute glaucoma Temporal arteritis Trigeminal neuralgia TMJ

Question 94

what causes tension headaches?

Answer 94

contraction of muscles/band like

Question 95

signs of a subarachnoid hemorrhage and management

Answer 95

sudden onset, "worst HA of my life", lOC, focal neuro signs, may have seizure, nuchal rigidity, need urgent ct (look for bright white blood) and need a cerebral angiography to visualize. tx with surgery or endovascular surgery (coil)

Question 96

how do brain tumors present?

Answer 96

often progressively worsening over days to weeks/months. starts mild and stays there, doesn't go away and may be progressively getting worse; worse in the morning +/- am vomiting. may also have motor/sensory deficits, ataxia, vision loss, seizures, altered mental status

Question 97

gold std for dxing brain tumors

Answer 97

MRI

Question 98

most common primary brain tumor of brain

Answer 98

astrocytoma (malignant)

Question 99

tx of astrocytoma

Answer 99

surgery + radiation +/- chemo

Question 100

Symptoms Headache Progressively worsening over days to weeks (not acute and sudden like subarachnoid hemorrhage) Often is worst in the morning, with AM vomiting- ­ interstitial fluid when lying flat Weakness, paralysis, sensory deficits, cranial nerve palsies Visual disturbance Ataxia Altered mental status Seizures- CT after first sz

Answer 100

astrocytoma

Question 101

Second most common type of brain tumor (2/100,000) Arise from the meninges Commonly on surface of brain, in concavity of skull May be single or multiple

Answer 101

meningioma

Question 102

tx of meningioma

Answer 102

Observation- if tumor is small and asymptomatic Need regular follow-up imaging Surgical- Best results if tumor is superficial and easily accessible Radiation- If surgical resection is incomplete or for recurrence chemo not effective

Question 103

Unilateral hearing loss The most common presenting symptom Can be sudden, persistent or fluctuating Tinnitus Vertigo Disequilibrium Headache Facial numbness or weakness- compression of brainstem and facial nerve

Answer 103

acoustic neuroma--notice how the tumor is in the cerebello pontine angle

Question 104

tx of acoustic neuroma

Answer 104

surgery (by expert), radiation (palliative to reduce tumor), can just observe if older and symptoms not too bad (won't die form these)

Question 105

T or F: cerebral metastases are more common than primary brain tumors

Answer 105

T; 1 in 5 cancer patients will have cancer go to brain. usually d/t lung or breast cancer

Question 106

multiple lesions found in brain is usu d/t what? tx?

Answer 106

mets; need sysemic workup: CXR, chest CT, abdomen, pelvis

Question 107

tx of cerebral mets

Answer 107

whole brain radiation therapy to get mets you can't see, can do stereotactic radiosurgery +/- chemo; surgery if ## Footnote Solitary lesion \> 3 cm Lesions in “noneloquent” portion of brain Limited systemic disease One symptomatic lesion with multiple asymptomatic lesions Symptomatic lesion resected, remaining lesions radiated

Question 108

what do these red flag signs make you think of? ## Footnote First severe HA or worst HA of pt.’s life, especially if acute onset HA that gets progressively worse over days to weeks Severe HA with fever Nuchal rigidity Decreased LOC or focal neuro signs

Answer 108

First severe HA or worst HA of pt.’s life, especially if acute onset (subarachnoid hemorrhage) HA that gets progressively worse over days to weeks (tumor) Severe HA with fever (meningitis) Nuchal rigidity (meningitis or subarachnoid hemorrhage) Decreased LOC or focal neuro signs (bad—work up; subarachnoid hemorrhage or tumor)

Question 109

MS: RFs eti pathophys

Answer 109

RFs: geography : 37th parallel, caucasians of scandinavian descent, age (younger onset in women), smoking, low vitamin D, some genetic involvement eti: autoimmune, t cells attack myelin, Cd4 cells activiated and leads to inflammation and damage, possibly microbial? no one bug ID'd yet pathophys: t cells attack myelin, inflammation by cd4, macrophages come in and "clean up" The end result is a shrunken area of demyelination called a plaque, or sclerotic area The axon cylinders and cell bodies are not destroyed, although the scar is capable of damaging the under lying axon fiber so that nerve fiber conduction is disrupted

Question 110

MS symtpoms

Answer 110

Primary Symptoms Visual complaints Gait problems Paresthesias Pain Spasticity Weakness Ataxia Speech difficulty Psychological changes(anxiety, depression) Cognitive changes Fatigue Bowel/bladder dysfunction Sexual dysfunction Tremor Secondary Symptoms Recurrent UTIs Urinary calculi Decubiti Muscle contractures Respiratory infections Poor nutrition Tertiary Symptoms Financial problems Personal/social problems Vocational problems Emotional problems

Question 111

signs of mS:

Answer 111

optic: blurred vision, color disturbances motor: hyperreflexia, spasticity, paraparesis, dysarthria, babinksi sensory: lhermittes sign, + rombergs, decrease in sensory and proprioception (dorsal column) cerebellar: ataxia, finger to nose test bad, heel to shin, loss of speech other: urinary incontinence, sexual dysfunction, cognitive and emotional abnormalities, fatigue, difficulty swallowing, dystonnia, +/- trigeminal neuralgia

Question 112

these signs on mRI are indicative of which diease? Plaques anywhere within the white matter of the CNS ↑ in immunoglobulin concentrations in the CSF studies in more than 90% of patients with MS. IgG index (a comparison between IgG levels in the CSF and in the serum) is elevated in many MS patients. Oligoclonal Immunoglobulin Bands can be identified in the CSF of MS patients via electrophoresis. (if you see this, ITS MS!) The overall protein level is also slightly elevated - up to 0.1 g/ · On T-2 weighted images, patchy areas of abnormal white matter (ovoid white lesions) are found most commonly in cerebral hemispheres in periventricular areas; can be present in the cerebellum and brain stem, cervical and/or thoracic spinal cord · Gadolinium enhancement on the MRI scan is considered a sign of an active lesion

Answer 112

mS

Question 113

gold std test for MS

Answer 113

MRI

Question 114

· Total volume of T2-weighted lesions (called T2 burden of disease) shows a significant (although weak) correlation with clinical disability in which disease?

Answer 114

MS

Question 115

differential dx of ms

Answer 115

Differential Diagnosis Any other condition that may potentially affect the nervous system, e.g. CNS vasculitis, especially lupus Sarcoidosis Syphilis HIV Lyme disease CVA/TIA Nutritional disorders, e.g. Vitamin B12 deficiency Often will do a rheumatoid type workup: ANA, sjogren’s, vitamin D; anything that can cause vague sx of fatigue

Question 116

Accounts for 85% of MS cases at onset Characterized by discrete attacks that generally evolve over days to weeks (rarely over hours) Often, but not always, there is complete recovery over ensuing weeks to months When ambulation is severely impaired during an attack, ~ 50% will fail to improve Between attacks, patients are neurologically stable Disease progression associated with more frequent attacks, tx aimed to prevent those relapses/attacks

Answer 116

relapsing remitting MS

Question 117

Always begins as RRMS A steady deterioration in function unassociated with acute attacks (which may continue or cease during the progressive phase) Approximately 50% of patients with RRMS will have developed SPMS after 15 years Appears to represent a late-stage of the same illness as RRMS

Answer 117

secondary progression MS

Question 118

Accounts for ~15% of MS cases Patients do not experience attacks but only a steady functional decline from disease onset Disease begins later in life (mean age 40 years) and disability develops faster

Answer 118

primary progressive ms

Question 119

Overlaps PPMS and SPMS and accounts for 5% of patients Patients experience a steady deterioration in their condition from disease onset—never get back to baseline like in RRMS They experience occasional attacks superimposed upon progressive course Early stages are indistinguishable from PPMS

Answer 119

progressive relapsing ms

Question 120

patient education for ms patients

Answer 120

· Multiple issues necessitate a team approach to care Patient Education- Educate the patient and their family about MS (www.nmss.org) get involved early Other Issues: 1. Life adjustments: Grief and loss, Depression common (suicide risk), Unknown future, walking devices, OT 2. Financial and Vocational Issues: Cost of therapy, Continued employment, Cognition 3. Sexuality, Family Issues & Pregnancy Physical Therapy- mobility issues Occupational Therapy- ADLs and job skills Speech Therapy- swallowing problems Cognitive Rehabilitation Vocational Rehabilitation- helps patients maintain their current job or find other employment opportunities despite disabilities Goal: optimize function and QOL

Question 121

differential diagnosis for neurological diseases

Answer 121

Neurological diseases Cerebrovascular diseases - CVA, subdural or epidural hematoma Demyelinating diseases - MS, Guillan-Barre Amyotrophic Lateral Sclerosis Neuromuscular Disorders - myasthenia gravis, botulism, organophosphate poisoning. Lambert-Eaton myasthenia syndrome Focal neurological diseases - trauma, tumor, inflammation, radiculopathies (cervical, lumbar) Neuropathies - peripheral, nerve plexus Spinal cord disease - injury, spinal muscle atrophy, disc disease Myopathy Infectious - Influenza, EBV Drug-induced - Alcohol, Corticosteroids, statins Endocrine - Adrenal insufficiency, Glucocorticoid excess, Hyperparathyroidism, Hypo and hyperthyroidism, acromegaly, hypopituitarism, Vitamin D deficiency Inflammatory - Polymyositis, dermatomyositis, vasculitis Rheumatologic – arthritis and autoimmune (RA, SLE) Genetic - Muscular dystrophy Metabolic - Disorders of carbohydrate,lipid metabolism Rhabdomyolysis Electrolyte disorders – hypocalcemia- ¯ threshold potential, hypercalcemia- ­ threshold potential, hyper and hypo -kalemia and –magnesemia Amyloidosis and sarcoidosis Various uncommon genetic and metabolic diseases

Question 122

meds that can cause motor weakness

Answer 122

Amiodarone Antithyroid Drugs Antiretroviral medications Chemotherapeutic agents Cimetadine Cocaine Corticosteroids Gemfibrozil Interferon Leuprolide acetate NSAIDS Penicillin Sulfonamides Statins

Question 123

infections that can cause motor weakness

Answer 123

Epstein-Barr Virus HIV Influenza Lyme disease Meningitis Polio Rabies Syphilis Toxoplasmosis

Question 124

motor weakness emergencies

Answer 124

Respiratory muscle weakness Tachypnea- consider Mechanical ventilation MG, GBS Pharyngeal muscle weakness Dysphagia, dysarthria- Intubation MG, dermatomyositis, polymyositis, West Nile Virus Vascular accidents Spinal cord compression

Question 125

causes of generalized weakness

Answer 125

Myasthenia Gravis Deconditioning Adrenal Insufficiency

Question 126

causes of asymmetric weakness

Answer 126

Multiple Sites- Multiple Sclerosis Unilateral- Cerebrovascular or spinal cord disease Mononeuropathy Compression neuropathy Radiculopathy

Question 127

causes of symmetric with proximal distribution weakness

Answer 127

Unable to rise from a seated position without the use of the upper extremities Unable to perform a deep knee bend Difficulty combing hair Duchenne Musclular Dystrophy Guillan Barre Syndrome Cushings syndrome

Question 128

weakness with distal distribution causes

Answer 128

Decreased grip strength Weakness of wrist flexion or extension Decreased plantar flexion strength, and foot drop Difficulty walking on heels or toes Peripheral neuropathy – Accompanied by sensory deficits DM, alcoholism, HIV

Question 129

characteristicd of uppe rmotor neuron issues and causes of upper motor neuron issue

Answer 129

babinski, hyperreflexia, spasticity, clonus; stroke, tumor, demyelinating, infection, trauma

Question 130

lower motor neuron lesion characteristics and causes

Answer 130

atrophy, flaccidity, fasiculations, fibrillations, hyporeflexia ## Footnote Lead poisoning, poliomyelitis, West Nile Virus, ALS, spinal muscular atrophy, Charcot-Marie-Tooth disease, progressive muscular atrophy, neuropathy

Question 131

lesion in muscle or myopathy: characteristics and causes

Answer 131

Findings: weakness, extramuscular symptoms May have normal or atrophied (replaced with scar tissue w/ contractures) or pseudohypertrophied bulk, normal or decreased tone, proximal distribution, normal or decreased reflexes Muscular Dystrophy Polymyositis, Dermatomyositis Influenza Rhabdomyolysis

Question 132

weakness d/t neuromuscular jcn: characteristic and cause

Answer 132

Progressive muscle weakness Myasthenia Gravis- Anti-ACh receptor antibodies Organophosphate poisoning- inhibits Ach ( insecticides) Lambert-Eaton syndrome- Interferes with presynaptic Ca2+ channel function Normal bulk, bone, reflexes

Question 133

what do each of these assoiated symtpoms mean when combined with weakness? ## Footnote Stones, bones, abdominal moans Rash Truncal obesity Legal problems, memory loss, unexplained trauma STD Relapsing and remitting symptoms

Answer 133

Stones, bones, abdominal moans – hypercalcemia Rash – SLE (malar), dermatomyositis- Heliotrope: dermatomyositis around eyelids Truncal obesity – Cushing’s syndrome Legal problems, memory loss, unexplained trauma – alcoholism STD – HIV, syphilis Relapsing and remitting symptoms – MS

Question 134

focal sensory loss causes

Answer 134

Focal Mononeuropathy Compression examples: UE – carpal tunnel LE – back pain and radiculopathy Peroneal neuropathy - crossing legs Lyme radiculopathy Trauma Nerve ischemia/infarct Signs and symptoms in nerve distribution Numbness, tingling, pain Associated weakness

Question 135

multifocal sensory loss causes

Answer 135

Sensory ataxia, absent reflexes, dysesthesia No motor involvement Sjogrens, DM, Sarcoidosis, HIV

Question 136

multifocal symmetric --proximal sensory loss causes

Answer 136

Porphyria Proximal is usually predominantly motor What is the pattern/distribution?

Question 137

multifocal symmetric distal sensory loss causes

Answer 137

Stocking-glove distribution Length dependent neuropathy – affects longest axons first Slowly progressive DM, alcohol, HIV What is the pattern/distribution?

Question 138

when should you check visual acuity

Answer 138

Before any testing to the eye or adnexa is done. This is the very first test!

Question 139

these initial signs are supportive of what dx? sensory loss, optic neuritis (vision changes, blurred or color changes), weakness, paresthesias (lhermitte's sign)

Answer 139

MS

Question 140

dxing MS

Answer 140

\>2 lesions in space and time on T2 weighted MRI images will show patchy, ovoid white lesions of abnormal white matter or increase in immunoglobulin concentrations in CSF or oligoclonal immunoglobulin bands

Question 141

ddx of ms

Answer 141

lyme, rheumatologic conditions work up (ANA, etc), stroke/tia, sarcoidosis, syphilis, hIV, nutritoinal disorders

Question 142

what's the most common type of ms at onset? what are the other types?

Answer 142

relapsing remitting. other types are secondary progressive, primary progressive and progressive/relapsing

Question 143

what test helps assesa and measure neuro impairmet in mS patients?

Answer 143

kurtzke expanded disability status score

Question 144

strabismus

Answer 144

eye turns

Question 145

term: disruption of normal vision development

Answer 145

ambylopia

Question 146

inflammation of cornea

Answer 146

keratitis

Question 147

squamous epithelium membrane covering globe

Answer 147

conjuctiva

Question 148

ectoprion and entropion: eyelids turn outward or inward

Question 149

what's a distinguishing feature of viral conjunctivitis?

Answer 149

usually watery, almost ALL are viral.

Question 150

gradual onset of ## Footnote Fixed deep injection of the blood vessels on the sclera Hallmark is deep, throbbing, severe pain that may radiate to jaw or temple Photophobia, Tearing, pain on palpation of globe, edema

Answer 150

scleritis

Question 151

Drainage cannot occur, pressure increases, PAINFUL Ocular emergency Often misdiagnosed Only form of glaucoma with sx They feel like they are going to vomit, head feels like its going to blow up, ER worthy

Answer 151

pathology of anterior chamber angle=acute angle closure glaucoma

Question 152

different sizes of pupils

Answer 152

anisocoria

Question 153

Dark unreflective layer, between the sclera and retina Absorbs light and stops reflection. Contains pigment and rich blood vessels

Answer 153

choroid

Question 154

Pain, decreased VA, photophobia, pupil irregularities (miosis or constricted) what has to be on your ddx b/c its severe??

Answer 154

iritis

Question 155

#1 cause of flashes and floaters; what else has to be on your ddx?

Answer 155

posterior vitreous detachment but need to refer in case of retinal detachment

Question 156

: restoring pain-free function of the legs, back, neck, shoulder, and torso, restoring independence and safety in transfers and gait

Answer 156

PT

Question 157

: restoring function of the upper extremity, especially hand therapy, as well as ADL’s and cognitive training to assist with planning and performing ADL’s

Answer 157

OT

Question 158

is working on cognition, sensory processing, ADLs, a part of PT or OT?

Answer 158

OT

Question 159

what are some important things to condsider before discharging someone--aka red flags that they need more care or supervision?

Answer 159

if can't do ADLs safely, can't take meds, can't handle emergencies, etc.

Question 160

what test scales cognition in someone recovering from a brain injury?

Answer 160

ranchos

Question 161

what is the best way to referr to pT/OT/

Answer 161

Do not specify # of visits- patient may plateau sooner but still want to come to PT, insurance will not cover sessions if no progress is being made Orders are best scripted as “evaluate and treat”- allows more freedom for therapist to treat