Neurology Clerkship Flashcards
Hearing loss Bilateral Progressive Predominantly high-frequency Sensorineural Difficulty hearing with competing noise Subjective bilateral tinnitus
Presbycusis
Keratinizing squamous epithelium
Destruction of ossicles and sensorineural structures in the inner ear
Conductive and/or sensorineural hearing loss
Intermittent ear discharge
Tinnitus
Balance problems
Otoscopic exam: White plaque on the tympanic membrane with or w/o perforation or retraction
Cholesteatoma
Excessive accumulation of endolymph in the membranous labyrinth
Recurrent episodes of vertigo (lasting 20 minutes to several hours)
Unilateral aural fullness, tinnitus, and sensorineural hearing loss
Meniere disease
Sclerotic changes within ossicles of the middle ear
Progressive conductive hearing loss
NORMAL otoscopic exam
Otosclerosis
Alzheimer’s disease treatment
a. SSRI
b. Cholinesterase inhibitor
c. Amantadine
Cholinesterase inhibitors.
Donepezil, rivastigmine, and galantamine
Fever Back pain Neurologic deficits Focal back pain that progresses over days to nerve root pain (shooting/electric) Motor weakness, sensory changes, etc
Spinal epidural abscess (most common Staph Aureus)
Acute headache Nausea/vomiting Blurry vision Unilateral sluggish/dilated pupil Conjunctival injection New medication recently started
Acute angle-closure glaucoma
Sudden rise in intraocular pressure due to impaired drainage of aqueous humor through the pupil into the anterior chamber.
Develops spontaneously or triggered by medications (e.g. decongestants, antiemetics, anticholinergics) in patients with predisposing anatomy.
What kind of medications can trigger acute angle-closure glaucoma?
Decongestants, antiemetics, anticholinergics, sympathomimetics. Basically, things that cause MYDRIASIS. Anticholinergic activity causes mydriasis which can cause acute angle-closure glaucoma in patients who have predisposing anatomy.
Name 2 sellar masses that can cause bitemporal blindness
- Craniopharyngioma
2. Prolactinoma
Gradual loss of peripheral vision in both eyes
Leads to tunnel vision
No headache or endocrine symptoms
Open-angle glaucoma
Ipsilateral hemiparesis
Ipsilateral diminished proprioception, vibratory sensation, and light touch
Contralateral diminished pain and temperature
Brown-Sequard syndrome
True or False: A right spinal hemisection at T10 would lead to Brown-Sequard syndrome with left-sided loss of pain and temperature sensation around the T10 level and below.
FALSE.
It would have a loss at T12 and below because the lateral spinothalamic tract tends to decussate 1-2 levels above the entry point for the corresponding sensory neuron.
Focal dystonia of the sternocleidomastoid muscle
Torticollis
Sustained muscle contraction resulting in twisting, repetitive movements, or abnormal postures
Dystonia
Focal = one muscle, diffuse = many muscles
Early executive dysfunction
Stepwise decline
Cerebral infarction and/or deep white matter changes on neuroimaging
Vascular dementia
Does Frontotemporal dementia or Alzheimer dementia have early personality changes?
Frontotemporal dementia
Early, insidious short-term memory loss
Language deficits & spatial disorientation
Later personality changes
Alzheimer disease
Early personality changes
Apathy, disinhibition, compulsive behavior
Frontotemporal dementia (aka Pick disease)
Frontotemporal atrophy seen on neuroimaging
Visual hallucinations
Spontaneous parkinsonism
Fluctuating cognition
Lewy body dementia
Behavioral changes
Rapid progression
Myoclonus and/or seizures
Creutzfeldt-Jakob Disease (prion disease)
Neurologic deficits disseminated in space and time
Women age 15-50
2 or more distinctive episodes of CNS dysfunction with at least some resolution
Cannot be explained by a single lesion
Multiple sclerosis
Internuclear opthalmoplegia
Demyelination of the medial longitudinal fasciculus resulting in impaired conjugate horizontal gaze in which the affected eye (ipsilateral to lesion) is unable to adduct and the contralateral eye abducts with nystagmus.
Rapidly progressive ascending muscle paralysis generally preceded by infection. Associated symptoms often include reduced/absent reflexes and paresthesias.
Guillain-Barre syndrome
Impaired vibration/propioception Sensory ataxia Instability during Romberg test Diminished pain/temperature sensation Reduced/absent deep tendon reflexes Miotic eyes. Pupillary constriction with accommodation but not with light
Tabes dorsalis (late neurosyphilis)
High-grade astrocytoma
CT/MRI: Butterfly appearance with central necrosis
Nausea, vomiting, headaches
Increased intracranial pressure
Glioblastoma multiforme
Which area is most likely affected by stroke if a patient is demonstrating hemi-neglect?
A. left frontal cortex B. left temporal cortex C. right parietal cortex D. right occipital cortex E. right frontal cortex
Right parietal cortex
Does hemi-neglect cause neglect of left or right side of a space?
Hemi-neglect syndrome is characterized by ignoring the LEFT side of a space.
What’s the difference between peripheral facial palsy (Bell’s palsy) and central facial palsy?
Peripheral facial palsy causes loss of forehead and brow movements while central facial palsy has preservation of forehead and brow movements. They both have loss of nasolabial folds and drooping of the lower lip.
Name 3 medications/supplements that can cause pseudotumor cerebri.
Glucocorticoids, vitamin A, oral contraceptives
What is the pathophysiology of pseudotumor cerebri?
Impaired absorption of CSF by the arachnoid villi causes increased intracranial pressure.
How do you treat pseudotumor cerebri?
Weight loss (if obese) and acetazolamide. Shunting or optic nerve sheath fenestration may be performed if needed.
What complication occurs if pseudotumor cerebri is left untreated?
Blindness
What vessel is injured in anterior cord syndrome?
Anterior spinal artery
Injury can be due to disc retropulsion, fragments of bone from vertebral burst fracture
Bilateral motor function loss at and below the level of injury with diminished pain and temperature sensation bilaterally that begins 1-2 levels below the cord injury. Proprioception, vibratory sensation, and light touch are unaffected. What’s the syndrome?
Anterior cord syndrome 2/2 anterior spinal artery injury
Usually bilateral, severe radicular pain Saddle hypo/anesthesia Asymmetric motor weakness Hyporeflexia/areflexia Late-onset bowel & bladder dysfunction
What’s the syndrome?
Cauda equina syndrome
Sudden-onset severe back pain Perianal hypo/anesthesia Symmetric motor weakness Hyperreflexia Early-onset bowel & bladder dysfunction
Conus medullaris syndrome
Upper or lower motor neuron damage? Spastic paralysis Clasp-knife rigidity Hyperreflexia Babinski sign
Upper motor neuron damage
Upper or lower motor neuron damage? Flaccid paralysis Hypotonia Hyporeflexia Muscle atrophy Fasciculations
Lower motor neuron damage
How can you tell the difference between caudal equina syndrome and conus medullaris syndrome?
Cauda equina defects are LOWER MOTOR NEURON defects as they are nerve roots of the peripheral nervous system. So, cauda equina syndrome will have hyporeflexia/areflexia while conus medullaris syndrome will have hyperreflexia. Also, cauda equina syndrome typically presents with asymmetric motor weakness while conus medullaris syndrome presents with symmetric motor weakness. This makes sense because it would be unlikely for the impingements/defects of the many nerve roots of the cauda equina to be symmetric in the damage distribution. Another difference is that cauda equina syndrome has late-onset bowel and bladder dysfunction while conus medullaris has early-onset bowel and bladder dysfunction.
What’s the difference in presentation between ischemic and hemorrhagic stroke?
Ischemic stroke usually has an abrupt onset of focal neurologic deficits but lacks headache and impaired consciousness. Hemorrhagic stroke (e.g. intracranial hemorrhage) classically presents with acute focal neurologic deficits that gradually worsen over minutes to hours (as it bleeds) and can be associated with symptoms of elevated intracranial pressure (e.g. headache, vomiting, altered mental status).
Unilateral, intermittent sharp pain of the cheek and lips that lasts several seconds and is triggered by minor stimuli (e.g. brushing teeth, drinking cold water) is likely what?
Trigeminal neuralgia
Trigeminal neuralgia more commonly effects which 2 branches of the trigeminal nerve?
V2 and V3 (maxillary and mandibular)
What is the pathophysiology of trigeminal neuralgia? (according to UW)
The pathophysiology is thought to be related to demyelination along the trigeminal nerve root (as it enters the pons), likely from localized compression (e.g. vascular structure).
What are two medications that can treat trigeminal neuralgia?
Carbamazepine, oxcarbazepine
Unilateral foot drop
Numbness/tingling over the dorsal foot and lateral shin
Impaired ankle dorsiflexion (walking on heels) and great toe extension
Preserved plantar flexion (walking on toes) and reflexes
Commonly caused by compression from leg immobilization, prolonged leg crossing, or protracted squatting
Common fibular neuropathy is a compressive injury to the common fibular nerve (aka common peroneal nerve) that travels near the fibular head. Manifestations are usually transient (lasting hours) and include foot drop and sensory changes over the dorsal foot and lateral shin. Physical examination shows impaired ankle dorsiflexion and great toe extension with preserved plantar flexion and reflexes.
Note that spinal nerve root entrapment of the L5 can also present with foot drop; however, patients with spinal nerve root entrapment typically have back pain radiating to the foot and impaired plantar flexion. With common fibular neuropathy, a peripheral nerve compression, plantar flexion and reflex is spared.
Unilateral Severe eye pain May see halos around lights Pupil dilated and poorly responsive to light Orbitofrontal headache, nausea, vomiting Eye appears injected
Acute angle-closure glaucoma
Acute angle-closure glaucoma is more common in what patient population?
Women
Asian and inuit populations
Individuals with farsightedness
Brief episodes of vertigo triggered by head movement (e.g. feeling dizzy when turning over in bed or looking up at objects on a high shelf). Dix-Hallpike maneuver helps to diagnose.
Benign paroxysmal positional vertigo (BPPV)
What’s the pathophysiology of benign paroxysmal positional vertigo (BPPV)?
BPPV is due to crystalline deposits (canaliths) in the semicircular canals that disrupt the normal flow of fluid in the vestibular system. This leads to contradictory signaling from the corresponding canals on each side, which is interpreted as a spinning/vertigo sensation.
What is the Dix-Hallpike maneuver?
This is a maneuver that helps diagnose benign paroxysmal positional vertigo. Vertigo and nystagmus are triggered as the patient quickly lies back into a supine position with the head rotated 45 degrees.
How do you treat benign paroxysmal positional vertigo?
BPPV resolves spontaneously in most cases but can recur months or years later. Symptoms can be relieved with the canalith repositioning maneuver. This involves having the patient lie down in a series of positions and holding their head in that position for 30-45 seconds.
How do you differentiate dizziness from cardiovascular causes (e.g. arrhythmia, aortic stenosis, hypovolemia) from vertigo (e.g. benign paroxysmal positional vertigo, meniere’s disease)?
Cardiovascular related dizziness usually causes global cerebral hypo perfusion and presents as lightheadedness or near-syncope rather than true vertigo. Also, physical exam findings of a crescendo-decrescendo systolic murmur at the aortic position radiating to the carotids with delayed and decreased carotid upstroke may also indicate a cardiac etiology of dizziness.
Slow movements
Shuffling gait
Masked facies
Rigidity
Parkinson disease
Cognitive impairment Low mood Feelings of worthlessness Sleep disturbance Low energy Psychomotor retardation (slowed speech, thinking, and movements)
Major depressive disorder
Elderly patients who are severely depressed often present with memory loss that is sometimes referred to as _____.
Pseudodementia
Action tremor (E.g. hands outstretched) Usually bilateral Hands > arms > head >> legs Family history of tremor often present 5% of population affected
Essential tremor
What is first line therapy for essential tremor? 2nd line?
1st) Beta blockers: propranolol
2nd) Anticonvulsants: primidone
What is central cord syndrome?
Central cord syndrome is a type of traumatic injury that typically occurs in elderly patients with pre-existing degenerative changes in the cervical spine. It typically occurs from hyperextension injuries and is characterized by weakness that is more pronounced in the upper extremities than the lower extremities and may be accompanied by a localized deficit in pain and temperature sensation.
Does anterior cord syndrome cause spastic or flaccid motor paresis?
Spastic
What is a cerebral contusion and how does it typically present?
Cerebral contusions are bruises of the brain that typically result from blows to the head that result in coup and contra-coup injuries. These injuries typically present with altered level of consciousness due to edema with the risk of seizure. Focal neurologic deficits may or may not be present.
Autosomal recessive
Younger individuals
Liver disease (ranging from asymptomatic elevation of LFTs to fulminant hepatic failure)
Neuropsychiatric disease (ranging from tremor and rigidity to depression, paranoia, and catatonia)
Wilson’s disease
Name 3 lab or physical exam findings unique to Wilson’s disease.
1) Decreased serum ceruloplasmin, 2) increased urinary copper, and 3) Kayser-Fleischer rings on slit lamp examination.
What biopsy finding can be found in both Wilson’s disease and alcoholic liver injury? How can you tell the difference between Wilson’s disease and alcoholic liver injury?
Mallory bodies can be found in both Wilson’s and alcoholic liver injury. However, Wilson’s disease typically presents with neuropsychiatric changes like tremor, rigidity, depression, paranoia, and/or catatonia. Alcoholic liver injury can be identified from a thorough patient history. Occasional drinking isn’t enough alcohol to cause alcoholic liver injury.
IV drug user
Fever/chills
Holosystolic murmur at cardiac apex
(Red cell casts with proteinuria)
Infective endocarditis
23 y/o anorexic hospitalized
Acute-onset confusion after IV hydration and parenteral nutrition
Horizontal nystagmus
Diminished bilateral ankle reflexes
Slow walk with short and wide-based steps
What is the first step in management?
Give thiamine because this is wernicke encephalopathy 2/2 anorexia.
Note that she got confusion after IV hydration and parenteral nutrition. This is because thiamine is a cofactor for many enzymes that have increased activity with high metabolic rate or glucose intake. Giving glucose to a thiamine deficient patient will exacerbate the problem.
In anorexic patients and alcoholic patients, what should cross your mind in terms of immediate management? What should you think about giving and what should you avoid giving?
Avoid giving glucose. Consider giving thiamine. Alcoholic and anorexic patients are often thiamine deficient and giving glucose to these patients can cause or worsen wernicke-korsakoff syndrome.
More than two-thirds of Guillian-Barre Syndrome patients have an antecedent respiratory or GI infection caused by which bacteria? Aside from this bug, what are 3 other precipitants of Guillian-Barre syndrome?
Campylobacter jejuni (2/3 of cases of GBS) Other culprits include herpes viruses, mycoplasma, and hemophilus influenza.
What is infectious cavernous sinus thrombosis?
Because the facial/ophthalmic venous system is valveless, uncontrolled infection of the skin, sinuses, and orbit can spread to the cavernous sinus. Inflammation of the cavernous sinus subsequently results in life-threatening cavernous sinus thrombosis and intracranial hypertension. Headache is the most common symptom and can become intolerable. A low-grade fever and periorbital edema usually occur several days later secondary to impaired venous flow in the orbital veins. Vomiting is also a result of intracranial hypertension, and funduscopy may reveal papilledema.
23 y/o male Worsening headache over past week Lost appetite, vomiting Fever Bilateral eyelid edema and swelling Bilateral extraocular movements restricted Face tender to palpation
Cavernous sinus thrombosis secondary to infection. Notice that extraocular movements (CN 3, 4, 6) are effected with cavernous sinus thrombosis.
Acute-onset agitation and confusion
Disorientation
Increased motor activity (e.g. climbing out of bed frequently)
Vacillating severity (better in morning, worse at night)
Delirium
How do you manage delirium?
Avoid polypharmacy and physical restraints, maintain normal sleep-wake cycle, provide frequent orientation, and treat underlying cause (e.g. infection, electrolyte disturbances, etc)
Where in the brain are metastatic brain tumors usually seen?
Grey-white matter junction
Brain metastasis is frequently seen in patients with which kind of cancer?
Non-small cell lung carcinoma
For metastatic brain cancer, when do you surgically resect and when do you do whole brain radiation therapy?
Surgical resection is recommended for solitary brain metastasis in patients with good performance status and stable extracranial disease. In patients with multiple brain metastases, whole brain radiation therapy is typically used.
Mood disturbances (depression, apathy)
Dementia
Chorea (facial grimacing, ataxia, dystonia, tongue protrusion, writhing movements of extremities)
Family history of similar symptoms
Huntington’s disease
What is the inheritance pattern of Huntington’s disease?
Autosomal dominant affecting both sexes equally typically between 30-50 years.
Fluctuating and fatiguable ocular/bulbar weakness
Myasthenia gravis
Patients with typical features of myasthenia gravis should undergo confirmatory testing by detecting the presence of which antibody?
Acetylcholine receptor antibodies (highly specific)
If a patient is found to have typical features of myasthenia gravis and confirmed presence of acetylcholine receptor antibodies in serum, what should be the next step in management?
Chest CT or MRI to evaluate for thymoma. Thymectomy can lead to long-term improvement.
56 y/o man Right-handed Right-sided weakness and speech difficulty Speaking in short sentences with considerable effort Fully follows written and verbal commands but has difficulty writing and repeating Lesion location? A. Dominant frontal lobe B. Dominant parietal lobe C. Dominant temporal lobe D. Nondominant frontal lobe E. Nondominant parietal lobe F. Nondominant temporal lobe
Dominant frontal lobe
Broca’s Aphasia
Gait disturbance Dementia Urinary incontinence Slow and progressive memory impairment Dilated ventricles
Normal pressure hydrocephalus
Describe the pathogenesis of subdural hematomas. Also, who is at highest risk for subdural hematomas?(name 4 groups)
Subdural hematomas are caused by shearing forces that tear the bridging veins, causing them to slowly bleed into the subdural space.
Elderly (cerebral atrophy and increased fall risk)
Alcoholic (cerebral atrophy and increased fall risk)
Infants (thin-walled vessels)
Patients on anticoagulants
Elderly patient
History of falls
Gradual worsening of headache, nausea, vomiting, impaired consciousness, and confusion (days to weeks)
Focal neurologic deficits
Subdural hematoma
How does chronic subdural hematoma look on a non-contrast head CT?
Crescent-shaped hypodensity that crosses suture lines
Painless, rapid, and transient (<10 minutes) monocular vision loss. Curtain descending over the visual field. Normal funduscopic examination, sometimes plaques and retinal whitening
Amaurosis fugax
What is the pathophysiology of amaurosis fugax?
Most commonly caused by retinal ischemia due to atherosclerotic emboli originating from the ipsilateral carotid artery; therefore, patients with vascular risk factors (e.g. HTN, HLD, smoking) should be evaluated with duplex ultrasound of the neck.
Unilateral headache Jaw claudication Fever Fatigue Proximal muscle weakness/pain
Temporal (giant cell) arteritis
Altered mental status
Core temperature >105 degrees F
Heat stroke
What’s the difference between exertional and non-exertional heat stroke?
Exertional heat stroke is most commonly seen in factory workers, military recruits, and athletes who are exposed to hot/humid environments with inadequate access to shade and fluids. Non-exertional heat stroke is most commonly seen in people incapable of obtaining adequate fluids and removing themselves from a hot environment (e.g. babies, disabled, elderly)
How many days after stroke until CT scan reaches greater than 95% sensitivity? How about MRI?
CT scan needs 4-5 days to reach greater than 95% sensitivity for stroke while MRI needs only 24 to 48 hours to reach greater than 95% sensitivity.
What is the best initial therapy for nonhemorrhagic stroke at less than 3 hours since onset of stroke? at more than 3 hours since onset? What’s the best initial therapy for hemorrhagic stroke?
Less than 3 hours since onset of nonhemorrhagic stroke: thrombolytics
More than 3 hours since onset of nonhemorrhagic stroke: aspirin. If they are already on aspirin, add dipyridamole or switch to clopidogrel.
Hemorrhagic stroke: nothing. Hemorrhagic stroke has no treatment for reversal and surgical drainage will not help outside of the posterior fossa.
Every patient with a stroke should be started on a _____.
Statin. Every patient with a stroke should be started on a statin medication regardless of LDL. Although target-based therapy for lipid management is unclear at this time, we want to bring the LDL to 70 or at least under 100.
True or False: Carotid angioplasty and stenting is first-line treatment for carotid stenosis of 70% and greater.
False. Carotid angioplasty and stenting is of no proven value for stroke patients and it is ALWAYS a wrong answer.
When is carotid endarterectomy indicated?
Carotid endarterectomy has no value for milder stenosis (under 50%) and is unclear if there is benefit with moderate stenosis (50-70%). Definitely do carotid endarterectomy in symptomatic cerebrovascular disease with more than 70% stenosis.
Name the 4 risk factor modifications for stroke prevention.
1) Control diabetes to hemoglobin A1C below 7%
2) Control hypertension
3) Reduce LDL to at least below 100 if carotid stenosis is the cause of the stroke
4) Tobacco smoking cessation
It is critical to start _____ without waiting for biopsy in giant cell arteritis.
Steroids
What is first line abortive therapy for cluster headache?
100% oxygen. If it doesn’t work, you can use triptans or ergotamine.
Cluster headache prophylaxis?
Verapamil
Migraine prophylaxis?
Propranolol is first line. Others include calcium channel blockers, TCAs (amitriptyline), SSRIs, topiramate, and botox injections.
Zoster vaccine is indicated in all persons above the age of __ to prevent herpes zoster (shingles)
60
True or False: EEGs should be ordered first when working up the cause of a seizure.
FALSE.
An EEG would not be the right answer unless all other tests were done and were normal including CT or MRI of the head. There is no point in doing an EEG to identify the cause of a seizure if there is a clear metabolic, toxic, or anatomic defect causing the seizure. Seizures can be caused by hyponatremia, hypernatremia, hypoxia, hypoglycemia, CNS infections, CNS anatomic abnormalities, hypocalcemia, uremia, hepatic failure, alcohol withdrawal, barbiturate withdrawal, benzodiazepine withdrawal, cocaine toxicity, and sometimes hypomagnesemia.
What is the best initial therapy for a persistent seizure (status epilepticus)? What if it persists?
Benzodiazepines such as lorazepam or diazepam. If it persists, give phenytoin or fosphenytoin.
1) Benzodiazepines
2) Fosphenytoin
3) Phenobarbital
4) General anesthesia
What is a partial seizure? What is a simple partial seizure? Complex partial?
A partial seizure is focal to one part of the body (e.g. limited to just an arm). Simple means that consciousness is intact while complex means there is a loss or alteration of consciousness.
What is a tonic-clonic seizure?
This is a generalized seizure with varying phases of muscular rigidity (tonic) followed by jerking of the muscles of the body for several minutes (clonic).
What is an absence seizure?
This is a seizure where consciousness is impaired only briefly. The patient remains upright and gives a normal appearance or just seems to be staring into space. Absence seizures occur more often in children.
It is typically not necessary to begin antiepileptic drugs for a single seizure episode. What are the 4 exceptions?
If the single seizure episode includes:
1) Presentation in status epilepticus
2) If there are focal neurologic signs
3) If there is an abnormal EEG or lesion on CT
4) If there is a family history of seizures
All anti-epileptic drugs have nearly equal efficacy. So, the goal is to choose a medication that has the least side effects for your patient. What anti-epileptic drug typically has the fewest adverse effects?
Levetiracetam (Keppra)
What is the best therapy for absence seizures?
Ethosuximide
When do you add a second seizure medication and when do you pursue surgical correction of a seizure focus?
If seizures are not controlled with a single agent, an alternate medication should be tried. If seizures are still not controlled, adding a second medication may help. If multiple medications do not control the seizure, surgical correction of a seizure focus may lead to resolution of recurrences.
When can you discontinue seizure medication?
The standard of care is to wait until the patient has been seizure free for 2 years.
What is the best study to tell if there will be a recurrence of seizure activity?
Sleep deprivation EEG. Sleep deprivation can elicit abnormal activity on an EEG but the test lacks high sensitivity.
Aneurysms are more common in patients with? (name 5)
1) Polycystic kidney disease
2) Tobacco smoking
3) Hypertension
4) Hyperlipidemia
5) High alcohol consumption
Sudden onset Severe headache Stiff neck Photophobia Fever Loss of consciousness
Subarachnoid hemorrhage. Note that the presentation of subarachnoid hemorrhage is similar to meningitis. The difference is that subarachnoid hemorrhage has a very sudden onset and can result in loss of consciousness. Subarachnoid often presents with fever due to meningeal irritation.
What is the best initial test (most sensitive) for subarachnoid hemorrhage work-up? How about most accurate?
Non-contrast CT head (95% sensitivity). Most accurate test is lumbar puncture demonstrating blood or xanthochromia (yellow discoloration)
What electrocardiographic finding can you sometimes observe with intracranial bleeding?
Large or inverted T waves suggestive of myocardial ischemia. This is thought to be from excessive sympathetic activity.
True or False: When looking for brain bleeds, use contrast with your CT.
FALSE. Do not use contrast when looking for blood.
When treating subarachnoid hemorrhage, what medication can be given to prevent subsequent ischemic stroke?
Nimodipine (calcium channel blocker)
Nimodipine has shown good results in preventing a major complication of subarachnoid hemorrhage–vasospasm. This is now the main use of nimodipine.
What are the 4 things that should be done for treatment of subarachnoid hemorrhage?
1) Nimodipine to prevent vasospasm causing subsequent ischemic stroke
2) Embolization (coiling). This is when a catheter is used to clog up the site of bleeding to prevent a repeat hemorrhage. IR places platinum wire into the site of hemorrhage. This has been shown to be superior to surgical clipping for survival and complications.
3) Seizure prophylaxis. Usually phenytoin.
4) Ventriculoperitoneal shunt only if hydrocephalus develops.
Meningitis and subarachnoid hemorrhage can both present with severe headache, fever, nuchal rigidity, and photophobia. How can you tell the difference between the two?
Meningitis will have a normal CT head while subarachnoid hemorrhage should have bleeding demonstrated on the non-contrast CT. Also, lumbar puncture shows CSF with increased WBCs in meningitis. A normal WBC to RBC ratio for CSF is 1 WBC to 500-1000 RBCs. A elevated WBC/RBC ratio suggests meningitis.
What’s the best initial therapy for bacterial meningitis?
Ceftriaxone and vancomycin (add acyclovir if viral is on the differential too)
True or False: When taking standardized exams, never answer “consultation” for anything.
True. Consultation is only the right answer when you want to do a particular procedure and the procedure is not given as a choice. If the right answer is “embolization” and it is not listed, but “IR consultation” is a choice, then you can choose it.
Loss of all function except for the posterior column
Flaccid paralysis below the level of infarction
Loss of DTRs at the level of infarction
Evolves into spastic paraplegia several weeks later
Loss of pain and temperature
Extensor plantar response
Anterior spinal artery infarction
Name 2 things that can cause subacute combined degeneration of the cord. How does this present?
B12 deficiency and neurosyphilis can cause subacute combined degeneration. This presents with loss of position and vibratory sensation.
Loss of pain and temperature bilaterally across the upper back and both arms. Loss of reflexes. Muscle atrophy.
Syringomyelia
What imaging do you order for syringomyelia? How do you treat it?
Order MRI. Treat with surgical removal of tumor if present and drainage of fluid from cavity.
Pathogenesis of brain abscess?
A brain abscess is a collection of infected material within the parenchyma of the brain tissue acting as a space-occupying lesion. A brain abscess can be a result of spread from contiguous infection in the sinuses, mastoid air cells, or otitis media. It can also be from anything that leads to bacteremia (e.g. pneumonia, endocarditis, etc).
Symptoms of brain abscess?
Headache, nausea, vomiting, fever, seizures, and focal neurological findings. Presentation is somewhat nonspecific and there is no way to distinguish a brain abscess from a cancer without a biopsy. Note that cancer can cause fever too. Both cancer and infection enhance with contrast. You cannot distinguish them based on CT scan appearance.
How do you treat a brain abscess?
You MUST biopsy to distinguish abscess from cancer and to determine the precise organism and sensitivity pattern. Abscesses can be from staph, strep, gram-negative bacilli, and anaerobes. Infections are frequently mixed, so a precise diagnosis is especially important. Duration of treatment is very long (6-8 weeks of IV antibiotics followed by 2-3 months of oral antibiotics).
Seizures Progressive psychomotor retardation Slowly progressive mental deterioration Reddened facial nodules (adenoma sebaceous) Leathery plaques on trunk (shagreen patches) Hypopigmented patches (ash leaf) Retinal lesions Cardiac rhabdomyomas
Tuberous sclerosis
Soft, flesh-colored lesions attached to peripheral nerves.
8th cranial nerve tumors
Cafe au lait spots
Meningiomas and gliomas
Neurofibromatosis
