Flashcards in Neuro 2 Deck (43):
A patient is brought in because of memory loss, shuffling gait, masklike facies, akinesia, rigidity, and a resting tremor. What is likely going on? What caused it?
Idiopathic dopamine depletion
Loss of dopaminergic striated neurons in the substantia nigra
Lew body (eosinophilic cytoplasmic inclusions in neurons) formation --> abnormal cholinergic input to cortex
How is parkinson disease treated?
Dopaminergic agonists (levodopa, carbidopa, bromocriptine, amantadine)
MAO-B inhibitors (selegiline)
Anticholinergic agents (benztropine)
How does levodopa work? When is it used? What are significant side effects?
Dyskinesia with chronic use
How does carbidopa work? When is it used? What are significant side effects?
Dopamine decarboxylase inhibitor that reduces levodopa metabolism
To augment levodopa
Reduces adverse effects of levodopa by allowing smaller dosage
How does bromocriptine work? What are significant side effects?
Dopamine receptor antagonist
Increases response to levodopa
Hallucinations, confusion, hypotension, cardiotoxicity
When is selegiline used? What are significant side effects?
Early disease...may delay need to start levodopa
How does amantadine work? When is it used? What are significant side effects?
Increase synthesis, release, or repute of dopamine
For rigidity and bradykinesia
What is necessary to diagnose ALS? How is it treated?
Lower motor neuron signs in at least 2 extremities AND upper motor neuron signs in one region
Riluzole may slow progression
A patient comes in with motor and mental dysfunction starting in middle age. Dad had similar symptoms before he died. What would be seen on genetic analysis? CT or MRI?
CAG repeats on chromosome 4...because this is Huntington disease
Caudate nucleus and putamen atrophy
How is Huntington disease treated?
Dopamine antagonist may improve chorea (haloperidol)
Tetrabenazine and reserpine inhibit vesicular monamine transport...limits how much dopamine gets packaged/released
What causes alzheimer disease?
What is seen on CT or MRI with alzheimer disease? How is it treated?
Cholinesterase inhibitors (donepezil, rivastigmine, galantamine)
Patient has come in because she has had many random things that will bother her, then go away, and then something else will bother her...often it's her vision. What is likely seen on LP? MRI?
This is MS:
LP shows increased protein, mildly increased WBCs, oligoclonal bands*, increased IgG
Asymmetric white matter lesions
How is MS treated?
Corticosteroids, methotrexate, avoidance of stress --> decrease length of exacerbations
Interferon-beta and glatiramer acetate --> decrease frequency of exacerbations
What causes syringomyelia? How is it treated?
Post-traumatic cystic degeneration of spinal cord from unknown mechanism (takes years) --> syrinx cavity expands and compresses adjacent neural tissue
Surgery...shunting if recurrent
A young woman comes in with periodic weakness and muscle fatigue that gets worse throughout the day, ptosis, diplopia, and dysarthria. What is this? What caused this? What is it associated with?
Antibodies bind to post-synaptic ACh receptors --> blocking normal neuromuscular transmission --> easy fatigue
Thymoma and thyrotoxicosis (get a chest CT after diagnosis)
How is myasthenia gravis diagnosed? Treated?
Edrophonium...a short acting anti cholinesterase
Anticholinesterase agents (neostigmine, pyridostigmine)
IVIG for refractory cases
A patient is diagnosed with, or likely has, SCLC and presents just like myasthenia gravis. What could this possibly be? How is it treated?
Lambert-Eaton syndrome...antibodies form to presynaptic calcium channels
A patient comes in after a recent viral illness with bilateral weakness in distal extremities with decreased sensation on exam. What is likely going on? What would be seen on LP? How is it treated?
Increased protein, normal glucose and pressure
Self-resolves...plasmapheresis or IVIG can speed it up
A person comes in concerned about a fixed oscillation of hands or head. What is this called? What is it associated with? How is it treated?
Benign Essential Tremor
beta-blockers, primidone, or clonazepam
Thalatomy or deep brain stimulation in refractory cases
Patient comes in with rapid flinching of distal limb and abnormal facial movements. What is it? What is it associated with?
Hyperthyroidism, stroke, Huntington disease, SLE, levodopa use, rheumatic fever
Patient comes in with writhing, snakelike movement in extremities. What is it? What is it associated with?
Cerebral palsy, encephalopathy, Huntington disease, Wilson disease
Patient comes in with sustained proximal limb and trunk contractions. What is it? What is it associated with? How can it be treated?
Wilson disease, Parkinson disease, Huntington disease, encephalitis, neuroleptic use (tardive dyskinesia)
Carbidopa, levodopa, botulinum toxin...treat underlying disorder
Patient comes in with flinging of proximal extremities. What is it? What is it associated with? How is it treated?
Stroke (subthalamic nucleus)
Patient comes in because s/he makes brief involuntary movements or sounds. What is this? what is it associated with? How is it treated?
Tourette syndrome, OCD, ADHD
Fluphenazine, pimozide, tetrabenazine
What is the most common primary brain tumor in adults? Where do they tend to be?
Glioblastoma (meningioma and schwannoma round out top 3)
What is the most primary brain tumor in kids? Where do they tend to be?
Astrocytoma (medulloblastoma [malignant] and ependymoma [may be malignant] round out top 3)
How is Neurfibromatosis type I diagnosed?
C- Cafe-au-lait spot b/w 5-15mm
O- Optic glioma
F- Freckling of axillary or inguinal area
F- Family history (1st degree relative)
I- Iris hamartomas more than 1 (Lisch nodules
N- Neurofibromas more than 1 or plexiform neurofibroma (tumors with mix of Schwann cells, fibroblasts, and mast cells)
S-Skeletal lesions (cortical thinning of long bones, sphenoid dysplasia)
How is hypersomnia (sudden occurrence of sleep) treated?
How is cataplexy (sudden loss of muscle tone) treated?
What do benzos do to the quality of sleep?
Decrease N3 and increase N2...do not reproduce normal sleep architecture
What is 'persistent vegetative state'?
Normal sleep cycles
Inability to perceive and interact wit environment
Preserved autonomic function
Patient is in a coma with large, nonreactive pupils. What is possible cause? Small reactive pupils? Pinpoint pupils?
Damage below midbrain (CN III involvement; possible uncal herniation)
Thalamic involvement, transtentorial herniation
Opioid OD; toxic effect
Patient is in a coma with immobile, reactive eyes. What is possible cause? Doll's eyes?
Patient is in a coma and you do a cold water caloric reflex test. Conjugate deviation toward that ear? No abduction/adduction? Conjugate nystagmus?
CN VI and III involvement
Patient is in a coma and has spastic paralysis. Where is the injury? Decorticate posturing (elbows flexed, legs extended)? Decerebrate posturing (elbows and legs extended)? No response to painful stimuli? Appropriate pain response?
High spinal cord injury
Cortical or thalamic compression
Pontine, medullary involvement
Superficial cause (not deep brain)
Where is the obstruction in noncommunicating hydrocephalus? Communicating hydrocephalus?
4th cerebral ventricle
Dysfunction of subarachnoid cisterns or arachnoid villi
What medications can be used to relieve symptoms of hydrocephalus? What is long term management and what is a possible side effect?
Acetazolamide or furosemide
Shunting...increases risk of meningitis
What enzyme is absent with Tay-Sachs?
What will be elevated during maternal screening if the child has a neural tube defect?
There are two types of cerebral palsy. What causes spastic CP? What else is often seen in these patients?
Damage of pyramidal tracts
There are two types of cerebral palsy. What causes dyskinetic CP?