Neuro Flashcards
How do you diagnose pseudo-seizure disorder?
Inpatient 24 hour EEG with video monitoring and induction of seizure with stimuli and sleep deprivation.
What is a possible treatment for neurogenic bladder?
neurogenic bladder can be side effect of MS
Use bethanechol to induce spasms in the bladder
How is stroke related to depression?
Stroke places patients at high risk for depression. Use of SSRI or SNRIs is indicated, unless contraindications exist.
What is the diagnosis of cluster headache?
Cluster headaches require one time brain imaging.
What is pseudodementia?
do not have dementia at all, just the depression that manifests as it
Fix the depression, fix the dementia. Treat depression with anti-depressants such as citalopram.
What is Eaton-lambert syndrome?
Paraneoplastic syndrome that presents with large-muscle weakness that improves with use.
Caused by the production of antibodies against presynaptic calcium channels.
How do you treat status epilepticus?
Escalation of therapy for status epilepticus is Benzos –> Levetiracetam –> Midazolam and Propofol –> Phenobarbital
How will Creutzfeldt-Jakob disease present?
Young dementia, rapid decline, and myoclonus is CJD.
What is myasthenia gravis?
Antibodies against acetylcholine-receptors
Weakness that worsens with use
Can be due to thymoma (do thymectomy)
Treat with stigmine (pyridostigmine)
What is Normal pressure hydrocephalus?
Weird, Wobbly, and Wet patient. This is dementia, ataxic gait, and urinary incontinence.
Get LP to diagnose
What is the treatment for Normal pressure hydrocephalus?
Removal of CSF is key to improve the condition and prevent worsening, a Ventriculoperitoneal shunt (VP Shunt) is required to maintain intracranial pressures at normal levels and reverse the dementia.
What is Cauda Equina syndrome?
Saddle anesthesia, loss of bowel and bladder continence in the setting of back pain.
Treat with IV steroids
How is a stroke diagnosed?
1st test- CT
Best test- MRI
Carotid stenosis treatment?
If carotid stenosis > 70% or > 60% with symptoms then you do a carotid endarterectomy.
If DVT, then heparin to Coumadin bridge.
If no clot, then just start Coumadin (no need for heparin bridge)
What is non-convulsive status?
Seizing but no outward signs of seizure activity
considered in the ICU setting with continued altered mental status after anoxic brain injury or trauma
Diagnosis of Myasthenia Gravis?
acetylcholine receptor antibody testing and positive anti-muscle-specific tyrosine kinase antibodies
a CT scan of the chest should be obtained to rule out thymoma.
What is Fronto-temporal dementia, or Pick’s disease?
loss of social graces often presenting as hypersexuality or violence, later in dz will lose memory.
What is Parkinson’s disease?
Pill rolling tremor at rest
cog- wheel rigidity
α- synuclein (intracellular eosinophilic inclusions)
< 65 + functional we use dopamine agonists (pramipexole) –> levodopa/carbadopa later in dz
What is brain death?
Absence of brainstem reflexes AND the absence of cortical function.
What is persistent vegetative state?
Brainstem reflexes are intact (eyes open/close, cough, pupillary, corneal reflex etc) BUT cortical function is lost forever (speech, memory, personality etc)
What if seen in a patient is indication of death?
Presence of either lividity (dark blue pooling of venous blood in dependent areas) or rigor mortis
What is lewy body dementia?
combination of dementia and Parkinsonian symptoms
verbal problems and visual hallucinations
First thing to do for a stroke?
If you think stroke get a CT scan to rule out a bleed
What is sensorineural hearing loss?
Lateralization to the normal ear on Weber testing and better air conduction is indicative of a cranial nerve lesion and central cause for vertigo. Evaluate with MRI.
What is conductive hearing loss?
Weber test should lateralize to the affected ear and the Rinne test should be louder when in contact with bone.–> peripheral cause
How is myasthenia gravis daignosed?
1st test- anti-acetylcholine receptor antibodies that block the binding of acetylcholine to the end-plate at the post-synaptic junction
Best test- EMG (electromyography)
Indication of impending brain herniation.
Cushing triad
1) widening pulse pressure
2) Irregular respirations
3) Bradycardia
Syringomyelia
Syringomyelia commonly occurs in patients with Arnold-Chiari malformations and is characterized by bilateral loss of pain and temperature one level below the lesion with bilateral flaccid paralysis at the level of the lesion.
It is commonly caused by cystic dilation of the central spinal canal.
consciousness can be assessed via the Glasgow coma scale (GCS)
Eye Response Spontaneous: 4 To verbal command: 3 To pain: 2 None: 1
Verbal response Oriented with normal conversation: 5 Confused speech: 4 Inappropriate speech: 3 Incomprehensible sounds: 2 None: 1
Motor response Obeys commands: 6 Localizes painful stimuli: 5 Withdrawal to painful stimuli: 4 Abnormal flexion (decorticate): 3 Abnormal extension (decerebrate): 2 None: 1
Total Possible Points: 15
GCS and need for intubation
GCS 13= Minor injury
GCS 9-12= Moderate injury
GCS 8 or less = severe injury
Intubation is indicated for patients with a GCS less than 8.
poisoning and its antidotes
Carbon monoxide poisoning= 100% oxygen
Amyl nitrite= cyanide poisoning
Dimercaptosuccinic acid or EDTA= Lead poisoning
Methylene blue= methemoglobinemia
autosomal recessive condition
25% normal
50% carrier
25% affected
TCA overdose
most common manifestations on electrocardiogram of TCA overdose is a wide QRS complex and prolonged QT interval. Patients need immediate infusion of sodium bicarbonate (NaHCO3) to help prevent cardiac collapse and fatal ventricular tachyarrhythmias.
Guillain- Barre syndrome labs
Normal opening pressure
Normal white blood cell count
Normal glucose
Large increase in protein (100 to 1000 mg/dL)
Clear yellow appearance
Histological/Structural findings of Alzheimer’s dementia
Neurofibrillary tangles made of hyper-phosphorylated tau protein
Senile plaques made of extracellular beta-amyloid Aβ plaques.
Huntington’s disease
Autosomal dominant
Trinucleotide cysteine-adenosine-guanine (CAG) repeat expansion on chromosome 4
Caudate atrophy
choreiform movements, behavioral change (depression), and executive impairment (memory imparment not typical until LATE in Dz)
Histological/Structural findings of Frontotemporal Dementia
Pick bodies (round inclusions of hyperphosphorylated tau proteins)
Histological/Structural findings of Lewy body dementia
Lewy bodies (α-synuclein aggregates)
Histological/Structural findings of Creutzfeldt-Jakob disease
Parenchymal vacuolation (spongiform cortex)
Prions (β-pleated sheets resistant to proteases)
Empiric Antibiotic Coverage for Less than 1 month old
Common Pathogens:
Streptococcus agalactiae
Escherichia coli
Listeria monocytogenes
Empiric Antibiotic choice
Ampicillin plus cefotaxime
OR
Ampicillin plus an aminoglycoside
Empiric Antibiotic Coverage for 1 month to 23 months
Common Pathogens: Streptococcus pneumoniae Neisseria meningitidis S. agalactiae Haemophilus influenzae E. coli
Empiric Antibiotic choice: Vancomycin plus Third-generation cephalosporin
Empiric Antibiotic Coverage for 2 years to 50 years
Common Pathogens:
N. meningitidis
S. pneumoniae
Empiric Antibiotic choice:
Vancomycin plus Third-generation cephalosporin
Empiric Antibiotic Coverage for
Common Pathogens: S. pneumoniae N. meningitidis L. monocytogenes Aerobic gram-negative bacilli
Empiric Antibiotic choice:
Vancomycin plus Third-generation cephalosporin plus Ampicillin
Study phases
Preclinical- testing on animals
Phase 1- Testing on healthy volunteers (<100)- is drug safe?
Phase 2- Testing on patients (100-300)- efficacy?
Phase3- Testing on patients (300-3,000)- therapeutic effect
Phase 4- Post marketing surveillance- long term effects
Brown-Sequard syndrome
Affects all of the tracts on one side of the spinal cord
Ipsilateral loss of vibration & proprioception
Ipsilateral weakness
Contralateral loss of pain and temperature below the lesion
Syringomyelia
Syrinx (fluid-filled cavity) then develops within the central canal
Bilateral loss of pain and temperature, often in a cape-like distribution, with bilateral flaccid paralysis at the level of the lesion and relative sparing of the dorsal columns
Middle cerebral artery (MCA) occlusion
Symptoms are usually more profound in the face and arms
Contralateral hemiparesis (weakness) Contralateral hypesthesia (decreased sensation) Contralateral hemianopia (blindness in half of the visual field) Gaze preference toward the side of the lesion.
Posterior cerebral artery (PCA) occlusion
vision and thought, producing contralateral homonymous hemianopia, symptoms of cortical blindness, and other visual disturbances. Signs of altered mental status and memory impairment are also likely
Emergent Treatment of Hyperkalemia (CIGAR-B)
C- Calcium gluconate (P IV) or Ca chloride (C IV)
I- Insulin (activates NaK pump)
G- Glucose (to prevent hypoglycemia)
A- Albuterol ((activates NaK pump)
R- Remove K from STOOL w/ Patiromer or sodium polystyrene sulfonate
Remove K from urine w/ furosemide or hemodialysis if ESRD
Budd-Chiari syndrome
Occlusion of hepatic veins or inferior vena cava
common in myeloproliferative disorders like polycythemia vera, tumors, and hypercoagulable states
Ascites
Spectrum of Monoclonal Gammopathies
< 10%= MGUS, No symptoms
10-60%=
No symptoms: Smoldering myeloma
Symptoms (CRAB): Multiple Myeloma
≥60%= MM
Graves disease
TSH Decreased
Thyroxine Increased
Radioactive Iodine Uptake High
Surreptitious ingestion- Exogenous
TSH Decreased
Thyroxine Increased
Radioactive Iodine Uptake Low
Hashimoto thyroiditis
TSH Increased
Thyroxine Decreased
Radioactive Iodine Uptake- not used for hypo
Pulmonary embolism (PE)
Commonly normal findings on chest x-ray unless very large–> wedge shaped infarct (hampton hump)
Lucency at the location of the embolus (Westermark sign)
Granulomatosis with polyangiitis (Wegener granulomatosis)
small vessel vasculitis, C-ANCA
triad of sinusitis, lung cavitary lesions, and glomerulonephritis
Alport syndrome
X-linked gentic disorder
Family history of hematuria
Loss of kidney function and sensorineural hearing impairment
Goodpasture syndrome
Antiglomerular basement membrane antibodies that activate the complement system and damage the basement membranes within the lungs and kidneys
Electron microscopy reveals linear line deposition of IgG and complement component 3 (C3)
Treatment for Goodpasture syndrome
Treatment includes plasma exchange and immunosuppression with corticosteroids and cyclophosphamide
IgA nephropathy
Deposition of the IgA antibody in the glomerulus
Episodic frank hematuria occurs in nearly 40% of all cases and usually starts within a day of an upper respiratory tract infection (compare to strep glom 2 weeks)
Associated w/ henloch purpura (systemic version of this?)
Huntington disease
cytosine-adenine-guanine (CAG) repeats in the huntingtin gene on chromosome 4
Autosomal dominant pattern
Prophylactic/preventative therapy of migraine headaches
Amitriptyline, venlafaxine, a beta blocker (propranolol), or topiramate
botox if more than 15 headaches/ month and nothing else works
Persistent neutropenic fevers
If treated with antibiotics and still no improvement, Consider addition of a broad-spectrum antifungal agent in the absence of an other obvious cause.
Lewy body dementia
- Fluctuating cognition with variations in attention
- Recurrent, detailed visual hallucinations
- REM sleep disorder
- Parkinsonian features: bradykinesia, rest tremor, rigidity
Eosinophilic cytoplasmic inclusion bodies within the substantia nigra and locus coeruleus of the brain.
Alzheimer disease
Most common cause of dementia in the elderly
Senile plaques and neurofibrillary tangles
Postdural puncture headaches
Headache after getting epidural
1) Conservative management
2) Epidural blood patch (EBP)- inject patient’s blood into the epidural space to create a blood clot to compress the area of cerebrospinal fluid leakage
3) Transnasal sphenopalatine block/ Greater occipital nerve block
Malignant hyperthermia
Abnormal ryanodine receptors on sarcolasmic reticulum react to anesthetics with unregulated flow of calcium into the cytoplasm and resulting in muscular tetany
Tx: Dantrolene (antagonizes these ryanodine receptors on the sarcoplasmic reticulum.
Intracranial berry aneurysms are associated with what diseases?
1) Polycystic kidney disease
2) Ehlers-Danlos syndrome
3) Pseudoxanthoma elasticum
4) Moyamoya syndrome
5) Glucocorticoid-remediable aldosteronism
Occlusion of the basilar artery
Bilateral pontine infarction–> quadriplegia, inability to speak or swallow
Consciousness, vertical eye movements, and the ability to blink are spared.
How to diagnose orbital cellulitis?
- Orbital cellulitis is a vision threatening condition
- Contrast enhanced CT scan or MRI needs to be urgently performed to confirm the diagnosis of orbital cellulitis
Otosclerosis
Autosomal dominant (AD) inheritance pattern
Overgrowth of the middle ear bones, most commonly the stapes, which interferes with sound conduction
Tx: Hearing amplification or surgery (stapedectomy)
Conductive hearing Loss
Rinne test: Bone conduction > air conduction
Weber test: Lateralizes to affected ear, Midline if bilateral
Examples include outer and middle ear etiologies
Sensorineural Hearing Loss
Rinne test: Air conduction > bone conduction
Weber test: Lateralizes to nonaffected ear, Midline if bilateral
Examples include Inner ear etiologies
Trinucleotide cytosine-guanine-guanine (CGG) expansion
Fragile X syndrome
Mutation in the FMR1 gene. Clinical features include intellectual delay, facial dysmorphism, and autism
Trinucleotide cytosine-thymine-guanine (CTG) expansion
Myotonic dystrophy
Muscle weakness, myotonia, cardiac-endocrine-gastrointestinal disease, and intellectual delay
Trinucleotide guanine-adenine-adenine (GAA) expansion
Friedreich ataxia
Clinical features include ataxia, sensory loss, weakness, diabetes mellitus, and cardiomyopathy
Creutzfeldt-Jakob disease (CJD)
Rapid progression of cognitive and motor decline
Myoclonus (quick involuntary muscle jerks)
End-stage CJD can manifest as akinetic mutism
Pathophysiology of CJD
Caused by prions
Fatal within 1 year of symptom onset
Diagnosis of CJD
Periodic sharp waves seen on EEG
Elevated 14-3-3 proteins in the CSF
MRI abnormalities in the caudate/putamen
Lyme Neuroborreliosis
Advanced Lyme disease can cause post-viral cerebellar ataxia and is tested by the finger to nose test.
A positive test indicates a lesion within the cerebellum
frontotemporal dementia (FTD)
Personality change, disinhibition (eating multiple meals a day), and her relatively young age of onset (in her 60s).
Pick bodies consisting of hyperphosphorylated tau proteins
Hyperphosphorylated tau proteins can be found in both Alzheimer disease (AD) and Frontotemporal dementia FTD
In FTD, tau proteins are found as intracytoplasmic round aggregates
In AD, tau proteins are described as intracellular neurofibrillary tangles.
Glioblastoma multiforme
Most common and worst prognosis
“butterfly glioma”
Dx: MRI- lobulated, ring enhancing lesions that cross corpus collusum
Tx: Surgery, radiation, chemo (temozolomide)
Ependymoma
Most commonly present in the 4th ventricle, and may result in an obstructive hydrocephalus
Histology: Perivascular pseudorosettes
Hemangioblastomas
Benign central nervous system vascular neoplasms and are most often found in the cerebellum
May produce erythropoietin, leading to secondary polycythemia
Histology: Foamy cells and high vascularity
If found with retinal angiomas, is associated with von Hippel-Lindau syndrome
Medulloblastomas
Tumors of childhood
Obstructive hydrocephalus due to compression of the 4th ventricle
Differentiated from an ependymoma with MRI by observing that an ependymoma will extend further into the lateral recess of the 4th ventricle and into the cerebellopontine angle
Anterior cerebral artery (ACA)
Paralysis or weakness of the contralateral lower extremity
Urinary Incontinence anosmia
Posterior cerebral artery (PCA)
Supplies the occipital lobe
Cortical blindness and contralateral homonymous hemianopsia with macular sparing
May also not be able to recognize faces, objects, places
Middle Cerebral artery (MCA)
Contralateral paralysis/ sensory loss of the face and upper limbs
Aphasia if dominant (Left)
hemi-neglect if non- dominant side (Right)
Top of the basilar syndrome is caused by an embolus lodging in the rostral basilar artery.
If a stroke does not localize laterally, there is a good chance there is a lesion of the basilar artery.
Basilar artery stroke
impaired consciousness, pupillary abnormalities, neuro-ophthalmic abnormalities, especially of vertical gaze, and acute confusional state
Lateral medullary syndrome/ Wallenberg syndrome
Often caused by an ipsilateral vertebral artery or posterior inferior cerebellar artery occlusion
Anterior Circulation arteries
- MCA
- ACA
- Lenticulostriate artery
Posterior circulation arteries
- ASA
- PICA
- AICA
- PCA
- Basilar Artery
