Transcript neurology - University of Mississippi Medical Center

NEUROLOGY
Internal Medicine Board Review
Brad Ingram, MD
Neurology
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Demyelinating diseases
Stroke
Neuromuscular
Movement Disorders
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Dementia
Headache
Epilepsy
Neuro-oncology
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Demyelinating Diseases
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Multiple Sclerosis
• Diagnosis:
• Clinical—dissemination in time/space
• Paraclinical—MRI brain/c-spine, LP, evoked potentials
• Treatment:
o Exacerbation
• New si/sx lasting >48 hrs with infection/metabolic cause
ruled out (pseudo-relapse)
• Solumedrol 1 gram/day x 3-5 days
o Prevent Relapse
• 1st line: IFN b-1a, IFN b-1b, glatiramer acetate
• 2nd line: mitoxantrone (cardiotoxicity, leukemia);
natalizumab (PML); fingolimod (bradycardia, macular
edema)
Symptomatic Treatment
• Fatigue
o R/o medical causes: TSH, B12, CBC
o Address sleep hygiene
o Exercise and cooling measures
• Spasticity: PT, baclofen, tizanidine
• Bladder dysfunction: anticholinergics, timed
voiding, urology referral
• Paroxysmal symptoms: cooling, carbamazepine,
gabapentin
• Depression: TCAs, SSRIs
NMO (Devic’s disease)
• Neuromyelitis optica
• Recurrent optic neuritis and
transverse myelitis
• Long segment of
demyelination (3 vertebrae)
• Peripheral Ab to aquaporin4
• Acute tx: steroids, PLEX
• DMTx: rituximab,
azathioprine
STROKE
7
Basilar Artery Stroke
• Symptoms
o 75% have prodrome w/stuttering course, presentation very
variable
o Mild generalized weakness to comatose
o The 5 Ds: Dizziness, Diplopia, Dysarthria, Dysphagia, Dystaxia
o Hallmark of post. circ. = crossed findings
o Locked-in = Quadriplegia, bilateral facial and
oropharyngeal palsy but preservation of cortical function
and vertical gaze
• Treatment:
o Respiratory support
o IV TPA w/i 4.5 H, IA interventions even beyond 8 hours, heparin
infusion in some patients after treatment
o Angioplasty either acute or elective
• Very high mortality (>90% if locked-in)
Stroke etiology
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Cardio-embolism (30-40%)
Athero-embolism (LVD) (30-50%)
Small Vessel Disease (SVD) (20-30%)
Non-atherosclerotic vasculopaties (Rare)
Thrombophila (up to 15%)
Hemodynamic stroke (Watershed infx.) (unkown)
Cryptogenic (unknown cause) (up to 30%)
Frequency does not add up to 100% b/c etiologic frequency varies by
series/population)
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Basic Stroke Localization
Acute treatment of stroke
• IV tPA
o <4.5 hrs after onset
o CT head w/o contrast to r/o ICH absolute
mandatory for your hospital to consider stroke
treatment!
o Dose 0.9mg/kg with max 90mg; 10% bolus then
rest over 1 hour
o No ASA, NGT, Foley, other procedures x 24 h
post-tPA
tPA criteria
Inclusion Criteria
AIS by history and
exam
Time of onset w/i 3/4.5
hours
Normal noncontrasted CT-head
(early ischemic signs
allowed)
Age > 18 years
Exclusion Criteria
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Stroke or serious head trauma w/i 3 months
Lifetime history of ICH
Major surgery w/i 14 days
SBP > 185 or DPB >110 (sustained!) OR
needing aggressive tx to maintain BP in
above range
Rapidly improving or minor Sx
Sx suggestive of SAH
GI or UT-hemorrhage w/i 21 days
Arterial puncture @ non-compressible site w/i
7days
Seizure at onset of stroke symptoms
Coagulopathy: abnormal PT/PTT, Plt.<100000
Hypoglycemia (BG<50) or Hyperglycemia
(BG>400)
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Dense MCA
Blurred gray-white junction
ADC MAP
Diffusion weighted MRI
Apparent diffusion coefficient
Acute treatment of stroke
• IA tPA: less than 6 hours
• Endovascular intervention up to 8 hours
• If none of the above:
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Telemetry x 24 hours
Permissive HTN (to 220/120)
Maintain NPO until dysphagia screen passed
ASA 325mg in first 48 hours
PT/OT/Speech
TTE with bubble, vascular imaging
• Change in neuro examthink seizure, cerebral
edema, infection, arrhythmia
BP Management in AIS
Post-tPA
• Maintain SBP < 180, DPB <
105
• May continue use of
Labetolol 10-20 mg, 1-2
times
• If BP control
unsatisfactory, use
Nicardipine infusion (start
@ 5mg/hr)
• A-line not necessary, but
preferred
No tPA
• Do not treat BP unless SBP >
220 or DBP > 120
• Treat BP if patient shows signs
of cardiac ischemia AND has
clinical features of
decompensation (pain,
tachycardia, de novo
arrhythmia etc.)
• If BP requires tx, monitor
carefully for neurological
deterioration
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Secondary prevention
• Risk factors are universal for vascular disease
• Manage HTN, DLD, DM2
• Antiplatelet agent
o Aspirin 81mg or 325mg
o Aspirin + dipyridamole
o Clopidogrel 75mg
• Indications for warfarin
o Intracardiac thrombus
o Artificial heart valve
o Non-valvular Afib (lone Afib and secondary Afib may require other
considerations)
o Large areas of cardiac hypokinesis
TIA
ABCD2 score predicts risk at 2, 7, and 90 days after
stroke; helps determine urgency of w/u
• Age ≥ 60 y: 1 pt
• BP≥140/90: 1 pt
• Clinical features: U/l
weakness (2 pts),
speech change (1 pt)
• Duration: 10-59 min (1
pt), 60+ min (2 pts)
• DM: 1 pt
• < 4 low risk
• 4-5 moderate risk
• > 5 high risk
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Carotid Artery Dissection
Intimal
flap
Carotid artery dissection
• Unilateral HA in 2/3
• Miosis/ptosis (oculosympathetic dysfunction) in
<50%
• Transient monocular blindness in 50-95%
• Causes:
o Trauma (50%)
o Connective tissue disease
o Fibromuscular dysplasia
• Dx: CTA, MRA, angiography
• Tx: heparin infusioncoumadin, endovascular
stenting
Carotid artery stenosis
• Symptomatic CAS:
o Either CEA or angioplasty + stent
o Stent if radiation anticipated
o Surgery is best done within 4-6 weeks after stroke
• Asymptomatic CAS. Consider CEA or stent if:
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Stenosis >70%
age <80 years
life expectancy > 5 years
Center with low (<3%) perioperative complication rate
Neuromuscular
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65 y/o myasthenic woman is admitted with a
productive cough. She is given a dose of
levofloxacin for CAP. The next morning, she feels
weaker and complains of shortness of breath
worse with standing than with laying flat. She
can count to 10 on a single breath and is unable
to converse in full sentences. What is the best
next step?
A.
B.
C.
D.
E.
Increase Mestinon to 60mg q4h.
Increase prednisone to 60mg qday
Increase supplemental O2.
STAT pulmonary mechanics
Start plasma exchange.
Neuromuscular Respiratory Failure
¨
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Respiratory failure does not occur until the
respiratory muscle strength has fallen to 2030% of normal.
Signs of impending respiratory failure:
 Dysphagia
 Progressive quadraparesis with inability to
lift head off bed
 Weak voice
 Bifacial weakness
 Wet voice
 Inability to complete sentences
Neuromuscular
Respiratory Failure
• Pulmonary mechanics:
o FVC <15mL/kg
o NIF <-30 cmH20
• Rapid shallow breathing index
• Do not wait for ABG changes or sat
drop!!!!
• BiPAP doesn’t compensate for bulbar
dysfunction or evacuation of secretions.
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Myasthenia Gravis
• Ab-mediated attack on post-synaptic NMJ
• Dx: AchR Ab, MUSK Ab*, EMG, Tensilon test
• Tx:
o Crisis—PLEX, IVIg, respiratory support
o Suppression—prednisone (low, slow—may cause exacerbation),
azathioprine, mycophenolate
o Symptomatic—pyridostigmine (Mestinon)
o Consider thymectomy if young, AchR Ab+
• Avoid FQ, Li, aminoglycosides, Mg, CCBs,
and macrolides
Neuralgic amyotrophy
• Brachial neuritis/plexitis (Parsonage-Turner)
o Postinfectious, post-vaccination, idiopathic
o Severe pain followed by subacute, progressive
weakness/atrophy
o Tx: analgesics, PT/OT.
• Diabetic lumbosacral radiculopathy (Bruns-Garland)
o Subacute, progressive
o Unilateral, pain in thigh, buttocks, low back with LE weakness,
sensory loss, and ↓reflexes without bladder/bowel involvement
o Assoc w/rapid wt loss or change in glycemic control
o MRI L-spine normal. EMG peripheral dysfunction. CSF ↑protein.
o Tx: PT. Usually good recovery in months.
56-y/o WM c/o 1-month h/o intermittent weakness of the left foot, a 6month h/o progressive R UE weakness, and 1-year h/o muscle cramps. He
says he feels lately as if he is “catching” his foot on things when
ambulating. Denies dyspnea, dysphagia, pain, bowel or bladder
impairment.
Neuro exam reveals normal speech, language, and mental status. His
tongue appears atrophic with fasciculations. He has diffuse weakness and
atrophy of the proximal muscles in the R UE; fascics are noted. L UE
strength and bulk are normal. Mod weakness of the distal muscles in the L
LE is noted, with fascics present in both LE. DTRs are brisk in the UE and
LE, and toes are upgoing. Sensory exam is normal. Labs and imaging are
normal. What diagnosis is most likely?
A. Amyotrophic lateral sclerosis
B. Cervical myelopathy
C. Chronic inflammatory demyelinating
polyradiculoneuropathy
D. Primary lateral sclerosis
Motor neuron disease
Signs
DDx
UMN
Hyperreflexia
Spasticity
Weakness
ALS
PLS
Myelopathy
Spastic paraparesis
B12 deficiency
LMN
Weakness
Atrophy
Fasciculations
Decreased tone
Spinal muscular atrophy
Heavy metal exposure
Kennedy disease
• ALS
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Both UMN and LMN
Multisegmental (bulbar + at least 2 spinal regions)
Cognition, sphincter function, sensory spared
Likely to need trach/PEG
50% die in 3 years
Riluzole is the only disease modifying therapy.
Cervical myelopathy
• Symptoms:
o Intermittent neck/shoulder pain or stiffness
o May have pain, paresthesia, weakness in radicular
pattern
o “Numb, clumsy hands”
o Intrinsic hand muscle atrophy
o Spasticity, stiffness in LE. Gait change.
o Loss of vib/proprioception +/- sensory level
o Hyperreflexic. +Babinski –jaw jerk
o Emergency if bowel/bladder change
• DDx: B12 myelopathy, Cu-deficiency, NO-toxicity,
dural AV-fistula, spinal compression, HIV
myelopathy, ALS
• MRI c-spine is best study
• Tx: surgery, treat pain
Myopathies
 Critical illness
 Difficult to wean from vent
 Diffuse, flaccid weakness involving the limb, neck, diaphragm
 Avoid paralytics
 Steroid induced
 Normal CK, EMG
 Dx with muscle biopsy—type 2b atrophy
 Tx: PT, stop steroids
 Endocrine
 Proximal weakness, normal CK
 hyperthyroidism, hypothyroidism, hyperparathyroidism, or vitamin D deficiency.
 Toxic—statins, AZT, colchicine, hydroxychloroquine
Inflammatory Myopathies
 Inclusion body myositis
 >50yo. Quads/hand & feet flexors. Dysphagia
 Mild ↑ CK mild
 Ubiquitin+ inclusion bodies, denervation
 Polymyositis
 May overlap with connective tissue disease
 ↑CK, antiJo-1 Ab
 Endomysial inflammation. +Necrosis
 Dermatomyositis
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Older age = higher risk for underlying cancer
Painful proximal muscle weakness
Perivascular inflammation. No necrosis.
↑CK; antiMi-2 Ab
Myotonic dystrophy
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AD chr 19; CTG repeats
Difficulty releasing grip
Hand cramps
Hatchet facies
 Frontal balding
 Bilat ptosis
 Drooping mouth
Prog muscle weakness
Gynecomastia
Cataracts
Cardiac conduction
defects
 Diabetes
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Peripheral neuropathies
Classification
Signs and Symptoms
Major Diagnostic
Considerations
Autonomic neuropathy
Orthostatic hypotension
Constipation
Early satiety
Erectile dysfunction
Amyloidosis
Diabetes mellitus
Paraneoplastic syndrome
Small-fiber neuropathy
Burning extremity pain
without weakness
Normal reflexes
Diabetes mellitus
Impaired glucose tolerance
Acquired sensorimotor
neuropathy
Distal sensory loss and ↓
reflexes
Distal extremity weakness
Diabetes mellitus
Monoclonal gammopathy
Toxic (chemotherapy)
Polyradiculoneuropathy
Severe weakness
Sensory loss
Areflexia
GBS
CIDP
Amyloidosis
Motor neuropathy
Asymmetric weakness
Muscle atrophy
Multifocal motor neuropathy
Motoneuron disease
Guillain-Barre Syndrome
• Ascending paralysis is classic
• Evolves over days
• May progress to resp failure, autonomic instability or
involve CN
• CSF: ↑protein, normal cell count
• EMG/NCS: Slowed conduction/block
• Tx: Supportive, plasmapheresis, IVIg (NO STEROIDS)
• Good px: Young, mild disease, not hyperacute,
improvement within 1 week
MOVEMENT DISORDERS
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PD Medications
• Dopamine agonists
o ropinirole, pramipexole
o Initial tx for early disease
o AE: compulsive behavior, orthostatic hypotension, nausea, vomiting,
hallucinations, sleep attacks, pedal edema
• Levodopa-carbidopa
o Gold standard
o Long-term use assoc with tolerance and dyskinesias, difficult to distinguish
from disease progression
o AE: nausea, orthostatic hypotension, hallucinations
o **Watch out for NMS-like symptoms in pts who are NPO**
PD Medications
• COMT inhibitors
o Entacapone, tolclapone
o Delay metabolism of Sinemet; give with Sinemet
o AE: nausea, diarrhea, hepatotoxicity
• MAO-B inhibitors
o Selegiline, rasagiline
o AE: N/V, hallucinations, psychosis
• Amantadine, anticholinergics
o Mostly for tremor, very early disease
o AE: psychosis, cognitive decline
o Stop 1st if pt has altered mental status
Parkinson disease
• Tremor
o Resting
o “pill-rolling”
o asymmetric
• Rigidity
o Cog-wheel, lead pipe
o freezing
• Akinsesia/Bradykinesia
o Festination
o Masked facies
o Decreased blinking
• Postural Instability
o Stooped posture
o En bloc turns
o Falls (often backwards)
• Non-motor symptoms: constipation, depression, poor sleep,
autonomic instability, drooling, dementia (late)
Other diseases producing Parkinsonism
• Drug induced Parkinsonism
o Usually bilateral at presentation
o Exposure to antipsycotics, dopamine-blockade
• Progressive Supranuclear Palsy
o Early falls (backward), symmetric bradykinesia, axial rigidity,
vertical gaze impairment (can’t look up)
o Lack of tremor or dopa-response
• Lewy Body Dementia
o Parkinsonism, dementia, hallucinations, autonomic instability
o Worse with dopamine; sensitive to meds
• Multiple Systems Atrophy
o Ataxia, dysautonomia
DEMENTIA
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Dementia
• Must involve impairment in multiple
domains: memory, language, spatial skills,
judgment, and problem solving
• Decline in cognitive function with preserved
ADLs = mild cognitive impairment
o 10-15%/yr progression to dementia
• Work-up of dementia includes:
o
o
o
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CBC, TSH, B12, CMP
CT head or MRI brain
Screening for depression
Optional: RPR, HIV, LP
Alzheimer Dementia
By far most common type, Tau-opathy
50% prevalence by age 90
Short term> long-term memory impairment
1st language problem = anomia
Behavior impaired in late disease
(agitation/aggression)
• Usually no focal signs or gait impairment
• Tx:
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o Acetycholinesterase inhibitors (donepezil,
galantamine)
o NMDA receptor antagonists (memantine)—late
disease only
Less common dementias
• Vascular
o Step-wise deterioration
o Should have focal neuro deficits, but sometimes difficult
to determine due to multi-focality
o Will see multiple infarcts (typically) on MRI
• Frontotemporal lobar (Pick’s)
o Insidious, onset <65 yrs
o Behavior change: hypersexuality, disinhibition, irritability,
poor attention, perseveration
o Nonfluent aphasia
o Can Dx by PET
Less common dementias
• Diffuse Lewy body
o Fluctuating cognition
o Parkisonism, hallucinations, autonomic dysfunction
• Creutzfeldt-Jakob Disease
o Rapidly progressive dementia with myoclonus
o ↑ CSF 14-3-3
• Normal pressure hydrocephalus
o Wet, wacky, wobbly
o MRI brain then CSF drainage
o Tx: low pressure VPS
• May improve gait and incontinence
• Symptoms <1 yr in duration
Wernicke Encephalopathy
• Encephalopathy, eye movement
abnormalities, ataxia
• Inadequate intake or absorption of thiamine
• At risk: alcoholics, malnourished patients
(any reason), chronic gastritis, repetitive
vomiting
• Always give thiamine before glucose!!
• Prognosis depends on severity.
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Transient global amnesia
Age >50
Paroxysmal, transient loss of memory
Immediate recall and long-term memory spared
Pts usually anxious, repeat same question
Mental status and neuro exam normal, although
temporal “UBO’s” have been described
• MRI brain and EEG usually normal
• Spontaneously resolves in <24 hours
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HEADACHE
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Migraine Diagnosis
• ~90% of pts w/CC of mod-sev recurrent HA
have migraine
• At least 2 of the following:
o Unilateral, not side locked, pulsating, worsens with routine
physical activity
• At least 1 of the following:
o N/V, photophobia, phonophobia
• Classic (~20%): with aura
• Common: no aura
• Variants: hemiplegic, basilar, acephalgic
Migraine treatment
• Abortive
o NSAIDS, caffeine containing analgesics
o Triptans
o Antiemetics + ergots
• Prophylactic—determined by freq of HA and
degree of interference with daily activities
o Propranolol, verapamil
o Topiramate, valproic acid
o SSRIs, amitriptyline
• Sleep hygiene and avoidance of triggers
• In pregnancy: Tylenol, Reglan, Fioricet
• Can use triptans in pts who are breast-feeding
Ménière’s disease
Recurrent, disabling vertigo
Usually 4th to 6th decades
Attacks last hours
N/V + cochlear symptoms (tinnitus, ear
fullness, and/or hearing loss)
• Tx:
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o Acute—meclizine, benzodiazepines, antiemetics
o Prophylactic—diuretics, low-Na diet
Giant Cell Arteritis
• Suspect if new onset HA after age 50
• Sx: HA, scalp tenderness, painless sudden blindness,
jaw claudication, arthalgias (PMR), weight loss,
fatigue
• ESR >100, low Hct, high plt, high CRP
• Start prednisone 60mg qd when suspected
• Dx with temporal artery bx
• Complications: blindness, stroke, MI, aortic
dissection
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Benign positional vertigo
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Most common cause of dizziness
Sudden, brief episodes of mod-intense vertigo
Nausea +/- vomiting, gait instability
Triggered by change in head position
Dix-Hallpike+
o upbeating torsional nystagmus with fast component that rotates toward
affected ear
o fatigable
• Tx: particle repositioning maneuvers, antihistamines,
anticholinergics
Causes of Vertigo
BPPV
Labyrinthitis Meniere’s
CP angle
tumour
Brain stem
Character of Paroxysmal
vertigo
Gradual onset Paroxysmal, Episodic or
over hours
spontaneous persistent,
insidious
Often constant
Course
Frequent
attacks then
recovery
Constant then Severe attacks Progressive
recovery
with remission
Usually
improves with
time
Duration
10-20 sec.
(< 1 min)
Persistent
Can be
persistent
Positional
Yes, turning
head to one
side
Days, dynamic Hours to days
symptoms
may persist
weeks
No, may be
No, may be
exacerbated exacerbated
by movement by movement
May or may
not
Yes
Hearing loss No
Yes
No, may be
No, may be
exacerbated exacerbated
by movement by movement
Usually no
CN 3 palsy
• Look at the pupil!
o Pupil sparing is usually ischemic and likely to be benign.
o If pupil involved, aneurysm until proven otherwise.
• Examine CN IV, VI, V to r/o cavernous sinus
involvement.
• Risk factors: age>50, DM, HTN, giant cell
arteritis
• Diabetic 3rd nerve palsy:
o Painful, ptosis, EOM weakness, pupil spared
o Full recovery by 3 months
CN 3 palsy
• Just remember that any isolated 3rd nerve
palsy, partial or not, deserves a w/u
• Always consider the worst case scenario:
aneuryms
• Less likely with pupil sparing partial 3rd, but
if uncertain, perform w/u to r/u aneurysm
• Don’t let anybody tell you otherwise!
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EPILEPSY
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Seizures
• Partial—originates from a focus
o Simpleretained consciousness
o Complexaltered consciousness
• Generalized: GTC, absence, atonic, etc
• Symptomatic
o
o
o
o
o
Hyper- or hypo- glycemia
Drug withdrawal—EtOH or benzos
Uremia
Meningitis
Tumor
• Risks: head injury w/LOC, h/o meningitis/encephalitis,
febrile sz, family hx
Single Seizure
• Was it a seizure?
• Look for provoking factor
o UDS, CBC, Chem8, ?LP
• Don’t usually start AED
• Risk for recurrence:
o partial seizure, Todd paralysis, a family history of
epilepsy, age greater than 65 years, and abnormal
findings on neurologic examination
• MRI brain with and without
• EEG
o Interictal EEG abnormal in 25-50% with epilepsy
o Sensitivity ~90% with 4 EEGs
Epilepsy
• 2 or more unprovoked seizures
• Start with monotherapy. Push to toxicity before
adding 2nd AED
• Trial of AED withdrawal if sz-free x 2 yrs
• Driving laws vary by state.
• Special considerations:
o Avoid valproate in child-bearing age ♀
o Monotherapy in pregnancy (not necessary to change
to Lamictal)
o Valproate for JME or myoclonus
o Levetiracetam not metabolized by liver
o Ethosuximide for absence ONLY
o Elderly, partial seizure: gabapentin, lamotrigine
Status Epilepticus
• Incidence 60/100 000 (varies)
• About 1% of patients with epilepsy will go
into status per year
• Mortality across the board is 2-35%*
• Factors associated with poor prognosis:
o
o
o
o
o
Advanced age
Prolonged (>60 min)
Hyperthermia
Associated hypoxia or stroke at onset
Other concurrent severe illness
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Status Epilepticus
Convulsive SE
• Generalized seizure
activity
• Subtle SE: dissociation
of EEG activity and
motor activity
• Mortality of > 30% (in
some series)
Nonconvulsive SE
• “Mental status
change”
• Behavioral changes
• Much lower morbidity
and mortality
• Difficult to recognize
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Status Epilepticus Tx
• ABC’s
• Treat the seizures aggressively without worrying
about causes initially
• While specific treatment for SE started, begin w/u
for possible causes if no history available or no
obvious cause apparent to you
• CT, LP and other labs must not delay treatment!
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Status Epilepticus Tx
• First line = benzodiazepines
o 0.1 to 0.2 mg/kg (for LZP), but mostly administered as bolus of 2 to 6 mg
IVP, up to 10 mg total
o DZP mostly used “on truck” IM
o Midazolam not useful IVP, but as an infusion
• Second line
o Fosphenytoin 20 PE/kg @ up to 150 mg/min.
• Brady-arrhythmia, more profound in older patients
• Goal level 15 to 25, check after 1 hour
o Phenytoin 20 mg/kg @ up to 100mg/hour (recommend 50)
o Phenobarbital 20 mg/kg over 15 minutes**
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Status Epilepticus Tx
• Any other AED (Depakote, Keppra, Vimpat)
administered in SE is “off label” use, which may be
fine, but should be seen as adjunctive medication
• Your main goal is to stop SE w/i the hour of it’s onset,
bad stuff starts to happen if permitted to persist
longer
• Co-morbidities are the main determinant of
Mortality/Morbidity related to SE
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NEURO-ONCOLOGY
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CNS Tumors
• 50% tumors are primary:
o Astrocytoma—50%of primary
• Low grade (WHO 1 and 2)
o Slow growing, present with seizure
o Resection may be curative with certain subtype
• High grade (WHO 3 and 4)
o Irregular enhancement, sig surrounding edema
o Surgery, radiation, chemo (temozolamide)
o Meningioma
• Benign, slow-growing, dural based
• Surgery or sterotactic radiation
o Pituitary adenoma
o Schwannoma
• MRI brain with and without contrast is best study
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Primary CNS Lymphoma
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Rare; <4% of CNS tumors
B-cell NHL
Present with neuro deficits, seizures
Single homogeneously enhancing deep lesion
“Vanish” with steroids
Check toxo serology, CSF EBV and flow cytometry
Tx: IT MTX and WBRT
Brain Mets
• More common than primary CNS tumors
• Lots of Bad Stuff Kills Glia
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•
•
•
•
Lung
Breast
Skin (melanoma)
Kidney (renal cell)
GI
• 70-80% are multiple
• Occur anywhere, but favor gray-white junction
early
• Tx: steroids, surgery if single/few, whole brain
radiation if multiple
Mets from Renal Cell
Cancer
CT
MRI T1 with Gd
Paraneoplastic syndromes
Syndrome
Antibodies
Associated tumor
Myasthenia gravis
Nicotinic Ach Receptor
Striated muscle
Thymoma
Lambert-Eaton
P/Q voltage-gated Ca channel SCLC
Cerebellar degeneration
Hu
Yo
other
SCLC, neuroblastoma
SCLC, ovary, breast
Hodgkin lymphoma
Brainstem encephalitis
Ma-1
Ma-3
SCLC
testicle
Limbic encephalitis
Voltage-gated K channel
NMDA receptor
SCLC
Ovary
Neuropathy
Mag
Hu
Waldenstrom
macroglobulinemia
SCLC, prostate
Amphiphysin
SCLC, breast
Stiff-man syndrome