Neurology Flashcards
Work up required for stroke, and what is the best initial test? What is the most accurate test for stroke?
EKG, e-lytes, Doppler of carotids, ECHO
But best initial test is CT head without contrast to see if ischemic or hemorrhagic stroke.
Most accurate test for stroke is MRI.
What number is stroke on the leading cause of death in the US?
And what are the risk factors for stroke?
3rd leading cuase of death
RF: hypertension , diabetes, hyperlipemia and tobacco smoking
Acute treatment for ischemic and hemorrhagic stroke?
Acute ischemic stroke: -within 3 hours thrombolytics, within 6 hrs intra-arterial thrombolytics, more than 3 hours ASA
Acute hemorrhagic stroke: no reversible treatment, control BP with beta blockers, ACE, or CCB, control intracranial pressure with mannitol.
Chronic/ long-term treatment for ischemic and hemorrhagic stroke?
Treat the underlying cause of the stroke and manage risk factors.
Valve repair, PFO, warfarin for afib, endarterectomy for 70% stenosis with symptoms .
DM goal hemoglobin A1C <100
Stop smoking
What is one hypertension medication that should be avoided in hemorrhagic stroke?
Nitroprusside because it can increase inter cranial pressure
Name five common differentials for headache and their characteristics.
1) migraine: photophobia, aura, N/V, relationship to food and menses
2) tension headache: most common, neck tenderness, stress related
3) cluster headache: M>F, cluster in time, unilateral behind one eye, rhinorrhea, lacrimation
4) Giant cell arteritis: visual disturbance, jaw claudication, systemic muscle pain fatigue and weakness
5) PSeudotumor cerebri: obese female, papilledema, morning headache, N/V ands associate with venous sinus thrombosis, oral contraceptives and vitamin A toxicity.
What work up should be done for a new onset headache or if the diagnosis is unclear?
CT head or MRI to r/o intracranial mass, LP if pseudotumor cerebri
Give treatment for 5 common causes of headache.
1) Triptan and ergotamine - migraine
2) NSAIDS- tension headache
3) oxygen, Triptan and ergotomines, prednisone, Li+- cluster headache
4) prednisone- giant cell arteritis
5) weight loss, acetezolimide, steroids, serial LP, shunt
Prophylaxis for cluster headache and migraine.
What is the criteria for starting prophylactic therapy in migraine?
Cluster verapamil
Migraine propranolol, CCB, TCA, SSRI
3 migraines/ month
What do you do if a patient who is already on aspirin has an ischemic stroke?
Change to clopidogrel or add dipyridamole
What is trigeminal neuralgia and how is it treated?
It is a disorder of the fifth cranial nerve resulting in an intense pain disorder of the face induced by light touches, chewing or talking.
Treated with carbmazepine or oxcarbazepine, baclofen or lamotrigine.
If medication does not help then gamma knife surgery for nerve decompression.
What is post herpetic neuralgia, presentation and treatment?
Shingles or herpes zoster reactivation, with pain after resolution of the vesicles.
Treatment with acyclovir, famcyclovir, valganciclovir reduce the time of the herpetic neuralgia. Pain can be controlled with TCA, gabapentin, pregabalin, benzos of phenytoin.
Name common causes of new onset tonic clinic seizure that must be ruled out or considered?
Hypo or hypernatremia Hypoxia Intracranial bleeding/ increased intracranial pressure Brain mass/tumor/trauma CNS infection Alcohol, benzo or barbiturate withdrawl Amphetamine/cocaine intoxication Hypoglycemia Hepatic failure Renal failure with uremia Hypocalcemia D
What is the treatment for persistent seizure (status epilepticus)?
Start with benzos
Add phenytoin
Add phenobarbital
If seizure continues then paralyze , anesthetize and intubate
When a person comes to the ER with Altered consciousness or stupor/coma what treatments should be given prophylactically without delay?
Glucose, thiamine opens naloxone
In what patients can anti- seizure medications be started after one seizure?
When family history of epilepsy is present
Status epilepticus
Abnormal EEG or head CT
What medications are used for epilepsy?
First line: Valproic acid, phenytoin, carbamazepine
Alternate treatments: lamotrigine, gabapentin
Ethosuximide for absent seizures
When is it ok to discontinue epilepsy medication? And what test can be done to assess readiness to do so?
Standard of care is to wait for seizure free period for 2 years assessed with a sleep deprivation EEG
What are the causes of subarachnoid hemorrhage and risk factors?
Subarachnoid hemorrhage share due to aneurysms, usually at the ACA and PCA.
Risk factors for SAH are alcohol use, hypertension, hyperlipidemia, tobacco smoking, PCKD
Symptoms of subarachnoid hemorrhage.
Sudden onset headache, photophobia, meningeal irritation symptoms like neck stiffness. May have LOC due to ICP
What is the best initial test for SAH and what is the most accurate?
Best initial test is CT head without contrast
Most accurate test is LP showing xanthochromia, may show increased WBC bit should not exceed 1 WBC for each 500-1000 RBC.
How can one definitively determine the site of bleeding in SAH?
Angiography or MRA
Treatment for SAH
Like hemorrhagic stroke there is nothing that can reverse the bleeding in a SAH, but we can try to limit the bleeding and prevent seizure.
Nimodapipine (CCB), embolization (coiling), shunt
Phenytoin for seizure prophylaxis
How would a stroke of the middle, posterior and anterior cerebral arteries present?
MCA: contra lateral weakness/ sensory deficit upper extremity/face, contralateral homonymous hemianopsia (“look toward lesion), aphasia (90% left brain)
ACA: personality/ cognitive deficits, urinary incontinence, contralateral lower extremity weakness/sensory deficits
PCA: ipsilateral sensory loss of the face, 9-10 th cranial nerves, contralateral sensory loss of the limbs, limb ataxia
How does anterior spinal artery infarction present?
Loss of all function except for posterior column (vibratory and proprioception): flaccid paralysis distal to infarct (eventual spastic paralplegia), loss of deep tendon reflexes, loss of pain and temperature
What does subacute combined degeneration of the cord due to B12 deficiency or neurosyphillis look like?
Loss of dorsal column function, loss of positional and vibration sense
How does sudden spinal trauma present and what is the best treatment to start as soon as possible?
Sudden onset of weakness and sensory disturbance below the level of the spinal injury. Sphincter functions impaired. Loss of deep tendon reflexes at levels of the injury and hyperreflexia below.
Give glucocorticoids to limit inflammatory response.
Describe the presentation of Brown-Sequard syndrome.
Due to unilateral hemidisection of the spinal cord from injury or mass lesion.
Loss of pain and temperature on contralateral side
Loss of motor and vibration/proprioception ipsilateral
What is syringomylia and how does it present?
What is the most accurate test for diagnosis and what is the treatment?
It is a fluid filled sad that causes a dilated central canal in then spinal cord.
Cape-like distribution loss of pain and temperature. If severe enoughs will start to show muscle weakness and eventual atrophy of muscles.
Assessed with MRI and treated with drainage or shunting
What is the best initial test for suspected brain access?
What is the most accurate test?
Best initial test is head CT or MRI, however no definitive diagnosis can be given without the most accurate test, the biopsy. Without the biopsy brain access and mass cannot be differentiated.
What organisms should be suspected in brain access?
What is the empiric treatment?
Duration of treatment?
Staphylococcus, streptococcus, gram-negative bacilli and anaerobes.
Penicillin, metronidazole and ceftriaxone/cefepime
-> exchange penicillin for vancomycin if staph aureus is suspected as in neurosurgery patients
6-8 weeks of intravenous antibiotic followed with 2-3 months of oral antibiotics
Describe the constellation of symptoms seen in tuberous sclerosis.
What is the treatment?
Neuro: seizures, slowly progressive mental deterioration, psychomotor retardation
Skin: adenine sebaceous, shagreen patches, ash lead spots
Cardio: rhabdomyomas
Retinal lesions
No treatment control seizures
What is the constellation of symptoms seen in neurofibromatosis?
Type 1: chromosome 17
Type 2: chromosome 22, bilateral acoustic neuromas
Neurofibromas attached to peripheral nerves, cafe au lait spots, meningiomas, iris harmatomas, axial lady/inguinal freckles.
Describe the constellation of symptoms in Sturgeon-Weber syndrome.
What is the treatment?
Port-wine stain, seizures, mental sub normality, homonymous hemianopsia .
No treatment, control seizures
How does essential tremor present and what is the best initial therapy?
This is a tremor that occurs both at rest and with intention.
Most present in the hands and head.
The rest of the neuro exam is normal.
Patients may comment that caffeine makes it worse with alcohol makes it better.
First line treatment: propranolol
What should Be included in a patient presenting with new dementia?
Mini-mental; must be <24/30, if normal consider pseudodementia CBC to r/o infectious causes Urinanalysis to r/o UTI Electrolytes with bun/creat LFT and TFT Serology for syphillis and HIV B12 levels MRI is absolutely necessary to rule out multi-infarct dementia
Parkinson’s disease: pathophysiology, presentation
Loss of dopaminergic cells of the susbtantia nigra, Lewy body formation with increased acetylcholine release.
Patients 50-60 years old, pill rolling tremor that stops with intention movement, mask-like facies, hypokinetic shuffling gait, micrographia, cog wheel rigidity, Bradykinesia, postural instability.
Parkinson’s disease: treatment for mild and severe disease
What medication is thought to slow the progression of the disease
Mild disease: anticholinergic medications (benztropine and trihexyphenidyl) to relieve movement disorder. Amantidine may increase release of dopamine.
Severe disease: levodopa/carbidop, dopamine agonist (pramiprexole and ropinirole), COMT inhibitors and MAO inhibitors (selegiline, rasageline)
MAOIs are thought to slow progression of Disease
Alzheimer’s disease: pathophysiology, presentation, CT findings and risk factors
Caused by neurofibrillary tangles, amyloid protein deposits, and plaque formation that leads to decreased acetylcholine.
Patients often had confusion with inability to complete common everyday tasks, slow and progressive short term memory loss with sparing of long term memory, do not recognize they are having memory issues. If severe may have hallucination or personality changes.
CT may show diffuse cortical atrophy, non-specific
Risk factors: age, family history, Down syndrome , female sex
Alzheimer’s disease treatment.
Donepizil, rivastigmine, galantamine (cholineaterase inhibitors) and mimantine (NMDA receptor antagonist)
What characteristics differentiate pick’s disease and Lewy body dementia from the other more common causes of dementia?
Picks disease: personality and behavior changes may often occur before dementia symptoms (socially inappropriate) and aphasia mah be present.
Lewy body dementia: dementia, Lewy bodies, Parkinsonian symptoms, with visual hallucinations. May present due to repeated and unexpected falls.
How to treat restless leg syndrome?
Pramiprexole a dopamine agonist
Huntington disease: cause, presentation, diagnostic test and treatment
Hereditary disease of the 4th chromosome resulting in CAG repeats.
Presentation between 30-50 years old, choreoform movements, dementia and behavior changes (crazy), decreased acetylcholine, changes in caudate nucleus and putamen.
Use specific genetic testing for hunting tons and offer to family members with counseling
Treatment: no treatment reverses this condition. Dyskinesia treated with tetrabenazine. Psychosis treated with haloperidol, quetapine and other anti-psychotics.
Presentation and treatment of Tourrete’s disorder.
Vocal or motor tics for more than one year before the age of 18
OCD behavior.
Treat with fluphenazine, clonazepam, pimozide or other neuroleptic treatment. Methylphenidate and ADHD treatment are used as well.
Multiple sclerosis : pathophysiology, presentation, diagnostic test and treatment
Thought to be an autoimmune attack of the white matter (myelin) of the brain and spinal cord.
Presentation of 20-40 year old with multiple unrelated focal neurological deficits usually separated in time; had a progressive course with remissions between exacerbations.
-unilateral optic neuritis: painful eye movement with central vision loss and loss of addiction.
-inter nuclear ophthalemoplegia
-motor and sensory disturbances
Best initial and most accurate test is MRI brain and spinal cord
LP will show increased proteins and oligoclonal bands.
Treatment for acute exacerbations: high dose steroids
Treatment for chronic disease: interferon beta and glatiramer; prevent exacerbation.
Amyotrophic lateral sclerosis: pathophysiology, presentation, diagnostic tests and treatment
Loss of upper and lower MOTOR neurons. Sensory is spared.
Presentation in 20-40 year old patient, unilateral asymmetric weakness and than lead to spastic and/or flaccid paralysis, issue with chewing/swallowing and gag so mcc death is respiratory failure. *weak cough suggests a poor prognosis.
Diagnose with electromyography showing nerve deinnervation in different muscle groups. Elevated CPK.
Treatment: Riluzole decreases glutamate toxicity. Baclofen for spasticity. CPAP/BiPAP and eventual trach with vent to protect airways
Facial nerve palsy: causes, presentation, how to differentiate with stroke, test, treatment
AKA Bell’s palsy/ cranial nerve VII. Most causes are idiopathic, but can be seen Lyme disease, sarcoidosis, herpes zoster and tumors.
Presents with unilateral paralysis of upper and lower face; as differentiated from stroke where only lower face shows paralysis. Can have complication of corneal drying/ulceration because patient cannot close eye. May also complain of hyperacusis and taste disturbances.
No test is usually done due to the characteristic presentation but an electromyography and nerve conduction studies can be done.
This is usually a self limiting condition that will resolve on its own; presents 1-2 days, progresses 3 weeks, improvement with resolution 6 months; 60% have full recovery. Can give eye drops and steroids.
Guillan-barre syndrome: cause/associations, presentation, complications, diagnostic tests, treatment, prognosis.
Autoimmune attack on myelin of the peripheral nervous system. Associated with recent infections: campylobacter jejuni, HIV, CMV
Presents with symmetrical lower extremity weakness that ascends; loss of DTR. Autonomic dysfunction (tachycardia mc, hypotension, hyper tension).
Complications and most common cause of death due to respiratory failure and dysautonomia.
Tests:most specific nerve conduction studies, CSF with increased protein but normal cell count (albuminochtologic dissociation). Do PFTs to assess respiratory function and need to intubate.
Treatment: IVIG Or plasmapheresis.
Prognosis: 80% will spontaneously regress and recover within one year, 10% relapse, 10% prolonged disease and rest die.
Myesthenia gravis: pathophysiology, presentation, associations, best initial/most accurate test, treatment
Autoimmune disorder with anti-acetylcholine receptor antibodies at neuromuscular junction.
Presentation is a pt complaining of easy fatiguabilty that progresses throughout the day, double vision, difficulty chewing.
Associated with thymoma and thyrotoxicosis; so must do chest X-ray.
Best initial test: acetylcholine receptor antibodies, anti-MUSK antibodies (muscle specific kinase). Can do edrophonium tests.
Most accurate test: electromyography showing decreased strength with repetitive movements.
Treatment: first line is neostigmine and pyridostigmine (acetylcholinase inhibitors). If medical treatment fails 60 years give steroids.
What is the management of acute myasthenia crisis?
Sudden severe overwhelming disease with profound weakness and respiratory involvement.
Treat wi IVIG or plasmapheresis.
What is Lambert-Eaton syndrome? Treatment?
Paraneoplastic disease most commonly seen with small cell carcinoma of the lungs; caused by presynaptic calcium channel antibodies.
Similar presentation to myasthenia gravis but big difference is that muscle weakness improves with muscles use.
Treatment: immunosuppressant and plasmapheresis.
What are the most common primary CNS tumors in adults vs children?
What must be done with the identification of a CNS tumor?
Although metastasis is the most common CNS tumor in adults the most common primary tumors are glioblastoma multiforme, meningiomas and schwannoma.
Children:astrocytoma, medulloblastoma, epindeymoma
Full body scan must be done to see if tumor is primary or metastasis; biopsy. Resection and radiation.
What are the most common origin sites of CNS metastasis?
Lungs, kidneys, breast, colorectal CA, prostate, melanoma
What is a common complication of giant cell arteritis? And how should this be managed?
Aortic aneurysm and follow with serial chest X-rays
