neuro Flashcards
angiogram indications
• Evaluate blood vessels • Aneurysm • AV malformation
plain film indications in nuero
• Evaluate for stenotic arteries in patients with TIA stroke
• Nerve Conduction Studies (NCS) –
integrity of peripheral nerves: axons, myelin
• Electromyography (EMG)
– electrical activity of muscle fibers
EEG indications
− Seizure, seizure disorder − Altered level of consciousness, coma − Encephalopathy
bacterial meningitis: etiology and pathophsyiology, RFs, clinical presetnation, lab findings, plan, sequelae of untx’d
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
bacterial meningitis presentation in infants
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
lumbar puncture side effects
• Post-LP headache • Infection • Bleeding • Cerebral herniation (since lowering pressure in spinal cord, risk that brain will herniate there) • Back pain • Minor neurological symptoms
ddx of meningitis
Differential Diagnosis • Fever − Pneumonia − Influenza − URI − Viral infection − Gastroenteritis • Headache − Subarachnoid Hemorrhage- sudden, worst headache • Nuchal Rigidity − Musculoskeletal causes − Injury − Arthritis − Sleeping position
aseptic meningitis patho, eti, clinical, dx, eval, tx
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
encephalitis dx, patho, tx, eti
• 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
seizures: all possible causes
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
what are the phases of grand mal seizures?
tonic, clonic, post ictal
do petit mal seizures have post ictal phase?
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
what are simple partial seizures?
• 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
what are myoclonic seizures?
• 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
what criteria fit a generalized seizures?
• Near-simultaneous activation of entire cerebral cortex • Causes abrupt LOC
what is a complex partial seizure?
• 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)
what’s in the ddx for a seizure?
• 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
when would CT, MRI, EEG be used in people with seizures?
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
what should all patients be warned about after having a seizure?
• 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
status epileptics definition and causes, action steps (tx in pharm)
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
what is delirium?
• 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
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
delirium
possible causes in development of delirium
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
what is the most common reversible cause of delirium?
• Medications are the most common reversible cause of delirium (22-39%)
what are risk factors for delirium?
Cognitive impairment (dementia, mental retardation) Sleep deprivation Immobilization Psychoactive medications Vision impairment Hearing impairment Dehydration
what are the types of deliirum/
• 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
how would you manage delirium?
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)
what is dementia?
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
potential causes of dementia
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
what are the reversible causes of dementia?
uremia, liver failure, ethos, medications, heavy metals, b12, thiamine, hydrocephalus, neoplasms, respiratory failure, CO poisoning, neurosphyilis, tour, hypothyroidism, calcium, depression, schizophrenia
what parts of the brain are affected in cortical dementia (like AD)
Temporal cortex (medial) Parietal cortex Frontal lobe cortex
what parts of the brain are affected in subcortical dementia (like parkinson)
Thalamus Striatum Midbrain Striatofrontal projections
what is vascular dementia?
• 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
what is levy body dementia/
• 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
what is frontotermporal dementia/
• 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.
creutzfeldt jakob dz
• 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
patho pays of AD
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)
genetic influences in AD
• 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)
how do you dx alzheimers?
history: onset, time course, meds, any other illnesses. tests: baseline cognitive testing (mini mental status exam, neuropsych testing, depression)
what tests would be recommended to r/o other causes of alzheimers?
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
what should be included in family education for pt with dementia?
• 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
what are ways to differnetiate delirium from dementia?
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
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
Assessment: Delirium from UTI- treat UTI, delirium will subside
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.
Delirium- unfamiliar environment, opioids for post-op pain management, potential catheter- consider changing analgesic to non-opioid medication, bring in familiarity, remove catheter¬
parkinsons: eti, epi, pathpphys, features, dx, tx
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
risk factors for parkinson
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 (
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-
• 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”
how should parkinson dz be managed/
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
what are the most common COD in parkinson patients?
• The most common causes of death: pulmonary infection/aspiration, urinary tract infection, pulmonary embolism and complications of falls and fractures
what is restless legs syndrome? mean age of onset, patho pays
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
essentia tremor: definition, classifications
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
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
- 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)
what are some ways to “tx” or overcome essential tremor?
• 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
dystonia
neurologic movement disorder characterized by sustained muscle contractions that frequently cause twisting or repetitive movements and abnormal, sometimes painful, postures or positions.”
what is the difference between primary and secondary dystonia?
primary : its the only sign; secondary can be d/t parkinsonism, post traumatic, drugs
what are some examples of focal dystonia?
• 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)
what important things should be considered in the hx of someone suspected of having dystonia?
• 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.
what is spasticity?
“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.
what is ataxia and what is a good way to test for it?
• 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
what is hunting tons disease?
• 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
what is the genetic basis of huntingon’s dz?
automsomal dominant disorder with CAG repeat in huntington’s gene
huntington’s dz: diagnostic eval, pathophys
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
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
astrocytoma
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
meningioma
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
acoustic neuroma–notice how the tumor is in the cerebello pontine angle
multiple lesions found in brain is usu d/t what? tx?
mets; need sysemic workup: CXR, chest CT, abdomen, pelvis
· Total volume of T2-weighted lesions (called T2 burden of disease) shows a significant (although weak) correlation with clinical disability in which disease?
MS
