neurology Flashcards
tension headache character
30 minutes to 7 days Typically bilateral location Pressure or tight quality Does not prohibit activity Not associated with nausea
tension headache tx
Treat acute headache with NSAIDs
A tricyclic antidepressant may be needed for prophylaxis
trigeminal neuralgia symptoms
Brief paroxysms of unilateral lancinating pain in the V2 or V3 distribution of the trigeminal nerve, often
triggered by light touch of the affected area
imaging needed for trigeminal neuralgia
MRI to rule out intracranial lesions and MS
tx for trigeminal neuralgia
Select carbamazepine for treatment
medication overuse headache symptoms
Chronic headache that occurs ≥10 days per month in patients using combination analgesics,
ergotamine products, or triptans; chronic headache that occurs >15 days per month in patients using
simple analgesics
chronic migraine characteristics
Headache occurring ≥15 days per month for >3 months
Headache possessing the features of migraine ≥8 days per month
Risk factors include migraine headache frequency or acute medication use >10 days per month
1st and 2nd line tx for migraisn
nsaids
then use triptans if lack of response or severe
treatment for . Migraine that is present on awakening, is associated with vomiting, or is found to escalate rapidly
intranasal triptans or subcutaneous
tx for migraine assoc nausea
Metoclopramide and prochlorperazine
indications to use prophylaxis for migraine
migraines do not respond to therapy
• headache occurs ≥10 days per month
• disabling headache occurs ≥4 days per month
• use of acute migraine medications is >8 days per month
options for ppx tx of migraines
amitriptyline, metoprolol, propranolol, timolol,
topiramate, valproic acid, and venlafaxine. Onabotulinum toxin A is indicated in chronic migraine.
contraindications to triptans
CAD and cerebrovascular disease, brainstem aura, and hemiplegic migraine.
characteristics of cluster headaches
Pain usually periorbital, duration 15-180 minutes, several times per day. Repeating over weeks then
disappearing for months or years. Unilateral tearing and nasal congestion or rhinorrhea, eyelid
edema, miosis and/or ptosis
tx of cluster headaches
acute - triptan and oxygen
chronic veramapil
symptoms of chronic paroxysmal hemicranias
Occurs at least five times daily lasting 2-30 minutes. Responds completely to indomethacin.
Short-lasting Unilateral Neuralgiform headaches with Conjunctival injection and Tearing
Dozens to hundreds of times per day, with durations of 1 to 600 seconds. Typically resistant to treatment.
Hemicrania continua symptoms
Persistent strictly unilateral headache that responds to indomethacin
red flag symptoms for headache (9)
- first or worst headache
- abrupt onset or thunderclap attack
- progression or fundamental change in headache pattern
- abnormal physical examination findings
- neurologic symptoms lasting >1 hour
- new headache in persons >50 years old
- new headache in patients with cancer, immunosuppression, or pregnancy
- association with alteration in or loss of consciousness
- headache triggered by exertion, sexual activity, or Valsalva mane
testing for headaches when red flag symptoms are present
MRI over CT in nonemergency situations
• CT for suspected acute ICH
• ESR or CRP for suspected giant cell arteritis
• LP for suspected infectious or neoplastic meningitis or disorders of intracranial pressure
Subarachnoid hemorrhage
(SAH) clues
Sudden onset of “worst headache of my life”
Many patients have warning “sentinel” headaches
before SAH
carotid or vertebral dissection clues
Neck pain and ipsilateral headache; neurologic
findings in territory of involved vessel
tx with asa heparin or anticoag
clues for thrombosis of cerbral vein or dura sinus
Exertional headache, papilledema, neurologic
findings
Consider in hypercoagulable states, pregnancy, use of
oral contraceptives
Tx LMWH followed by warfarin
Reversible cerebral
vasoconstriction syndrome clues
Recurrent thunderclap headache syndrome, more
frequent in women. Associated with pregnancy,
neurosurgical procedures, exposure to adrenergic or
serotonergic drugs. Imaging shows strokes,
hemorrhages, or cerebral edema
Idiopathic intracranial hypertension (pseudotumor cerebri) is
characterized by
intracranial pressure without identifiable structural pathology. Patients are typically female, obese, and
of child-bearing age. Papilledema is nearly always present.
diagnose and tx pseudotumor cerebri
Diagnosis is confirmed by a CSF pressure >250 mm H2O with normal fluid composition. MRI may be normal or show small ventricles, widened optic nerve sheaths, or a partially empty sella.
tx acetazolamide
epilepsy diagnosis
two or more unprovoked seizures occurring more than 24 hours apart or one unprovoked seizure with a significant ongoing risk of further unprovoked seizure
Focal seizure without alteration of awareness
(formerly simple partial seizures) charateristics
Normal consciousness and awareness
Single neurologic modality (sensory, motor, olfactory, visual, gustatory) involving a
single region of the body, such as the hand or arm
Focal seizure with alteration of awareness
(formerly complex partial seizure) characteristics
Conscious but unresponsive or staring
Automatism (lip smacking, swallowing, or manipulating objects)
Postictal confusion
Primary generalized seizure characteristics
Loss of consciousness or awareness at onset
No prodromal or localizing symptoms
Whole-body stiffening (tonic) and/or jerking (clonic) seizures
Temporal lobe epilepsy
Focal seizures with alteration of awareness preceded by an aura before losing consciousness. Often unaware that they have become impaired and may have no recollection of the seizure. Medial temporal sclerosis is a characteristic finding on MRI.
Idiopathic (genetic)
generalized epilepsy
Any combination of tonic-clonic seizures, absence seizures, and myoclonic seizures. MRI typically normal. EEG may show generalized spike-wave abnormality.
Frontal Lobe epilepsy
Nocturnal complex seizures that awaken patients from sleep. Often associated with underlying structural
pathology (e.g., tumor, vascular malformations).
Myoclonic seizure
A generalized seizure associated with brief, lightning-like jerks of the arms, not associated with loss of
consciousness (misdiagnosed as “jitteriness”).
Convulsive status epilepticus
Characterized by continuous seizure for ≥5 minutes. Most common cause is low AED level. Complications
include aspiration pneumonia, fever, hemodynamic instability, acidosis, PE, and rhabdomyolysis;
associated with a mortality rate of approximately 20%.
symptoms of PNES
- forced eye closure
- long duration
- hypermotor activity that starts and stops
- pelvic thrusting
evaluation needed after first unprovoked seizure
• EEG (although a normal EEG does not rule out a seizure)
• CBC, electrolyte and glucose levels, and toxicology screen
• brain MRI (or head CT in an emergency)
• CSF examination if the patient has fever, prolonged altered mental status after the seizure, is immunosuppressed, or has
a severe headache
how do you diagnose PNES and what population is susceptible to pNES
Inpatient video EEG monitoring is required to make the diagnosis of PNES
PTSD in military
carbamazepine SE
interactions with other hepatically metabolized drugs and increased risk for osteoporosis and
hypercholesterolemia
• valproic acid SE
weight gain, hypercholesterolemia, PCOS, teratogenicity, hepatotoxicity
tompiramate and zonisamide SE
increased risk of kidney stones
• carbamazepine and oxcarbazepine SE
hyponatremia, pancytopenia
all AED have a potential SE of
drug hypersensitivity syndrome, SJS, and suicidal ideation
when can you stop AED
seizure free for 2-5 years
AEDs that are relatively safe in preg
lamotrigine (dose adjustment)
and levetiracetam
most common cause of status epileticus
low blood AED levels
tx for status epilepticus
First-line treatment is IV lorazepam, IV diazepam, or IM midazolam. Patients not taking AEDs should then be treated with phenytoin or fosphenytoin, administered after
5 minutes of continuous seizing
when is Surgical clipping or endovascular coiling of aneurysms are indicated
patients with aneurysms ≥7 mm in the posterior circulation or ≥12 mm in the anterior circulation.
all patients with TIA require
- emergent head CT without contrast (to rule out intracranial hemorrhage)
- ECG and telemetry or event monitoring (to rule out AF)
- vascular studies (cerebrovascular ultrasonography or cerebrovascular MRA, CTA)
- echocardiography (to rule out LV or valvular thrombus
abcd2 scoring system
Age ≥60 y 1
Blood pressure ≥140/90 mm Hg 1
Clinical Symptoms
• focal weakness with the TIA 2
• speech impairment without weakness 1
Duration of TIA
• ≥60 min 2
• 10-59 min 1
Diabetes mellitus present 1
what abcd2 score do you hospitalize
> /=3
what kind of stroke should you consider in older adults with persistent, acute-onset vertigo
vertibral basilar
how quickly do you need to administer tpa
within 3 hours or 4.5 hrs in selective patients
exclusion criteria for tpa
- age >80 years
- severe stroke
- diabetes mellitus with a previous infarct
- anticoagulant use
increased risk of bleeding, diagnosis of ICH, or SBP
>185 mm Hg and DBP >110 mm Hg
additional stroke treatment acutel
- treat temperature >38.0 °C (100.4 °F) with acetaminophen
- administer normal saline to maintain euvolemia
- give aspirin, 325 mg, unless thrombolysis is planned
- start DVT prophylaxis within 48 hours
only times to start antihypertensive therapy early in acute stroke instead of permissive htn
- SBP is >220 mm Hg, DBP is >120 mm Hg, or MAP is >140 mm Hg
- thrombolytic therapy is planned, and SBP >185 mm Hg or DBP >110 mm Hg
- ACS, aortic dissection, or end-organ damage is present
whats considered a small SAH
<7 mm posterior or <12 mm anterior circulation can be monitored by MRI
most common location/cause of SAH
results from the rupture of saccular (“berry”) aneurysms of the circle of Willis.
eye symptoms in SAH
(third nerve palsy and dilated pupil
what should you do if SAH is suspected but CT negative
Do CSF to look for erythrocytes or xanthochromia.
Tx for SAH
• Treat ruptured aneurysms with surgical clipping or endovascular coiling within 48 to 72 hour
• Maintain BP <140/80 mm Hg to prevent rebleeding.
• Select oral nimodipine for 21 days to prevent vasospasm and improve
neurologic outcomes.
what needs to be done in the setting ICH and cocaine use
Cerebral angiography is indicated for patients <45 years of age with ICH related
to cocaine use
what score on mini mental is associated with dementia
<24
routine testing/imagining for dementia
Routinely obtain brain imaging with CT or MRI to detect nondegenerative causes that would alter management, such as cerebrovascular disease, neoplasm, subdural hematoma, or hydrocephalus. Screen all patients for depression.
when to obtain LP in dementia
- rapidly progressive dementia
- age of onset <60 years
- history of malignancy or paraneoplastic disorders
- suspicion for acute or subacute infection; immunosuppressed or immunodeficiency state
- positive syphilis or Lyme serology
- systemic autoimmune disease; suspected CNS autoimmune or inflammatory disorder
diagnose Gradual memory loss, aphasia, apraxia, agnosia, inattention, and decrease in
executive function
alzheimer disease
diagnose: Imaging or history positive for stroke responsible for impairment of at least
one cognitive domain
Common findings include focal neurologic findings, depression, pseudobulbar
palsy, gait abnormalities, and urinary difficulties
vascular neurodegenerative disorder
Mild parkinsonism characterized by postural instability and gait difficulty,
fluctuating cognition, delusions, and visual hallucinations
dementia with lewy body
Early and prominent personality changes, behavioral disturbances including
disinhibition and impulsivity, diminished frontal and/or temporal lobes on MRI,
onset before age 60 years
Frontotemporal dementia, behavioral variant
Dementia, shuffling gait, urinary incontinence, and ventriculomegaly in the
absence of past history of meningitis, SAH, or trauma
Normal-pressure hydrocephalus
Choreoathetosis and dementia, autosomal dominant pattern of
inheritance
Huntington disease
Prominent myoclonus, characteristic EEG pattern of triphasic sharp waves, CSF
protein 14-3-3, rapidly progressive onset at early age
Creutzfeldt-Jakob disease
Early postural instability and falls, apathy, parkinsonism poorly responsive to
levodopa, and vertical gaze palsy
Progressive supranuclear palsy
History of head injury followed by delayed development (10 years) of
impaired concentration, short-term memory, executive dysfunction, and
judgment; aggression, depression, irritability, violent behaviors, and
suicidality; and parkinsonism, unsteady gait, shuffling gait, and slurred speech
Chronic traumatic encephalopathy
treatment for mild to mod dementia
(donepezil, rivastigmine, and galantamine)
side effects of ach inhibitors
bradycardia, diarrhea, heart block, nausea and vomiting, and syncope
best option to delay cog decline in moderate alzheimer
Memantine
tx for lewy body
ach inhibitors
tx for normal cephalic hydrocephalus
large volume LP
parkinsons cause
degeneration of dopaminergic neurons in the substantia nigra of the midbrain
parkinsons diagnosis requires 2 of the following
bradykinesia (slowed movement and decreased amplitude of repetitive movement)
• rigidity (cogwheel type)
• resting tremor (or with movement)
• postural reflex abnormality (falling)
Early dementia within the first year of the appearance of parkinsonism is a
hallmark of
dementia with Lewy bodies.
early signs of parkinsons
loss of smell, constipation, and acting out dreams may
precede the onset of motor symptoms by years
cutaneous associatio with parkinsons
sebhoreic dermatitis
Multiple system atrophy
Severe orthostatic hypotension and ataxia
MRI showing “necrosis” of the putamen and cerebellar atrophy
Progressive supranuclear palsy
Unexplained falls (typically backward), inability to move eyes vertically, and parkinsonian features
Medication-induced parkinsonism
Antiemetics (prochlorperazine, metoclopramide), antipsychotics (haloperidol),
reserpine, lithium, and methyldopa
what are some concerns of levadopa and how to counteract them
associated with motor fluctuations,
including dyskinesias, and a “wearing-off” effect (enhanced parkinsonian symptoms). Initiating therapy with a dopamine
agonist (pramipexole, ropinirole) in patients younger than 65 years avoids the early appearance of these side effects
side effects of dopamine agonist
sedation and an increase in compulsive behaviors such as gambling, shopping, and
hypersexuality
manifestations of Essential tremor
Typically slowly progressive or stable over time
Bilateral postural or kinetic tremor; improves with alcohol
Family history positive in 50%
treatment for essential tremor
Propranolol, primidone, or topiramate
manifestation of huntingtons
Most common neurodegenerative cause of generalized
chorea
Also progressive dementia and psychiatric
manifestations
Autosomal dominant
tx for huntingtons
Symptomatic treatment with
tetrabenazine and deutetrabenazine
manifestations of Drug-induced dystonia
Tardive dyskinesia associated with choreiform and
dystonic craniofacial movements
Can be caused by neuroleptic, antiemetic, and
serotoninergic medications
tx for drug induced dystonia
Stop the offending drug
Valbenazine, clonazepam, tetrabenazine,
anticholinergic agents, and clozapine`
Cervical dystonia (torticollis) manifestations
Cervical muscle contractions resulting in abnormal
posture of the head and neck
Cervical dystonia (torticollis) treatment
Botulinum toxin (first line)
Tourette syndrome manifestations
Childhood onset, multiple complex motor tics, and
presence of vocal tics (e.g., echolalia)
Tourette syndrome treatment
Reassurance or cognitive behavioral
therapy
Myoclonus manifestations
Rapid, shock-like, jerky movements of isolated body parts
Underlying metabolic disorder, serotonin syndrome,
postanoxic, Creutzfeldt-Jakob disease, corticobasal
degeneration
myoclonus treatment
Treat the underlying metabolic disorder
what should you screen patients <40 years with “essential tremor” or dystonia for
Wilson disease with serum ceruloplasmin and
24-hour urine copper measurements.
what is MS
episodes of dysfunction resulting from demyelinating lesions (plaques) in different areas of the CNS
(brain, brain stem including optic nerve, or spinal cord) at different times.
what is Relapsing-remitting MS
Clinical episodes of neurologic dysfunction, typically lasting weeks before improving, that may lead
to the accumulation of disability.
what is Secondary progressive disease in MS
Disappearance of evidence of clinical relapses in the relapsing-remitting form and by
progressive disability.
what is Primary progressive MS disease
Progressive disability accumulation from the time of disease onset.
Optic neuritis description
Subacute visual deficit in one eye along with pain with eye movement
Afferent pupillary defect MS involvement
Paradoxical dilation of the pupil when light is rapidly shifted from the
unaffected to the affected eye
Papillitis MS involvement
Inflammatory changes in the retina causing a flared appearance of the optic
disc
Myelitis MS involvement
Focal inflammation within the spinal cord manifesting as sensory, autonomic,
or motor symptoms below the affected spinal level
Lhermitte sign MS involvement
A shock-like sensation radiating down the spine or limbs induced by neck
movements
Bladder MS involvement
Urinary frequency, urgency, or retention
Cerebellum MS Involvement
ataxia and vertigo
Brainstem MS involvement
(internuclear ophthalmoplegia) Inability to adduct one eye and nystagmus in the abducting eye
Uhthoff phenomenon in MS
Transient worsening of baseline neurologic symptoms with elevations of body
temperature
how to diagnose MS
evidence of CNS demyelination disseminated in both space and time as demonstrated through a combination
of documented clinical relapses, signs on physical examination, and the distribution of lesions on an MRI.
CSF finding in MS
oligoclonal IgG bands or an elevated IgG index
Treatment of MS flare
IV methylprednisolone followed by oral glucocorticoids speeds recovery from acute exacerbations, most effectively in acute
optic neuritis.
Treat fever and look for underlying cause of fever before starting steroids
chronic treatment for MS after first flare
interferon beta or glatiramer acetate if imaging suggests MS.
what vitamin is helpful additive for MS patients
Vitamin D added to interferon beta reduces the accumulation of MRI lesions and is recommended for all patients with MS
Tx for r confirmed relapsing-remitting MS (RRMS).
Prescribe interferon beta or glatiramer acetate
MS Spasticity tx
Physical therapy, stretching, massage therapy
Baclofen, benzodiazepines, cyclobenzaprine,
tizanidine
MS Neuropathic pain
Carbamazepine, duloxetine, gabapentin,
pregabalin, topiramate
MS Fatigue tx
Proper sleep hygiene, regular exercise
Amantadine, amphetamines, armodafinil,
modafinil
MS Depression tx
Individual or group counseling
Antidepressants (SNRIs, SSRIs)
MS cognitive dysfunction tx
Cognitive rehabilitation and accommodation
strategies
No medication has been proven effective
MS mobility tx
Physical and occupational therapy; use of braces,
canes, rolling walkers, or electrostimulatory walkassist devices
Dalfampridine
MS Urinary retention tx
Manual pelvic pressure, intermittent catheterization
• Interferon agents are contraindicated in patients with …
Liver disease or depression
is getting pregnant with MS increase risk of disability
NO
does Combining glatiramer acetate with interferon beta provide greater therapy
NO
what is Neuromyelitis optica
Devic disease
Recurrent episodes of myelitis and optic neuritis without the brain lesions typical of MS; NMO-IgG
autoantibody may be present
what is Idiopathic transverse
myelitis
Subacute onset of weakness, sensory changes, and bowel/bladder dysfunction, typically after a viral infection
Distinguished from MS by the presence of complete myelitis, no oligoclonal bands or elevated IgG index in
the CSF, and no lesions on brain MRI
b12 myelopathy characteristics
Paresthesias, lower-extremity weakness, and gait instability
Findings may include paraparesis, vibration and position sense loss, and sensory ataxia.
Anemia may be absent
Copper deficiency myelopathy characteristics
Mimics vitamin B12 deficiency
May develop after bariatric surgery or from excessive zinc ingestion
Infarction of the spinal
cord characteristics
Acute onset of flaccid paralysis or weakness and pinprick sensation loss below the level of the infarction
Potential causes include emboli, hypotension during cardiovascular/aortic surgery, and AV malformations
Clues to the cause of compression myelopathy: • fever • anticoagulation • cancer • trauma • elderly with chronic back/leg pain
- fever — epidural abscess
- anticoagulation — epidural hematoma
- cancer — metastases
- trauma — vertebral fracture
- elderly with chronic back/leg pain — spinal stenosis
tx for transverse myelitis
IV methylprednisolone
Spinal cord compression caused by leukemia, lymphoma, myeloma, and germ cell tumors may be treated urgently with surgery or radiation?
radiation!
signs of ALS
combination of upper motoneuron signs (e.g., hyperreflexia, spasticity, and extensor plantar
response) coexistent with lower motoneuron findings (e.g., atrophy and fasciculation). Sensory deficits are characteristically absent.
how does ALS symptoms present
Muscle weakness in patients with ALS usually begins distally and asymmetrically, although 20% of patients have bulbar-onset
ALS with difficulty speaking and swallowing
tx for ALS
Riluzole may increase survival by about 3 months. Begin noninvasive ventilatory support for patients with respiratory insufficiency. Placement of a percutaneous endoscopic gastrostomy tube is indicated when weight loss or swallowing difficulty occurs.
cause of myasthenia Gravis
antibodies directed against the acetylcholine receptor, which results in impaired neuromuscular transmission.
signs of MG
ptosis or diplopia (first manifestation in most patients)
• muscle weakness, including dysphagia and dyspnea
• positive anti–acetylcholine receptor antibody titer (found in 90% of patients; negative titer does not rule out MG)
• normal deep tendon reflexes and sensation
• decremental response to repetitive stimulation on EMG
Difference between botulism and MG
cranial nerve involvement, including diplopia, dysphagia, and sluggish or nonreactive pupils, whereas the pupils are normal in MG
Lambert Eaton symptoms
progressive proximal weakness and diminished tendon reflexes that improve
with repetitive movement of affected muscles
diagnosing lambert eaton
Diagnosis is confirmed by detection of serum anti–voltage-gated calcium channel
antibodies and the EMG finding of facilitation of motor response to rapid repetitive stimulation.
what disease is lambert eaton associated with
SCLC
how to diagnose MG
Single-fiber EMG can establish the diagnosis. Look for elevated serum TSH levels because of the association of MG with autoimmune thyroid disorders. Perform CT of the chest to detect thymoma.
what drugs can precipitate MG crisis
aminoglycosides, quinolones, magnesium, β-blockers, or
calcium channel blockers as precipitants of myasthenic crisis
Treatment for MG
pyridostigmine
Thymectomy if thymoma present
Tx for MG crisis
plasmapheresis or IV immune globulin.
Pyridostigmine monotherapy should be avoided in this scenerio due to increased resp secretions
diagnosis: Isolated anterolateral thigh numbness
without weakness
Meralgia paresthetica (a compressive neuropathy of the lateral femoral cutaneous nerve)
Tx: Locate and relieve pressure
diagnosis Sensory loss over palmar surface of first
three digits and weakness with thumb
abduction and opposition
Median neuropathy (carpal tunnel syndrome)
Diagnose: Numbness of the fourth and fifth fingers
and weakness of interosseous muscles
Ulnar neuropathy
Tx: Elbow splinting or elbow pads
Diagnose: Pain, tingling, and numbness in great toe
and along medial foot
Tarsal tunnel syndrome
Tx Local glucocorticoid injection;
decompression surgery if severe
Diagnose Upper and lower face weakness
Bells Palsy
Tx: Prednisone within 72 hrs
Painful, Multiple, noncontiguous nerve deficits
mononeuritis multiplex
Vasculitis
diagnose: Distal and symmetric (stocking-glove)
sensory or sensorimotor
Axonal polyneuropathies; diabetes and alcohol
are the most common causes;
diagnose Severe unilateral leg pain, numbness,
proximal weakness, atrophy, and weight
loss
dm amyotrophy
Diagnose: , ascending, areflexic paralysis and
paresthesias often preceded by GI
illness (usually Campylobacter infection);
CSF shows elevated protein and a
normal cell count (albuminocytologic
dissociation)
Guillain-Barré syndrome
Tx Plasma exchange or IV immune
globulin
Dont do steroids may slow recovery
Diagnose: Progressive proximal motor and sensory
neuropathy that evolves over months.
Initial EMG and CSF findings similar to
Guillain-Barré syndrome
Chronic inflammatory demyelinating
polyneuropathy
Prednisone, plasma exchange, or IV
immune globulin
Diagnose: Symmetric distal sensory neuropathy in
the setting of MGUS, multiple myeloma,
amyloidosis, and cryoglobulinemia
Paraproteinemic neuropathy
How to differentiate myopathy from neuropathy
Myopathies typically present with symmetric weakness of the proximal muscles.
• Normal sensory and reflex examination differentiates myopathy from neuropathy.
• Serum CK level is elevated and falls in response to treatment.
• EMG confirms the presence of myopathic changes (low amplitude, short duration, and polyphasic motor unit potentials)
Type of myopathy: Diffuse myalgia, proximal muscle weakness, delayed relaxation phase of deep tendon reflexes, and
elevation of CK
Hypothyroid myopathy
Type of Myopathy: Myopathy, brisk reflexes, fasciculation, and ophthalmoplegia
Hyperthyroidism
Type of Myopathy: Proximal muscle weakness, myalgia, fatigue, and osteomalacia-related bone pain
Vitamin D deficiency
Type of Myopathy: Proximal weakness and myalgia, normal CK levels, and normal EMG findings
Glucocorticoid myopathy
type of myopathy: Subacute toxic myopathy associated with rhabdomyolysis
statin myopathy
Type of myopathy: Myotonia (manifested as delayed hand-grip release) and distal weakness
Myotonic dystrophies
which statins are more likley to cause myopathy
Lipophilic statins (atorvastatin, simvastatin, and lovastatin) have a higher propensity to cause statin myopathy
characteristics of meningioma
benign
. CT scan of the head will show a partially calcified, homogeneously
enhancing extra-axial mass adherent to the dura and an enhancing dural “tail.”
Tx resect growing or symptomatic meningioma
common primary source for lung met
evaluate the patient for lung cancer, breast cancer,
and melanoma.
Parenchymal metastases on MRI
multiple, ring-enhancing, centrally necrotic lesions
What kind of brain met is likely in leukemia and lymphoma
leptomeningeal metastases
first line tx for parynchamal or leptomeningial tumor
Glucocorticoids are a first-line treatment for parenchymal and leptomeningeal tumors.
initial therapy for patients with leptomeningeal metastases from leukemia and lymphoma
Chemotherapy (methotrexate and cytarabine)
cardinal features of brain death
coma, absence of brain stem reflexes, and apnea.
