Neurology II Flashcards
List 3 closed head injuries
1) Concussion
2) Post concussion syndrome
3) Traumatic brain injury (TBI)
1) What typically refers to moderate to severe head trauma leading to functional and structural dysfunction?
2) What is a mild TBI with functional disturbance but with preserved structure?
1) TBI
2) Concussion
1) Define concussion.
2) What may it result in?
1) Head injury resulting in altered consciousness < 6 hrs. Usually, recover in seconds to minutes.
2) Retrograde and anterograde amnesia around the time of the event
Concussion:
1) Pathophys?
2) Epidemiology?
3) Etiologies?
1) Acceleration/deceleration movements of the head cause stretching and shearing of axons result in LOC at moment of impact (transient dysfunction of upper brainstem reticular activating system)
2) ~3 mil/ yr thought that about ½ aren’t reported
3) Trauma, sport, recreation
Concussion:
1) What are some DDxs?
2) What are some Txs?
1) HA, seizure, meningitis, encephalitis, infection, drug toxicity
2) ABCs, Supplemental O2, tight BP control, repeat neuro checks, rest
What are 3 sideline assessment tools for concussion?
1) Sports concussion assessment tool 6 (SCAT6) – validated for age 13+
2) Child SCAT6: validated for kids 5-12 y/o
-Validated during acute phase, less utility 3-5 days post-injury, widely utilized
-The incorporated symptoms checklist may be useful for monitoring recovery
3) Canadian CT
-Not used <16
What can’t assess concussion under 16?
Canadian CT
1) Describe concussion Tx.
2) Are there any specific meds?
1) Individualized and based on symptom presentation
Brief period of rest followed by gradual return to activity
2) No specific medications; Rx for symptom management same as in patients without concussion
Concussion:
1) How long should the acute rest period last? Then what should you do?
2) What leads to better outcomes?
1) ~4-48 hours is appropriate, then symptom limited cognitive and physical activity should be introduced
2) Early symptom limited activities
Concussion:
1) When should a pt return to activity?
2) What should you tell the pt after the initial rest period?
3) When may they return to full activities?
1) Individualized return to activity
2) Encourage to return to normal ADLs as tolerated
3) May return to full activities once fully recovered (ADLs) and not taking any symptomatic medications
Concussion: After initial 24-48 hours of acute rest, what should the pt do?
1) Cognitive activities at home with frequent breaks – should not worsen symptoms
2) Light physical activity that does not worsen symptoms or pose risk for repeat injury – walks
Concussion:
1) When the pt resumes part time school/work with expectation to resume full time school/work, what may be needed?
2) When can a pt restart their sport?
1) +/- short term accommodations
2) Once return to full time school/work without accommodation, asymptomatic, caught up on academics: return to play protocol with medical supervision
Concussion:
1) When do Sx typically present?
2) What is important in Tx?
3) When do they often resolve?
1) Symptoms typically present immediately
-Can be delayed by minutes to hours
2) Serial monitoring important
3) In 72 hours
When do most ppl recover from concussion?
Most adults fully recover by 2 weeks and kids within 4 weeks
Which of the following is the keystone to management of concussions?
A. medication for symptoms
B. brief rest from cognitive and physical activity
C. hospitalize for monitoring
D. STAT neuroimaging
B. brief rest from cognitive and physical activity
Post Concussion Syndrome:
1) What is it
2) What are the Sx?
3) What may the neuro exam/ imaging look like
1) 40 % of patients with concussion (but not necessarily LOC) will have lingering symptoms for a few weeks to years.
2) HA, dizziness, fatigue, insomnia, hypersomnia, blurred vision, tinnitus, irritability, restlessness, inability to concentrate, anxiety, depression.
3) Neuro exam and imaging may be normal
Post Concussion Syndrome:
1) What may happen over time?
2) Who is more likely to experience this?
3) What is the pathophys?
1) Affected area of brain may atrophy and result in symptoms c/w that specific lobe.
2) Patients with baseline psych disorders
3) Cerebral contusions, diffuse axonal injury
PCS (post concussion syndrome):
1) Etiology?
2) Epidemiology?
3) DDxs?
4) Txs?
1) Head
2) 40% of patients with concussions will have PCS
3) Depression, ADHD, behavioral conditions, malingering, emotional lability, anxiety, sleep disorders
4) Gradual improvement many months
anxiolytics, antidepressants, cognitive and vocational therapy
Traumatic Brain Injury (TBI):
1) What does a TBI require?
2) What are the Sx?
3) What does imaging reveal?
4) What is it a major cause of?
1) Evidence of trauma
2) Focal neurologic deficits with progressive mass effect; delayed inflammatory response can be delayed 1-3d
3) Skull fracture, intracranial bleed and/or cerebral edema
4) Death and disability
What is the pathophys of TBIs?
Depends on cause; tissue destruction, perivascular edema, contusional or perivascular bleeding within the cerebral parenchyma, and hypoxic-ischemic brain injury may develop secondarily.
TBI:
1) Epidemiology?
2) Etiologies?
3) 2 DDxs?
1) Incidence is rising 2/2 increasing MVAs in low- middle-income countries as well as increasing falls in the aging population; ~ 2 mil patients with TBIs treated in US EDs/yr; peak age 15–25-year-olds; leading cause of death in people <25. M»>F
2) MVAs, GSW, crush or blast injuries
3) Stroke or spontaneous intracranial hemorrhage
TBI Txs?
1) ABCs, eval and stabilize C spine, fluids, GCS (intubate <8)
2) ? Supplemental O2, strict control of BP, frequent neuro checks, assess for other sites of trauma, reduce ICP,? CSF leak? (Halo sign,) pupils? CT/MRI, reverse any comorbid factors as able (ex/ coagulopathy,) monitor for infections, seizures, PTSD
How do you stratify the risks of pts with TBIs?
1) Low/Moderate: GCS = >15 (alert, fully oriented and following commands) and CT neg ; may d/c home with close observation
2) Mod: GCS 9-14, CT findings do not require surgery; admit to ICU for close observation/neuro checks and repeat CT in 24 hrs
3) High: GCS <=8 serious head injury admit to ICU for neurosurgical consultation; stabilize patient, intubate; do not delay surgery as time is brain cells
A 27 y/o male patient presents with h/o Ha, 2-3 times a month, lasting from 30 minutes to several days, bilateral band-like quality, mild to moderate intensity, not aggravated by routine physical activity (walking or climbing stairs). Denies N/V but does endorse some sensitivity to noise. Some improvement noted with Excedrin migraine tablets. Remainder of ROS & PMHx is non-contributory. PE non-focal
Dx?
A. tension headache
B. migraine headache
C. cluster headache
D. secondary headache
A. tension headache
38 y/o male presents with h/o of disabling pain behind his right eye lasting about 60 minutes. He notes his eye gets red and tears and he becomes very agitated. Occurs several times a day for a couple of weeks then seems to go away for months then can return. HA gets worse with any activity. Remainder of ROS, PMHx is non-contributory. PE is non-focal
Dx?
A. tension headache
B. migraine headache
C. cluster headache
D. secondary headache
C. cluster headache (no CT needed)
Ataxia:
1) Define it
2) Pathophys?
3) Epidemiology?
1) Disordered coordination of movements (often thought of as gait)
2) Typically: cerebellar dysfunction, other lesions of nervous system, proprioception, and/or vestibular system
3) Uncommon, 150,000 people in US
Ataxia:
1) Etiologies?
2) DDxs?
3) Tx?
1) Acute infections, post-inflammatory, toxins, tumors, trauma, migraines, BPPV, Guillain–Barré
2) Above etiologies
3) Treat underlying cause
Essential tremor:
1) How does it typically present?
2) Is it fast or slow onset? Explain
3) DDxs?
1) Typically involves the bilat hands and is brought about by intentional movements, ex/ drinking/eating, writing, tying shoes
2) Slowly progressive and can also involve the head, voice and legs
3) Parkinson’s Dz, dystonic or orthostatic tremors, hyperthyroidism
Essential tremor:
1) Pathophys?
2) Epidemiology?
3) Etiology?
1) Pathophys: dysfunction of cerebellar – brainstem-thalamic–cortical circuits
2) Most common cause of action tremor in adults, < 1 % worldwide, 5% of adults > 60 M= F
3) Unknown, but thought to be cerebellar dysfunction or genetic
What is the goal of treating essential tremor? How do you Tx?
To minimize tremor enough to prevent disruption of ADLs:
1) Typically, in primary care, d/c caffeine and any aggravating meds
-exclude secondary causes
2) Propranolol or primidone (B Blockers have central depressive effect; primidone works to increase GABA)
3) Refer to neurology if not comfortable treating it
Essential tremor:
1) What may Sx be aggravated by?
2) What can make Sx better?
1) Stress, fatigue, caffeine, temperature extremes
2) Alcohol
Parkinson’s disease:
1) Define it
2) What is the pathophys?
3) Epidemiology?
1) Adult-onset neurodegenerative disorder with slow progression
2) Dopamine depletion (disrupts thalamus and motor cortex connections)
3) 90,000 new cases/yr; rising as population ages M>F
>10 mil PD patients worldwide
Parkinson’s disease: What are the 3 hallmark features?
1) Pill rolling tremor at rest; often unilateral, resolves with intentional movement
2) Cogwheel rigidity
3) Bradykinesia/shuffling gait and freezing movements
Parkinson’s disease:
1) Etiology?
2) How is it diagnosed? DDxs?
3) Tx goal? What are some Txs?
1) Genetic, lower lifetime estrogen exposure, exposure to environmental toxins
2) Clinical diagnosis (though clinical response to levodopa is diagnostic); hydrocephalus, trauma, tumor, toxins, or metabolic imbalance
3) Symptom control; can’t cure
-Dopaminergic meds
Parkinson’s disease:
1) Assoc. Sx?
2) Non-motor Sx?
1) Along with bradykinesia: rigidity, micrographia, postural instability, shuffling gait
2) Depression, sleep disturbance, cognitive impairment, autonomic dysfunction (orthostatic hypotension, urinary urgency, constipation, excessive sweating)
List 2 medications that can Tx Parkinson’s, and what group of meds each is in
1) Levodopa-Carbidopa (Sinemet; dopamine agonist)
2) Benztropine Mesylate (anticholinergic (indirectly increases dopamine))
Which part of Levodopa-Carbidopa (Sinemet) is adjunct to reduce peripheral side effects (nausea/vomiting, dreaming, psychosis, dyskinesias) & increase CNS bioavailability of levodopa (dopamine agonist)?
Carbidopa
Huntington’s disease:
1) What is it?
2) Pathophys?
1) Involuntary and unpredictable movements of extremities that also includes dementia and behavioral changes. Gradual onset and progression. (chorea + dementia.) onset usually between ages 30-50. Progressive and fatal in 15 -20 years
2) Under-activity of GABA and acetylcholine and overactive dopamine
Huntington’s disease:
1) Define chorea
2) Epidemiology of Huntington’s?
3) Etiology?
1) involuntary rhythmic movements - may appear purposeful; dysarthria, ataxia
2) Worldwide, all ethnic groups, 5 in 100,000 +genetic
3) Inherited genetic defect (repeat in the Huntingtin gene, too many (37) repeats is dx of HD)
Huntington’s disease:
1) DDxs?
2) Txs?
1) Stroke, SLE, HIV, paraneoplastic syndromes, meds, post-infectious, other causes of dementia, other genetic movement disorders, myoclonic epilepsy
2) Symptomatic, cannot be cured or halted; Tetrabenzine can help treat dyskinesia; dopamine blockers. Genetic testing of offspring should be offered with counseling
True or false: ALL HD patients should be referred to neurology
True
Tourette’s:
1) Define & describe it
2) What is the pathophys?
1) Chronic disorder of involuntary motor or vocal tics prior to age 21 (<11,) often assoc with ADHD and OCD.
Sudden, repetitive gestures, sounds, or words; decrease with concentration
2) Thought to be dopamine hypersensitivity
Tourette’s:
1) Epidemiology?
2) Etiology?
3) DDxs?
4) What is the goal of Tx?
1) Worldwide, M»F, <=4% of general population
2) Unknown – not genetics, but familial
3) Parkinsonism, dystonia, chorea, genetic or acquired neurologic injury, trauma, infection, stroke, Huntington’s, PANDAS, transient tic disorder, other chronic tic disorders
4) Treat underlying conditions (psych) as able, goal is for “normal” life
Tourette’s: What are some Txs?
1) Symptomatic, behavioral therapy (habit reversal training)
2) Clonidine
3) dopamine antagonists
4) Haloperidol
5) Tetrabenzine
6) Botox if tics limited to a small area
Stimulants contraindicated
-Choose treatment with best SE profile for specific patient
-Treat any underlying comorbidities (ex/ ADHD, OCD)
Tourette’s: ____% of children with Tourette’s syndrome will have tics resolve prior to 18, but tics may return later in life
50%
Restless leg syndrome (RLS):
1) What is it? Describe the feeling
2) Pathophys?
1) Restless legs accompanied by unpleasant sensations in the Bilat legs( arms and trunk not affected,) intolerable tingling, crawling, creeping; relieved by moving or walking; associated with IDA, uremia, peripheral neuropathy. Not cramping
2) Unknown, thought to be affected by dopamine pathways (responds to dopaminergic meds)
Restless leg syndrome (RLS):
1) Epidemiology?
2) Etiology?
1) Common, affects 3-10% of populations, begins in middle age, worsens over time
2) Familial, circadian disorder, occurs in the evenings and may worsen throughout the night
Restless leg syndrome (RLS):
1) DDxs?
2) Txs?
1) Akathisia, Parkinson’s, peripheral neuropathy, radiculopathy, nocturnal seizures
2) Dopaminergic agonists (ropinirole,) gabapentin, clonazepam, treat underlying cause (IDA,) optimize sleeping habits, stretching, or massage. A lifelong disorder but can typically be controlled.
Tardive Dyskinesia:
1) Define
2) Pathophys?
3) Etiology? What in particular?
1) Chronic, persistent, hyperkinetic movement disorder/restlessness of face and distal extremities
2) Muscle spasms caused by DRBAs; permanent alterations in synaptic dopaminergic sensitivity
3) Iatrogenic, esp chronic exposure to agents that block central dopamine receptors (DRBAs (dopamine receptor blocking agents). ex: neuroleptics, like risperidone also metoclopramide)
Tardive Dyskinesia:
1) Epidemiology?
2) DDxs?
3) Txs?
4) Can it be permanent?
1) Globally 15-50% of patients on antipsychotics
2) Huntington’s, idiopathic dystonias, chorea, facial tics
3) Early recognition; immediate gradual removal of offensive agent
4) Can be permanent; provider needs to educate patient on symptoms to watch for.
>Dopamine depleting drugs (ex: tetrabenazine for depression)
-Low rate of spontaneous remission, often causes permanent disability
61-year-old male withinvoluntary movements of the left hand, which occur only at rest.The symptom has been obvious to his wife for two months. Exam reveals apill-rolling tremor at rest; a significant lack of arm movement, stooped posture and shuffled gait while walking, and cogwheeling of the shoulder jointswith passive ROM.
1) What is the most likely diagnosis?
2) What is it caused by?
3) How do you want to treat it?
1) Parkinson’s
2) Dopamine depletion
3) Give dopamine meds
Define Alzheimer’s Disease
Gradual progression of memory loss plus dysfunction in at least one of the following areas:
a) Cognition
b) Language
c) Visuospatial
d) Executive functions
Alzheimer’s disease:
1) Assoc Sx?
2) What is it the most common type of?
3) Epidemiology? Demographics?
1) Depression, insomnia, agitation, hallucinations, restlessness, lack of ability for independent ADLs
2) Dementia in the elderly
3) Incidence increases with age, 5% of people >65
-50% of people > 85, F>M
Alzheimer’s disease:
1) Etiology?
2) Protective factors?
3) DDxs?
1) Age, genetics, environmental and lifestyle factors (DM, stroke, vascular disease, HTN, obesity)
2) Healthy lifestyle, no smoking, education, intellectual achievement
3) Metabolic derangement, Lyme ds, syphilis, HIV, paraneoplastic syndrome, stroke, tumor, infection, hydrocephalus, Lewy Body dementia, meds, toxins
List 4 Txs for Alzheimer’s and the side effects
1) Cholinesterase inhibitors
2) Donepezil (but major GI and psych SE)
3) Rivastigmine patch (less GI SE)
4) Memantine (less SE)
Meningitis- meningococcal:
1) What are the Sx?
2) What are some positive signs?
3) What will you see in CSF?
4) How do you Dx?
1) Fever, HA, vomiting, convulsions, delirium; neck and back stiffness, petechial rash
2) +Kernig and Brudzinski signs
3) Purulent CSF, Gm (–) diplococci.
4) Blood or csf culture (Neisseria meningitidis)
Meningitis- meningococcal:
1) Pathophys?
2) Epidemiology?
3) Etiology?
4) DDx?
5) Tx?
1) Neisseria meningitidis invades nasopharyngeal mucosa to meninges to CSF
2) Highest <1 yo, next 1-4 yo, next >85 yo
3) Neisseria meningitidis
4) Other meningeal infections (Rickettsial, echovirus, staph)
5) IV PCN G q 4hr x 5-7 d
Encephalitis (viral):
1) What is it?
2) What is the pathophys?
2) Epidemiology?
1) Acute inflammation of the brain: HA, AMS with neurologic dysfunction, personality changes and hallucinations; most commonly from viruses (HSV and arthropod-born)
2) Invasion of the brain by viruses, damages neurons, can cause hemorrhagic necrosis
3) Anytime of year worldwide; 1000/yr in US during mosquito season; US, <1000/yr (except West Nile has been more common some years)
Encephalitis (viral):
1) Etiology?
2) DDxs?
3) Tx?
1) HSV 1, arthropod-born viruses
2) Meningitis: bacterial, fungal, parasitic, autoimmune, meds, carcinomatous
3) HSV = IV acyclovir; West Nile = supportive
(Tick-born infections must be reported to local health dept or CDC)
What are the 2 main types of tumors? Give examples of and describe each
1) Primary tumors: Solitary lesion
-Meninges, Neuroepithelium, glioblastoma
2) Metastatic tumors: Often multiple lesions
-Lung, melanoma, breast, renal, testicular, GI
Neoplasms:
1) ~_____are glial cell origin tumors
2) ~________are meningiomas
3) What makes up the remaining fraction of neoplasms?
1) 1/3
2) 1/3
3) Vestibular schwannomas, pituitary adenoma, neurofibroma, lymphomas
The most common CNS tumors in adults are what? (4)
1) Gliomas
-of the cerebral hemispheres, particularlyglioblastoma - cancerous
2) Menengiomas
-most common benign tumor
3) Schwannomas
-e.g., acoustic neuroma
4) Primary CNS lymphomas
Astrocytoma, ependymoma, and oligodendroglioma have what in common?
All malignant glial cell tumors
1) How are astrocytomas graded?
2) Which grade is glioblastoma? How common is glioblastoma?
1) Four grades with worsening prognosis
2) Grade four = glioblastoma; most common primary malignant brain tumor; has poor prognosis.
A primary glial cell tumor that occurs in the ependymal cells that line the ventricles and spinal canal is called what?
Ependymoma
Metastatic neoplasms: The most common sources ofintracranial metastasis in adults are carcinomas from what?
(LaMB)
Lung
melanoma
Breast
What are 3 times more common than primary intracranial tumors and have a mostly hematogenous spread?
Metastatic neoplasms from (LaMB)
Lung
melanoma
Breast
1) What are some causes of primary neoplasms?
2) What is the origin of most primary neoplasms?
3) What are some other correlations to primary neoplasms?
1) Genetics and exposure to high-dose radiation
+FH brain tumors
2) Most are sporadic
3) Toxins and exposures, military history
Describe the clinical presentation of CNS neoplasms
General vs. focal symptoms
2) General: Headache and seizure are secondary to increased intracranial pressure
2) Focal neurologic symptoms: unilateral weakness or personality changes due to local destruction/compression
Seizure is an example of what kind of Sx of CNS neoplasm?
General
1) What are some Sx of secondary increased ICP (from brain tumor)?
2) What are the most common Sx?
1) Increased intracranial pressure (ICP)
Irritability
Lethargy
Changes in behavior/personality
Gait and balance disorders
2) Headache,Nausea and vomiting, and seizures
1) What are headaches with brain tumors like?
2) Describe general brain tumor Sx
1) Severe HA, worse in morning, + N/V
2) Chronic, persistent HA with N/V, seizures, change in HA pattern, + neurologic symptoms/signs, or positional worsening should prompt an evaluation for brain tumor (SNNOOPPPP red flags)
SNNOOPPPP mnemonic for red flag symptoms in patients with headaches
Systemic symptoms – fever, rash, myalgia, weight loss, HTN
Subdural hematoma, vascular condition
Neoplasm – history of cancer
Neurologic deficit or dysfunction – focal exam, Sz, MS & cognitive changes
Nonvascular IC pathology
Onset abrupt (thunderclap HA)
Older patient (> 50 y/o)
Painful eye + autonomic symptoms
Papilledema*
Pathology of immune system
Pattern – new HA or change in pattern in usual HA
Position exacerbates or relieves HA
Pregnancy
Posterior fossa, pituitary, cavernous sinus
Posttraumatic onset – acute or chronic
Precipitating event – sneezing, cough, exercise, sex
Progressive and atypical presentation
Postpartum
Posterior fossa, Arnold-Chiari malformation
List some other headache red flag Sx
IC Hypertension, IC condition
HIV or opportunistic infection
IC pathology
IC hypotension or hypertension
HTN/pre-eclampsia, epidural HA
Thunderclap HA, fever with meningismus, papilledema with focal neuro signs or impaired MS, and
acute glaucoma all warrant what?
Emergent evaluation
Describe how CNS neoplasms are diagnosed
1) Clinical suspicion
2) Gadolinium enhanced MRI
3) Brain biopsy for pathologic Dx, multispecialty team:
Medical oncology, XRT, Surgical
4) Treatment regimen based on tumor type, location, malignant potential, and patients age and physical condition
Primary intracranial tumors
1) What is the Tx for gliomas (usually cancer)?
2) What is the Tx for meningiomas?
3) What can help with Sx due to obstructive hydrocephalus?
4) What are some presenting Sx of both of these?
1) Surgical resection with adjuvant chemotherapy
2) Benign, space-occupying - Surgical resection
3) Surgical shunting can provide significant benefits
4) HA n/v, seizures, AMS, focal neuro deficit, cognitive/personality changes
Most common primary malignant brain tumor is what?
Astrocytoma/ tumors coming out of the glial/supportive cell tissue
1) What is the most common primary malignant brain tumor?
2) Where are these tumors?
3) What is the prognosis and Tx?
1) Glioblastoma; grade 4 (high grade) astrocytoma
2) Coming out of the glial/supportive cell tissue
3) Poor prognosis < 30% survival rate @ 1 year
Resection and adjuvant Chemo
Meningiomas:
1) What are they? How do they present and who are they more common in?
2) How are they diagnosed?
3) Tx?
4) When do they worsen?
1) Tumors of meninges, usually benign, women > men, ages 40-60, variable presentation depending on location
2) MRI + GAD
3) Surgical resection
4) Worsen with hormone exposure/fluctuations
Intracranial and spinal neoplasms: neuroimaging
1) What is preferred?
2) What has a characteristic appearance on MRI that is virtually diagnostic? What do these look like? Where are these typically?
3) What effect can occur?
MRI with gadolinium is preferred
2) Meningiomas: Homogeneous area of increased density, enhances uniformly with contrast
-typically coming from meninges
3) Mass effect
Schwannoma:
1) Define
2) Where is it usually?
3) Sx? How do you Dx?
1) Benign tumor of Schwann cells which myelinates the neurons
-Solitary tumor of peripheral nerves that’s usuallybenignandgrow very slowly
2) Usually arise on cranial nerve 8 (acoustic neuroma) causing hearing loss
3) Sx vary greatly depending on location of tumor; Dx is byMRIwith contrast agent
Primary intracranial tumors: What is the Tx? Describe
Depends on type and site of tumor:
1) Radiation therapy and chemotherapy: long-term cognitive deficits may complicate radiation therapy and chemotherapy
2) Corticosteroids to reduce edema/increased IC pressure, often started prior to other therapy
3) Seizures: phenytoin
What are some brain tumor treatments?
1) Surgical shuntingof obstructivehydrocephalus: dramatically reduce clinical deficits
2) Radiation and/or chemotherapy: increase median survival rates in malignant neoplasms, regardless of any preceding surgery
3) Corticosteroidshelp to reducecerebral edema: usually started before surgery or if symptomatic
4) Anticonvulsantsare commonly administered in standard doses to prevent seizures
5) Intramedullary cord lesions are treated by decompression and surgical excision and irradiation
6) Treatment of epidural spinal metastases consists of radiation, irrespective of cell type
7) Surgery if solitary, accessible
Metastatic intracranial tumors:
1) What is the most common source?
2) Where are most metastatic tumors?
3) When is surgical resection appropriate?
4) What are other Txs?
1) LUNG
-Other sources = melanoma, breast (LaMB)
2) Supratentorial
3) If limited number and surgically accessible is standard of therapy for mets
4) Radiation, steroids for swelling, phenytoin for seizures
