Quiz 2 Flashcards
What pathology can occur as a result of failure of the optic fissure (choroidal fissure) to close?
During embryological development of the eyes, what new artery/vein do the hyaloid artery/vein become?
The central retinal artery/vein
What is the etiology of Coloboma?
A failure of the optic fissure (choroidal fissure) to close during embryological development of the eye
What role does the cornea have in refraction of light entering the eye?
The cornea has a major role, being responsible for approximately 65-75% of the refraction of light entering the eye
Into what structure does aqeuous humor drain from the ciliary body?
The scleral venous sinus or Canal of Schlemm
How can obstruction of the scleral venous sinus (Canal of Schlemm) lead to glaucoma?
Increased intraocular pressure can lead to a depressed or cupped optic disc, collapsing retinal veins. The collapse of vascular outflow can lead to retinal edema and risk of retinal detachment
What is presbyopia?
Presbyopia is the age-associated increasing rigidity of the ocular lenses
What are cataracts?
Cataracts are opacifications of the ocular lense, often associated with age.
What are “eye floaters”? What is their significance?
Aggregations of vitreous material
They are generally normal but sudden appearance could be a symptom of retinal disease
What is the function of the retinal pigment epithelium? What is the concern if it has a weak junction with the retina?
Primarily it does three things:
1) Absorbs light, decreasing reflection
2) Phagocytoses discs in outer segments of photoreceptors
3) Resynthesizes photopigments
Weak junction with retina is site of retinal detachment
What artery is responsible for perfusion of the inner layers of the retina?
The central retinal artery
What artery is responsible for perfusion of the outer segments of photoreceptors?
The ciliary arteries
Does the optic disc depress or bulge in an environment of increased intraocular pressure? What is a notable pathology that could cause this?
The optic disc depresses with increased intraocular pressure
Glaucoma is a common pathology
Does the optic disc depress or bulge in an environment of increased intracranial pressure? What is a notable pathology that could cause this?
The optic disk bulges with increased intracranial pressure
A tumor could be responsible for increasing ICP (just as an example)
What is papilledema? What are the two direct effects on ocular function?
Papilledema is the swelling of the optic nerve as it enters the back of the eye due to increased intracranial pressure
1) Axonal conduction block
2) Ocular edema
What is optic neuritis? What are common etiologies?
Inflammation of the optic nerve causing swelling and damage
It is seen with multiple sclerosis, drugs, and toxins
What is a scotoma?
A scotoma is an area of depressed vision within the visual field
They can be physiological (blind spot) or pathological
Expansion of which gland, situated inferior to the optic chiasm can be a notable cause of bi-temporal heteronymous hemianopsia? Which visual fields are disrupted in this pathology?
The pituitary gland
Bi-temporal heteronymous hemianopsia produces lateral or temporal vision deficits in both eyes due to interruption of the ducussating portion of the optic nerve tract
What is uveitis?
Uveitis is inflammation of the uveal tract, which includes the choroid, ciliary body and iris
Where is the cornea located and what does it do?
The cornea is a clear, dome-shaped, avascular collagenous structure that acts as a lens to refract light entering the eye
Where is the sclera of the eye?
The sclera is the thick, tough collagenous wall of the eye, continous with the cornea, covered by conjunctiva anteriorly
What are the conjunctiva of the eye?
The conjunctiva are mucous membranes that cover the sclera and lines the inside of the eyelids
Where is the iris? What is its function?
The iris controls the amount of light entering th eye
The iris is controlled by both the sympathetic and parasympthaetic divisons of the ANS
What is the pupil?
It is the empty space or hole within the center of the iris
Where is the lens of the eye located? What is its purpose?
The lens is a clear, crystalline, avascular structure that refracts or focuses light onto the retina.
It accomplishes this by changing shape
Where is the ciliary body located? What is its function?
The ciliary body makes aqeuous humor for the anterior chamber, holds the lens in place via the zonules, and controls accomodation, or the focusing of the lens
What is the angle of the eye?
The angle of the eye is the crevice where the iris meets the cornea and where aqeuous humor is drained out of the eye.
What is vitreous gel (vitreous humor)?
Vitreous gel is a clear, jelly-like material that provides form to the young, developing eye
Where is the retina? What is its function?
The retina of the eye is neural tissue that converts the image from light energy to an electrical signal
What is the macula? Where is it located?
The macula is the central portion of the retina that corresponds to central vision
What is the fovea?
The fovea is the very center of the macula, corresponding to our most central point of focus and sharpest quality of vision
What is the optic nerve?
The optic nerve (CN II) carries afferent axons from the retina to the lateral geniculate nucleus or LGN
What cellular layer is most superficial in the retina? Which is most deep (or closest to the pigment epithelium)?
The ganglion cell layer is most superficial
The photoreceptor cell layer is most deep
What is the pathway of light from entering the retina to the retinal nerve? (four steps)
Retina nerve fiber layer: Ganglion cell axons run to the optic disc
Why is the cornea clear as opposed to the sclera, which is white?
Cornea
-Avascular
-Dehydrated (endothelial pump)
-Collagen fibrils in a lattice
Sclera
-Vascular
-Normally hydrated
-Collagen fibers not in lattice (NOT highly organized)
What pathology is seen here? What is it? What is the main cause and symptoms it is associated with?
Pterygium
Pterygium is a fleshy overgrowth of the conjunctiva, most often caused by sun exposure
It can cause astigmatism and/or blurry vision
What level of vision is needed for an unrestrictive driver’s license? At what level of vision is somebody legally blind?
20/40- needed for uDL
20/200- legally blind
How is visual acuity tested? Is it tested binocularly or monocularly? When is a pinhole occluder used?
Visual acuity is tested with charts that compare your monocular vision at 20 feet with a normal vision standard at different adjusted distances
A pinhole occluder can be used if initial testing is abnormal
What is the medical term for farsighted? Is light focused before or past the fovea? What type of corrective lens is needed?
Light is focused behind the fovea
What is the medical term for nearsighted? Is light focused before or past the fovea? What type of corrective lens is needed?
Light is focused in front of the fovea
What causes astigmatism? Does it create issues with near or distance vision?
Astigmatism is occurs when the cornea or lens is curved more steeply on one side than another. It can cause problems with near and distance vision
What is presbyopia? What causes it? Does it affect the near or far vision field?
Presbyopia is the hardening of the lens that occurs with aging. It makes it more difficult for accomodation to occur with near objects
What may be indicated if a patient does not experience vision improvement with pinhole occluder during a visual acuity test?
The pathology is non-refractive, or cannot be fixed with corrective lenses
What eye exam would be used to assess each of the following:
-Visual pathway
-Pupils (innervation)
-CN III, IV, and VI
What happens to visual images as the enter the eye? On which side of the retina do the right and left visual fields end up, respectively?
The images are focused upside down and backwards on the retina
Left visual field
Left eye- Nasal retina
Right eye- Temporal retina
Right visual field
Left eye- Temporal retina
Right eye- Nasal retina
In which area would a lesion to the optic nerve tract cause right monocular blindness?
Distal to the optic chiasm
In which area would a lesion to the optic nerve tract cause bitemporal heteronymous hemianopsia?
The optic chiasm
In which area would a lesion to the optic nerve tract cause contralateral homonymous hemianopsia?
What are one notable pathology that could cause compression of the optic chiasm in children and in adults?
Child- Craniopharyngioma
Adult- Pituitary tumor
What is a craniopharyngioma? What visual deficits can it contribute to?
it is a rare, virtually benign tumor of the CNS. It has been known to contribute to bitemporal heteronymous hemianopsia due to compression of the optic chiasm.
In which area would a lesion to the optic nerve tract cause ipsilateral nasal hemianopsia?
Note that it is extremely uncommon, but does happen.
In which area would a lesion to the optic nerve tract cause contralateral upper quadrantic anopsia?
The lesion is affecting the lower optic radiations, which pass through Meyer’s loop and then through the temporal lobe.
This is called superior quadrantanopia, and is sometimes called “pie in the sky”.
In which area would a lesion to the optic nerve tract cause contralateral lower quadrantic anopsia?
The lesion is affecting the superior optic radiations, which run through the parietal lobe.
This is called inferior quadrantanopia
In which area would a lesion to the optic nerve tract cause contralateral homonymous hemianopia with macular sparing?
Macular sparing is associated with posterior cerebral artery (PCA) occlusion, which supplies everything in the visual cortex except the macula
The MCA supplies the posterior calcarine cortex, preserving central vision bilaterally.
When visual field loss is homonymous, how does that help to localize the lesions?
Homonymous vision loss is retrochiasmal or potentially post-geniculate
What part of the optic tract would be lesioned to produce bilateral superior altitudinal defects?
Prechiasmal, often due to ischemia or a hemi-vessel occlusion
Where is the lateral geniculate nucleus or LGN located?
In the sympathetic innervation of the eye, how many neurons are involved? Where are the synapses between the hypothalamus and the opthalmic nerve tract?
There are three neurons
The first and second order neurons synapse between C8 and T12 in the spinal cord
The second and third order neuron synapse in the superior cervical ganglion or SCG
What are potential events/pathologies that can occur at these five locations that can produce Horner’s syndrome?
How can you tell if anisocoria is caused by a sympathetic or parasympathetic tract lesion?
In the sympathetic tract innervating the eye:
-Will a first order neuron lesion cause CNS findings?
-Will a second order neuron lesion cause CNS findings?
-Third order lesions typically involve what vscular structure(s)?
In diagnosis of Horner’s syndrome, what is indicated if the anisocoria does NOT resolve with cocaine drops? What is indicated if it does NOT resolve with hydroxyamphetamine drops?
In a cranial nerve III palsy, will a compressive or ischemic etiology present with a blown pupil before motility deficits?
A compressive lesion of CN III is most common caused by what pathology affecting what area of the brain?
An aneurysm of the PCOM or PCA
What pathology is seen here and how is it caused? Is it infectious?
This is called a chalazion. It is caused by obstructed Meibomian glands, or oil glands. It is non-infectious.
An infection behind the orbital septum is referred to by what name?
Orbital cellulitis
What pathololgy is seen here? What symptoms are commonly concurrent?
Orbital cellulitis
Notable findings:
-ptosis
-poor EOM
-compartment syndrome
If the patient is showing signs of optic nerve compromise, an immediate lateral canthotomy/cantholysis is indicated.
Is orbital cellulitis considered an emergency? What is the treatment protocol?
Orbital cellulitis is an ophthalmologic emergency.
Tx:
-CT scan
-IV abx
-admit and close monitoring
Is this orbital cellulitis or preseptal cellulitis?
Correctly identify each type of conjunctivitis pictured here:
Top- Allergic
Middle- Bacterial
Bottom- Viral “Pink eye”
What pathology is seen here? What are characteristics of a history and exam? Are they most often bacterial, viral or other?
This is uveitis. It is most often caused by bacteria.
What pathology is seen here? Does it affect visual acuity, visual fields or both?
This is caused by HSV or Herpes Simplex Virus. It can drastically affect visual acuity, but visual fields and motility should be normal. This is because it is a superficial infection, and primarily affects the cornea.
Herpetic eye infections are painful and can cause photophobia.
What finding is indicated on the fluorescent imaging? What is it pathognomonic of?
Dendritic branching, indicative of herpetic eye infection (can be simplex or zoster)
Should herpetic eye disease be treated with steroids? What is preferred?
Herpetic eye diseases should NOT be treated with steroids. Start oral acyclovir and refer to ophthalmology.
What is a normal intraocular pressure?
20 or less
Which line is the optic cup and which is the disc? What is contained in each space?
Blue circle- Optic disc
Yellow circle- Optic cup
What is Primary Open Angle Glaucoma? What causes it? Is it painful? What are RF? How is it treated?
How are acute high IOP and gradually high IOP differentiated by color and pain perception?
Acute high IOP
-Painful
-Red eye
Gradual chronically high IOP
-Painless
-White eye
What is Primary Angle Closure Glaucoma? How does this mechanism differ from POAG?
What pathology is shown here?
Pupillary block
Note that the anterior chamber is cut off from the posterior, and fluid will build up in the posterior chamber.
What are two universal features of all glaucomas? What type is at risk for acute angle closure crisis? What are treatmetns for POAG vs PACG?
What pathology is seen here?
Albinism
There is a lack of pigment (especially notable in the iris)
Anytime the lens of the eye (crystalline lens) is not clear it is called a what?
Cataract
What pathology is seen here?
Cataracts
What is the leading cause of reversible blindness worldwide? How long does the corective procedure take?
What pathology is seen here?
Macular degeneration
It is a slowly progressive loss of central vision
What is the difference between atrophic or dry-type macular degeneration and wet macular degeneration? How are they treated?
What is metamorphosia?
Distortion of vision
What pathology is seen here?
Diabetic retinopathy
What principle feature leads to this being classified as proliferative diabetic retinopathy?
What is the leading cause of blindness in the middle aged population of the US?
Diabetic retinopathy
What are four visible fundoscopic exam findings characteristic of diabetic retinopathy?
What are the two main types of diabetic retinopathy? How is proliferative diabetic retinopathy treated?
Picture of of laser induced retinal tissue death
What is a Central Retinal Artery Occlusion? How is it treated?
AKA Stroke of the Eye
What is the pathology seen here? How is it differentiated from other similar conditions?
What are the 3 ways the optic nerve can be damaged? Name one common cause of each.
What is Giant Cell Arthritis?
A systemic, inflammatory, granulomatous vasculitis affecting medium and large vessels
What are four symptoms and one signifiant lab finding in Giant Cell Arthritis? What patient population is it most common in?
It is almost always seen in white patients over 50.
In which patients should Giant Cell Arthritis be suspected? What is the gold standard for Dx? What treatment should be initiated if GCA is suspected?
What are three classic elements of optic neuritis? What underlying disease should be suspected?
1) More common in younger ages (20-40’s) but can present in outside range
2) Pain in the eye that is losing vision, with worsening pain on eye movement
3) Colors seem less saturated (especially red)
You should suspect Multiple Sclerosis but remember it can be idiopathic, or due to other inflammatory processes like Sjogren’s or Lupus.
What is another name for Idiopathic Intracranial Hypertension or IIH?
Pseudotumor cerebri
What are 3 classic RF for Pseudotumor cerebri? What are classic signs? How is it diagnosed?
What are common causes of unilateral optic nerve edema vs. bilateral?
What pathology is seen here?
Central Retinal Artery Occlusion
What pathology is seen here?
A cherry red spot. As compared to CRAO, there is no cilioretinal artery and no area of spared retina
What syndrome is most likely if there are palsies of CN III, IV, V1 and VI?
Superior orbital fissure syndrome
What syndrome is most likely if there are multiple cranial nerve palses (any of the following: III, IV, V1, VI) in addition to optic nerve involvement?
Orbital apex syndrome
What syndrome is most likely if there are multiple cranial nerve palses (any of the following: III, IV, V1, VI) in addition to CN V2 involvement?
Cavernous sinus syndrome
What is Internuclear Ophthalmoplegia (INO)?
It manifests as reduced adduction or abducting nystagmus. It is named for the side of the MLF lesion or side of weakened adduction
It is most commonly caused by MS or stroke.
What two pathologies make up One and a Half Syndrome?
Gaze palsy (usually PPRF)
INO (usually MLF lesion)
With what section of the brainstem is horizontal gaze associated?
The pons
What characterizes Dorsal midbrain syndrome i.e. Parinaud syndrome? What is the most common cause?
It involves an up-gaze paralysis, a light-near pupillary dissociation and sometimes a convergence retraction nystagmus.
The most common cause is a pineal tumor pushing on the dorsal midbrain.
It is most common in young men.
What are Saccades?
What are three other names for the Primary Visual Cortex?
Calcarine Cortex
Striate Cortex
V1
Where do the upper vision field and lower vision field projecto to in the primary visual cortex relative to the calcarine sulcus?
Superior vision field projects ventrally to the calcarine sulcus.
Inferior vision field projects dorsally to the calcarine sulcus.
What structure is seen here? What cortex does it identify?
The line of Gennari, which is found in the striate cortex.
Identify the arterial supply for the following components of the visual system:
-Retina
-Parietal optic radiations
-LGN and optic tract
-Calcarine cortex
Where is the pretectum located? What role does it have in vision?
It mediates the pupillary light reflex.
What response is used to maintain fixation on an approaching object? Does it require conscious vision? What are the three elements of this response?
Near Response
A subdural hematoma with uncal herniation would effect principally which part of the brainstem? Explain what symptoms would be observed based on involvement of the following structures:
-CN III
-Midbrain reticular formation
-Cerebral peduncles
-Posterior cerebral artery
What is the gold standard tonometry for measuring intraocular pressure?
Goldman applanation
Name 1 autoimmune and 2 infectious etiologies, 2 drug-induced and 1 vitamin deficiency-induced etiologies for optic neuritis?
Autoimmune
MS
Infectious
Cat Scratch Fever- Bartonella hensleii
Syphilis- Treponema pallidum
Drug-induced
Methanol
Ethanbutol
Vitamin deficiency-induced
Vitamin B12
What are two classic symptoms and two classic exam findings of optic neuritis?
Symptoms
-Decreased vision
-Central red-vision desaturation
Exam findings
-Afferent pupillary defect
-Pale or swollen optic nerve
What finding is notable on this MRI? What diagnosis is it supportive of? (with appropriate clinical history)
Dawson’s Fingers, which is supportive of Multiple Sclerosis
How is MS diagnosed?
Three additional confirmatory measures
1) MRI finding of Dawson’s fingers
2) Lumbar puncture (standard studies)
3) Oligocloncal bands and IgG synthesis in CSF
What is an appropriate acute treatment for an MS flare?
Short courses of high-dose steroids
*i.e. solumedrol 1g IV qd for 3 days
This helps to reduce reactivity of activated T cells, allowing time for the body to remyelinate
What is the prognosis for optic neuritis?
Most will improve without pharmacological treatment BUT the may improve more quickly with steroid treatment
There is a chance of residual defects
What is the purpose of contrast? (i.e. as used in a CT)
To enhance where blood flows, i.e. tumors, infection, inflammation, vascular disease, etc
What is a notable component of CT contrast?
iodine
What is notable about T1 MRI sequence?
Gray matter- gray
White matter- white
What is notable about T2 MRI sequence?
CSF- bright
Edema/tumors- bright
What is notable about FLAIR MRI sequence?
FLAIR or fluid attenuating inversion recovery
CSF- Dark
Edema/tumors- Bright
What is the DWI sequence on MRI especially sensitive for?
It is sensitive to detect stroke
What is the largest safety issue with an MRI?
The magnent is always on, and can affect any metallic devices
In the same vein, cardiac pacemakers are contraindicated
What is the most common primary brain tumor?
Glioblastoma
What are the three general causes of increased ICP? Give examples of each.
1) Increased size of brain tissue
-Malignancy
-Edema
2) Increased vascular pressure
Arterial- HTN, IC hemorrhage, epidural hematoma
Venous- Venous clot, subdural hematoma
3) Increased CSF pressure
-Communicating hydrocephalus
-Non-communicating hydrocephalus
What effect does increased CO2 have on ICP?
Clinical Pearl: Hyperventilation can reduce elevated ICP
Give the normal ranges for the following counts in a sample of CSF.
What are the 5 diagnostic reasons for ordering a spinal tap?
1) Infection
2) Malignancy
3) Subarachnoid hemorrhage
4) CSF drainage and pressure reduction
5) Infusion of medications
What can a spinal tap be used for therapeutically?
To reduce high CSF pressure i.e. IIP or pseudotumor cerebri
When should lumbar punctures be avoided (contraindication)?
1) Raised ICP is suspected
2) Coagulopathy (low platelets or elevated PTT)
3) Area of infection overlying spinal tap site
When must imaging of the brain be obtained prior to spinal tap?
1) Focal findings on neurological exam
2) Mental status changes
3) Papilledema
4) Seizures
5) Impaired immunity
Does Amyotrophic Lateral Sclerosis (ALS) principally affect the UMN or LMN tract?
Both upper and lower motor neurons
What best characterizes the triad of variability of presentation of ALS?
Bulbar onset- involving spastic or flaccid dysarthria
Limb onset
Trunk/respiratory involvement
Despite ALS being a motor disorder there is a high concurrence of fronto-temporal dementia.
What are four classic symptoms and two signs of bulbar involvement (i.e. ALS)?
What is the test of choice to verify is a patient has subclinical denervation from motor neuron disease?
What is collateral renervation? What role does it play in lower motor neuron disease?
Collateral denervation is the process by which neighboring nerves can project extensions to nearby dying (white) or dead (black) nerve cells.
What approximate perctange of patients with ALS have a familial etiology? What mutation is responsible for 20% of known mutations?
10-20% of ALS cases are familial
20% of known ALS mutations are due to a mutation in SOD-1
What is the pathophysiology of ALS?
Early spontaneous death of motor neurons in the brain, brainstem, and spinal cord. It is uniformly progressive in all patients.
What is the average survival from diagnosis of ALS?
30 months
Who is known as the father of neurology?
Jean-Martin Charcot
-He described and diagnosed the first case of ALS in the 1860’s.
He also discovered and treated many more diseases.
Besides ALS What are 6 other notable motor neuron diseases to include on the differential? (Not an exhaustive list)
Myasthenia gravis- Produces fatiguable weakness with preserved sensation
Brainstem lesion- Produces UMN and LMN findings, often seen with a tumor or demyelination. It should include CN findings
Multiple Sclerosis- Produces UMN findings with sensory changes
Subacute combined degeneration- Produces UMN spasticity from CST infolvement, and LMN in legs from peripheral neuropathy
Cervical Spondylosis- Narrowing at level of cervical spinal canal produces UMN findings below lesion, and LMN neuron at level of compression
West Nile Virus- Acute LMN apoptosis resembling polio
Also consider syphilis, sarcoidosis and Tay-Sachs disease.
What diagnostic evaluation should be performed for suspected ALS? What does each study contribute?
EMG studies- to confirm no sensory involvement
MRI-brain and cervical spinal cord- to rule out MS, multifocal ischemia, cervical stenosis or brainstem tumor
Lab testing of B12, RPR titer, RF, and monoclonal gammopathy.
What is a Spurling sign? How does it help to localize a lesion?
A positive Spurling sign would indicate a motor root lesion.
What is the best way to test the C8 myotome?
Resisting wrist extension
What is the best way to test the T1 myotome?
Resisting separation of the 1st and 5th digit
What spinal cord levels are tested by the biceps brachii reflex?
C5
What spinal cord levels are tested by the brachioradialis reflex?
C5 and C6
What three parts of the brachial plexus are generally important to understand for physicians? What are the disease categories for these three areas?
Upepr plexus- Erb’s palsy
Lower plexus- Klumpke’s paralysis
Posterior cord- Posterior cord lesions
What characterizes Erb’s palsy? What levels of the brachial plexus are involved? What is a common cause? What is the physical presentation?
What is Klumpke’s paralysis? What levels of the brachial plexus are involved? What is a common cause of injury? How does it affect sympathetic tone? What is the physical presentation?
What is a posterior cord lesion? What areas of the brachial plexus are involved? What is the classic cause of injury?
What three peripheral nerves of the brachial plexus should every doctor know?
The median nerve, the radial nerve and the ulnar nerve
Of the median, radial, and ulnar nerve, a neuropathy focused on which nerve would have the greatest impact on grip strength?
The median nerve
Classically lesioned at the wrist
What is the classic test of ulnar nerve function?
Finger abduction
it is most easily lesioned at the elbow
Though very uncommon, what can be an important differential not to miss when treating a radial neuropathy?
A bony tumor (as the radial nerve sits in the humeral groove and is usually protected)
What three signs are expected to be found with injuries to specific spinal cord levels of the brachial plexus?
Dermatomal- sensory changes
Myotomal- motor weakness
Reflexes- abnormal reflexes
What is the classic physical sign seen for complete nerve injuries to the following?
-Ulnar nerve
-Radial nerve
-Median neve
Note that these are rarely seen, as complete lesions are far less common than smaller neuroapthies
What movement is best able to test function of the L2 myotome?
What movement is best able to test function of the L3 myotome?
What movement is best able to test function of the L4 myotome?
What movement is best able to test function of the L5 myotome?
What movement is best able to test function of the S1 myotome?
What reflex is best able to test the integrity of the L4 spinal cord level?
What reflex is best able to test the integrity of the S1 spinal cord level?
What areas of sensation (general) are innervated by the femoral nerve? Weakness of the femoral nerve can be seen in what two classic movements? What are two common causes of femoral nerve lesions?
What areas of sensation (general) are innervated by the sciatic nerve? Weakness of the sciatic nerve can be seen in what classic movement? What are two common causes of sciatic nerve lesions?
What areas of sensation (general) are innervated by the peroneal nerve? Weakness of the peroneal nerve can be seen in what two classic movements? What are three common causes of peroneal nerve lesions?
What areas of sensation (general) are innervated by the tibial nerve? Weakness of the tibial nerve can be seen in what two classic movements? What is the most common location of tibial nerve lesions?
What areas of sensation (general) are innervated by the sural nerve? Weakness of the sural nerve can be seen in what classic movement? What is important for physicians to know about the sural nerve?
Define radiculoapthy:
The pinching or compression of a nerve root exiting the spine.
Describe the tempo, clincal findings and associated symptoms of Benign Paroxysmal Positional Vertigo or BPPV:
Describe the tempo, clincal findings and associated symptoms of Vestibular neuronitis:
Describe the tempo, clincal findings and associated symptoms of Meniere disease:
Differentiate the tempo, clincal findings and associated symptoms of Presbycusis versus Vestibular schwannoma:
The Dix-Hallpike maneuver is described here. Give the findings seen in the following:
Peripheral lesions or vestibulopathy
Central lesions
Normal/no pathology
PN- Latency and extinguishing with repeat testing
CL- Immediate sx with do NOT extinguish
How is the Weber test performed? What are the expected results for the following:
Normal hearing
Air conduction hearing loss
Sensorineural hearing loss
The Weber test screens hearing and involves placing a vibrating tuning fork (512 Hz) on the vertex of head/midline frontal bone.
Normal hearing- Sound appreciated bilaterally
ACHL- Sound is louder in affected ear
SNHL- Sound is louder in nonaffected ear
How is the Rinne test performed? What are the expected results for the following:
Normal hearing
Air conduction hearing loss
Sensorineural hearing loss
The Rinne test compares sound wave conduction between air and bone.
Normal hearing-Air conduction should be appreciated longer/better than bone
ACHL- Air conduction is either not appreciated or is for a much shorter time than the contralateral ear (assuming it is normal)
SNHL- Patients should experience shorter appreciation of both air and bone conduction in the affected ear
What is considered a normal ratio comparing the conduction of bone to air in a human ear?
Bone/Air
2/3
What are 5 important items on the differential if a patient has hearing loss?
1) Vestibular schwannoma/acoustic neuroma- note that impingement on nearby CN V and VII can produce facial numbness and weakness as well
2) Otosclerosis
3) Hair cell damage- often from exposure to ototoxic medications (i.e. gentamycin)
4) Tympanic membrane perforation
5) Presbycusis- usually affects higher pitches
What disease classically presents with opthalmoplegia, gait ataxia, and encephalopathy? How is it caused?
Wernicke encephalopathy
It is caused by a deficency in thiamine or vitamin B1
What are the symptoms of thiamine toxcitiy?
There are none known. Excess thiamine is excreted in the urine
What are symptoms of niacin toxicity?
Flushing
N/V
Pruritis
Constipation
What is the most common symptom of pyridoxine toxicity?
Peripheral neuropathies such as a small fiber neuroapthy
How is pyridoxine toxicity diagnosed?
History B6 supplementation + painful distal neuropathy
What is the relationship between Major Depressive Disorder or MDD and Major Depressive Episodes or MDE?
MDD is characterized by one or more MDEs.
How is a Major Depressive Episode diagnosed? (DSM-5 criteria)?
5 or more of the following, including 1 of the first 2:
Depressed Mood
Anhedonia
Change in appetite and/or weight
Sleep disturbance
Psychomotor retardation or agitation
Fatigue
Feelings of worthlessness or inappropriate guilt
Concentration difficulty
Recurrent thoughts of death, suicidal ideation or suicide attempt
What characterizes Major Depressive Disorder with atypical features?
Mood reactivity
Weight gain
Hypersomnia
Leaden paralysis
Rejection sensitivity
What characterizes Major Depressive Disorder with peripartum onset?
MD occuring within the course of pregnancy and in the postpartum period
What characterizes Major Depressive Disorder with seasonal pattern?
MD recurring and remitting around the same time each year
What characterizes Major Depressive Disorder with catatonia?
MD presenting with catatonic symptoms
What characterizes Persistant Depressive Disorder or Dysthymia?
1) Depressed mood for at least 2 years
In children and adolescents it is instead irritable or depressed mood for at least ONE year
2) Plus 2 or more of the following:
Appetite disturbance
Sleep change
Fatigue
Low self-esteem
Poor concentration
Feelings of hopelessness
What is are two hallmarks of Disruptive Mood Dysregulation Disorder? When is onset? How long must symptoms present for, and in which settings?
Hallmarks
-Recurrent temper outbursts approx. 3x/week
-Depressed-irritable mood most of the time most days
Onset must be before age 10. Symptoms must present for over 12 months in 2+ settings.
How is a diagnosis of Premenstrual Dysphoric Disorder made? What stipulations about diagnosis revolve around symptom presentation/resolution and menses?
PMDD is diagnosed based on presentation of 1+ of the following symptoms:
-Mood lability
-Irritability or anger
-Depressed mood or hopelessness
-Anxiety
AND
1+ of the following symptoms must be additionally present, to reach a total of 5 symptoms
-Anhedonia
-Difficulty concentrating
-Lethargy or fatiguability
-Change in appetite
-Sleep changes
-Lack of control
-Physical symptoms associated with menses
Give a short summary of the following disorders:
MDD
PDD
PMDD
Disruptive Mood Dysregulation Disorder or DMDD
What can be considered a sole treatment for mild or (sometimes) moderate depression?
Psychotherapy such as Cognitive Behavioral Therapy
What is the most effective treatment for moderate or severe depression?
Psychotherapy + Medications
What are the 3 C’s of TCA toxicity?
They are fatal in overdoses, notable for causing:
Cardiac complications
Convulsions
Coma
Why are MAOIs often tried last in antidepressant therapy?
The have a high risk for side effects and many drug-drug interactions
For example
MAO degrades tyramine, which normally causes catecholamine release. If a patient consumes tyramine, catecholamine release is unattenuated and can lead to a hypertensive crisis.
What is the FDA Black Box Warning for antidepressants?
Antidepressants carry a 4% risk of suical thinking or behavior, twice the risk of a placebo.
What is Antidepressant Discontinuation Syndrome? What does the acronym FINISH 5HT stand for?
What is Serotonin Syndrome? What does the acronym HARMED stand for?
What is the etiology of Lambert-Eaton Myasthenic Syndrome or LEMS? What is the defining symptom? With what type of malignancy is it associated?
Bilateral UE and LE proximal muscle weakness in the absence of sensory changes would help to localize a lesion to what levels of the nervous system?
The neuromuscular junction or muscle itself.
What are two classic exam findings of LEMS?
1) Proximal muscle weakness that improves with repeated manual motor testing
2) Absence of sensory deficits
What are 6 disorders of the NMJ that a medical student should know?
1) Myasthenia gravis (MG)
2) Lambert-Eaton myasthenic syndrome (LEMS)
3) Botulism
4) Organophosphate poisoning
5) Snake envenomation
6) Chemicals of warfare
How can EMG testing help to differentiate MG from LEMS?
How many cases of LEMS are associated with malignancy?
Over 50% of cases of LEMS are associated with malignancy.
If a diagnosis of LEMS is made, malignancy should be screened.
From most to least common: lung, breast, prostate, stomach, rectum.
How does the initial presentation of LEMS and MG differ?
LEMS: More often effects limb muscles at presentation
MG: Usually affects bulbar muscles at presentation
What is the target of the autoantibodies produced in LEMS?
Pre-synpatic voltage-gated calcium channels
What is the first step in management of a patient with LEMS?
First, evaluate for malignancy (usually pulmonary). If it is found, it should be treated as LEMS is likely paraneoplastic.
Second, begin treatment for LEMS:
-Azathioprine/Imuran- immunosuppression
-IV-Ig
-Plasma exchange
Where do muscular diseases first produce weakness? What are some symptoms that are common in adults vs children? How is sensation affected?
What are the three main types of Muscular Dystrophy? What is the common etiology of these conditions?
Muscular dystrophies result from genetic mutations.
Will muscular dystrophies present with UMN findings, LMN findings, or both?
Name how you could test for muscle disease in the following lab settings:
PE
Bloodwork
Radiology
Histology
Electrodiagnostics
What is the most common presenting symptom of Duchenne muscular dystrophy? By what age do symptoms usually appear?
What is Gower sign?
When a child lying supine is asked to stand up, they do so aytpically, walking their torso up from the floor with their hands.
What is a Trendellenberg sign?
A waddling gait produced by lack of pelvic girdle stabilization. It implicates weak hip abductor muscles.
What are four phenotypes produced in children with Duchenne muscular dystrophy?
-Lordosis resulting from weak hip extensors
-Heel cord shortening producing a classic “tip-toe” walking
-Gastrocneumius pseudohypertrophy
-Scoliosis can progress producing a secondary myelopathy, or spinal cord lesion (this finding appears as children become non-ambulent)
What are potentially expected levels of CK in children with Duchenne muscular dystrophy?
CK as high as 100,000 or 150,000
*Normal is <200 IU/L)
What histological changes would be expected in a patient with DMD?
Name one associated disease feature DMD with the following systems:
Respiratory
Cardiovascular
Neruological
Respiratory/accessory muscle wekaness leading to hypoventilation, somtimes apnea
Dilated cardiomyopathy
Intellectual impairment
What two kinds of testing are typical for confirming a suspected case of DMD?
Genetic testing is the gold-standard, and is 96% sensitive.
What is the purpose of dystrophin?
It is a cytoplasmic protein that combines in a matrix to anchor the intracellular cytoskeleton to the ECM.
It stabilizes the membrane during contraction and relaxation.
Note it is not the ONLY protein to participate in this process.
What are the two main treatments for DMD? What are some common additional measures?
What are the differences in onset, progression, and CK levels in Becker muscular dystrophy versus DMD?
What gene mutations are responsible for both Duchenne muscular dystrophy as well as Becker muscular dystrophy?
Mutations in the Duchenne gene
What is the difference in dystrophin protein function between DMD and BMD?
DMD: Dystrophin protein has no function
BMD: Dystrophin protein has some degree of function
What is the difference in treatment between DMD and BMD?
Becker muscular dystrophy has the same treatments as DMD with the exception of predisone not being used.
What is the most common type of muscle dystrophy?
Myotonic dystrophy
How does Myotonic Dystrophy get its name?
What is the classic presentation of myotonic dystrophy?
Weakness
Atrophy
Myotonia
Cataracts
Cardiac conduction defects
What is arthrogryposis?
A term used to describe a variety of conditions involving multiple joint contractures or stiffness. This can be a symptom of multiple pathologies that present in utero.
How does myotonic dystophy violate the rule of primary muscle diseases?
It presents first with distal muscle weakness, notably with symptoms such as:
weak grip
foot drop
What are important notable associated symptoms of myotonic dystrophy?
Though myotonic dystrophy can often be diagnosed with clinical features alone, what are two forms of testing that can be utilized to confirm diagnosis? What are the expected CK levels?
1) EMG: myotonia
2) Genetic testing: trinucleotide repeat expansion (CTG)
CK levels are typically normal, possibly slightly elevated.
What are expected histology findings in a muscle biopsy in myotonic dystrophy? What is a hallmark finding?
How are the following aspects of myotonic dystrophy treated?
-Heart block (cardiac complication)
-Somnolence
Heart block: Cardiac demand pacemakers
Somnolence: Methylphenidate/Ritalin and caffeine
What is the heritability of myotonic dystrophy?
Autosomal dominant, often with variable penetrance
What is the distribution of weakness in FascioScapuloHumeral muscular dystrophy (FSH-MD)?
Why is FSH-MD sometimes associated with Popeye arms?
The arm is thinner than the forearm, which is atypical in most people.
What are two notable associated symptoms with FSH-MD?
1) Hearing loss
2) Retinopathy
What are the expected lab findings in a patient with FSH-MD regarding CK, and muscle biopsy?
CK: Usually normal but can be elevated 5x (mildy; not like DMD or BMD)
Muscle biopsy: Varied findings, with changes being quite abnormal but usually mild
What is the inheritance of FSH-MD?
Autosomal dominant with sporadic de novo mutations
What treatments are typical for FSH-MD?
What are the 3 main subtypes of inflammatory myopathies?
What is the clinical phenotype of Dermatomyositis?
What is the expected elevation in CK in patients with Dermatomyositis? What hallmark finding on muscle biopsy is characteristic?
What are some associated findings of Dermatomyositis?
What should the next step be after a diagnosis of Dermatomyositis?
LOOK FOR THE CANCER
What is the treatment for Dermatomyositis?
What is the clinical phenotype for Polymyositis?
What are the expected lab abnormalities in Polymyositis?
What are associated symptoms of Polymyositis?
How is Polymyositis diagnosed?
How is Polymyositis treated?
Initially with steroids, then transitioning to steroid-sparing agents. (Just like with Dermatomyositis)
Where does Inclusion Body Myositis produce weakness?
What are the expected CK values for Inclusion Body Myositis? Why is an EMG often performed?
How is Inclusion Body Myositis diagnosed?
CK
EMG
Clinical phenotype
Muscle biopsy
How is Inclusion Body Myositis treated?
No known treatment, but sometimes low dose steroids are given (not alot of supporting research)
What is one significant result from each of the following that can indicate Dermatomyositis?
-Serum muscle enzymes
-Electromyography
-Muscle biopsy
Which of these test findings is diagnostic for Dermatomyositis?
What EKG finding is commonly seen in anorexia nervosa?
Sinus bradycardia
What are 4 risk factors for refeeding syndrome?
1) BMI of under 16
2) Rapid weight loss (generally more than 1lb/week)
3) Lack of food intake for more than 10 days
4) Low-energy diets (low fat, low carb)
Which complication of anorexia nervosa is most likely to be irreversible?
Osteoporosis
Refeeding syndrome is best described by pathophysiology involving depletion of what main electrolyte? What can result from failure to treat it?
Phosphorus
The intracellular stores of phosphorus are depleted due to malnutrition. Refeeding stimulates metabolic activity, causing an extracellular to intraceullar shift.
Failure to treat refeeding syndrome can lead to organ failure, cardiac arrhythmias and death.
What level of the nervous system is most likely given patient symptoms of motor weakness and dysautonomia with normal sensation?
The neuromuscular junction
What is the classical presentation of motor weakness in botulism?
Descending motor weakness (such as arms first, then legs)
What are the classic 5 disorders of the neuromuscular junction?
Myasthenia graivs
Lambert Eaton myasthenic syndrome
Botulism
Tetanus
Snake bite envenomation
What is the common cause of wound botulism?
IM or SUBQ injection of black tar heroin
What two neuromuscular junction disorders present with a small increment in motor response for repetitive nerve stimulation on EMG?
LEMS
Botulism
What are the ABCs of triage?
Airway
Breathing
Circulation
Where are giant pyramidal cells found in the brain?
What structure do the corticobulbar and corticospinal tract neurons traverse through between the giant pyramidal cells and the internal capsule?
Where is the synapse found between Upper motor neurons and Lower motor neurons? In other words, which part of the motor tract is composed of UMNs vs LMNs?
Why does a CNS lesion not always produce an UMN finding?
The corticospinal tract must be lesioned to produce an UMN finding.
On which side of the face will weakness appear if the left side of the corticobulbar tract is lesioned?
There will be right sided facial weakness.
List the 5 main bulbar lesion symptoms, and the 3 main signs. What is pseudo-bulbar affect?
What is the satellite sign? What does it help to manifest?
Regional weakness
What are the 3 components of the motor exam?
1) Strength/power
2) Bulk
3) Tone
Would an UMN or Basal ganglia lesion be best identified with a rigid tone?
UMN: More spastic tone
BG: More rigid tone
Label the following as UMN diseases, LMN diseases, or Both:
-Amyotrophic lateral sclerosis
-Spinal muscular atrophy
-Progressive muscular atrophy
-Primary lateral sclerosis (PLS)
-Poliomyelitis
-West Nile Virus
What is the symptom progression typically seen in Amyotrophic lateral sclerosis (ALS)? How is it diagnosed? How is it inherited, and with what protein is it associated?
Affected phrenic nerve can lead to fatal outcomes due to inability to activate the diaphragm in breathing.
What are characteristics of Spinomuscular atrophy (SMA)? Is it an UMN or LMN disease? What is the heritability?
What characterizes Primary lateral sclerosis (PLS)? Is it an UMN or LMN disease? What is the heritability?
Which two combined tracts are degenerating in Subacute combined degeneration? What are the two common causes? Which 3 labs may be helpful in diagnosis? What is likely to be found on MRI?
What nervous system disorder is caused by the Poliovirus? What are the premonitory symptoms? What two symptoms occur with onset? Which symptom attenuates? How is the poliovirus spread? How is prevented?
What is an example of a polio-like virus? When should these be indicated on the differential?
What is spondylosis? What is Cervical spondylosis most often associated with? Does it present with UMN or LMN symptoms? What other associated diagnoses or symptoms should warrant cervical spondylosis on a differential?
What disease should be first on the differential if UMN and LMN findings are present? What are other disorders on the differential?
ALS
Brown-Sequard syndrome
Cervical stenosis
Note the following ALS:
-Sensation is conspicuously normal
-Pseudobulbar affect
-Sighing and hiccoughing
How much of ALS is familial?
About 20% of cases (SOD-1 mutation)
What are the two broad types of neuropathies?
Axonal
Demyelinating or mixed
In which broad type of neuroapthy are the longest nerves affected first (in a symmetric distribution)? Why are longer nerves affected more?
Axonal type neuropathy
Do sensory or motor symptoms present first in Axonal type neuropathies? What is the difference between positive and negative sensory symptoms?
Do axonal type or demyelinating neuropathies present in a stocking-glove distribution?
Axonal neuropathies
What are four common examination findings in axonal type neuropathies?
Anhydrosis
Distal hair loss
Nail changes
High arches
This is in addition to distal sensory/motor loss.
What characterizes demyelinating neuropathies? How do they differ from axonal neuropathies?
Axonal neuropathies lose sensory first, then motor starting distally and progressing to more proximal segments
What are the two main types of primary demyelinating neuropathies?
How quickly do symptoms progress in Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP)? Are symptoms ascending or descending?
What is often the first symptom of AIDP? What are common sensory and motor symptoms?
Does AIDP present with sensory or motor dysfunction (or both)? Are atrophy or fasciculations seen? What reflexes are expected? What is an abnormal CSF finding?
Are the following effects of AIDP reversible?
-Primary monophasic demyelination
-Secondary axonal damage
What are the expected differences in outcomes between mild and severe AIDP? What is the preferred treatment? What does recovery depend on?
What is the unique triad that presents with the Miller Fischer variant of GBS or AIDP? What antibody is used to confirm this diagnosis?
What characterizes Chronic Inflammatory Demylinating Polyradiculoneuropathy? How much longer is the disease progression than in AIDP?
How is CIDP treated? How is this treatment different than AIDP?
What symptoms are expected at onset of **Charcot-Marie Tooth disorder*? What are four signs visible on exam?
What two steps should be taken in diagnosis of suspected CMT disorder? How is it treated?
Pathologies involving what body structure should be associated with the following mononeuropathies?
-Median nerve
-Ulnar nerve
-Radial nerve
-Peroneal-fibular nerve
-Tibial nerve
-Lateral femoral cutaneous nerve
Do mononeuropathies present with sensory or motor findings?
Oftentimes both, but in mild cases there may be no focal motor findings.
How can a mononeuropathy like Carpal tunnel syndrome be managed?
What characterizes mononeuritis multiplex disease?
What is the pathophysiology of mononeuritis multiplex? How is it diagnosed? How is it treated?
Do axonal or demyelinating peripheral neuropathies present with a stocking-glove distribution? Which presents with a distal and proximal presentation?
What are the two most significant causes of CIDP?
Idioapthic and infectious (i.e. HIV)
What is the most common cause of chronic primary axonal neuropathy world-wide?
What effects can be seen on an EMG in axon loss? What about with demyelination?
Explain the EMG associations for both Axonal lesions and Demyelinating lesions for the following:
-Amplitude
-Conduction velocity
-Late responses (F waves)
-Distal latency
What acronym is used to create the differential diagnosis for peripheral neuropathy?
What mnemonic describes the auditory pathway through the brainstem?
CNS lesions are VERY unlikely to produce hearing loss, and not frequently tested.
What are the 3 possible results from the Weber test and what does each result indicate?
Is a bone conduction or air conduction of sound better? What is the ratio of how long a patient should perceive conduction of sound through one medium to the other?
Air conduction is better than bone.
Bone conduction should last about 2/3 as long as air.
Is a CNS lesion or a Peripheral lesion of the nervous system more likely to cause hearing loss?
Which part of the vestibular apparatus of the inner ear is associated with angular motion? Which is associated with linear motion?
What high levels of electrolytes characterize endolymph? Which characterize perilymph?
T/F: Vestibular symptoms can result from CNS lesions only
False, they can also arise from PNS lesions. These involve secondary motor neurons from the midbrain to the caudal pons.
Describe what occurs within the semicircular canals during head motion toward the right. Reference the following:
-Endolymph movement
-Axis of hair cells
-Ampulla
-Firing rate of afferent CN VIII fibers
What is the difference between physiological nystagmus and pathological nystagmus?
What test can be used to simulate head turning in order to test the VOR (vestibulo-ocular reflex)?
Caloric stimulation
For which phase (slow or fast) is nystagmus named?
It is named for the direction of the fast phase.
What are the 3 outcomes of a caloric stimulation test? Which direction is the fast/slow phase of each outcome? What is signified by each outcome? What is the meaning of the acronym “COWS”?
Which part of the nervous system controls the slow phase of nystagmus? Which part of the nervous system controls the “fast phase”?
Slow phase: Peripheral control
Fast phase: Cortical control
Does the acronym “COWS” used in VOR testing describe normal or abnormal findings?
COWS described normal test results, and COWS will not be seen in pathological results, i.e. comatose patients.
Cortical function is lost in comatose patients
What is the cause of BPPV? Whatis the tempo of the vertigo induced in BPPV? What provokes it? How is it diagnosed?
BPPV is caused by a benign otolith crystal that rolls around in the inner ear.
What is the tempo of vestibular disruption in vestibular neuronitis? What is it caused by? Patients tend to fall to which side of their body?
What is the tempo of development of vestibular schwannoma? What are clinical signs? What area of the brainstem is affected, and which CN can be impacted? What disease processes may vestibular schwannoma be associated with? What type of tumor is common to see on MRI?
In what patient popular is presbycusis most often seen? What are 7 significant associated factors to development of presbycusis? What type of frequency hearing loss is seen on audiometry?
Age is generally the most important risk factor.
What best describes the onset and progression of Meniere’s disease? What type of hearing loss is seen on audiometry? What is the clinical tetrad seen?
It can be a very debilitating disease to live with.
When a patient presents with low frequency hearing loss what should be high on the differential?
Meniere’s disease
What are the biggest RF for a brainstem stroke? How quick is the onset? What clinical findings of long tract involvement are seen? What are three important syndromes to check for?
Internuclear Ophthalmoparesis or INO is caused by a lesion to what tract? Which eye defines the side of the lesion?
Downbeat nystagmus would be indicative of a lesion affecting what part of the brain?
What is the biggest cause of lateralized nystagmus?
Vestibular neuronitis
What type of antibiotics have the highest risk for ototoxicity?
Aminoglycosides
-Gentimycin
-Tobramycin
-Streptomycin
What visual field defect would most likely associated with see saw nystagmus?
Bitemporal contralateral hemianopsia
These are both causes by lesions/impingements at the OPTIC CHIASM.
What anatomic structure is stimulated by a cochlear implant?
The **hair cells*
What is cyto-albuminemic dissociation? What is it characteristic of?
High protein content in the CSF without an elevation of WBC count.
It is characteristic of AIDP or GBS.
What is tested in a nerve conduction study versus a needle electromyography?
NCS: Looks at nerves
nEMG: Looks at muscles
Both are part of an EMG, which is a 2 part study.
What are three pathogens that GBS has been associated with?
Epstein-Barr Virus
HIV
Campylobacter jejuni
Fill in the blank: Always think of _____ in an areflexic patient.
Guillan-Barre Syndrome
What desribes generaly amyotrophy?
A typically monomelic, exceedingly painful neuropathy with a limited time course.
What characterizes Diabetic amyotrophy? How can it be treated?
It is often treated with GABA-ergic medications, like gabapentin or pregabalin. These help to address the neuropathic pain, which does not respond well to NSAIDs, steroids, or narcotics (i.e. opioids).
Compare Diabetic amyotrophy and Diabetic polyneuropathy in the following areas:
Onset
Symmetry
Site
Weakness
Pain
Course
What part of the brain may be less active in people with anorexia nervosa? What is effect is hypothesized on interoceptive processing?
What is the main electrolyte affected by refeeding syndrome? What other two electrolytes also play a role?
Descrieb the multi-modal treatment approach used to treat Anorexia Nervosa?
In summary:
-medical management
-Nutrition rehab
-Individua/group/family therapy
Medical management typically includes monitoring for refeeding syndrome, and monitoring ECG for prolonged QT etc
How does the DSM-5 define binge eating?
What is the DSM-5 criteria for Bulimia?
What are three classic signs of Bulimia seen on physical exam? (there are many more less specific findings)
1) Dental enamel erosion
2) Sialadenosis (salivary gland enlargement)
3) Russell’s sign (knucle abrasions)
What drug class is FDA approved to treat Bulimia? Which medication is preferred? How long is treatment needed to reduce chance of relapse? What are 3 non-FDA approved drugs for treating Bulimia, and how do they work?
Are other treatments besides drugs recommended for Bulimia?
Absolutely.
CBT is preferred, but Family based treatment (FBT) and other types of therapy can be helpful.
What is Binge Eating disorder?
Binging without purging in addition to subjective feelings os loss of control, and guilt associated with eating
What are treatment options for Binge Eating Disorder?
What are three types of Avoidant-Restrictive Food Intake Disorder?
What is Pica? What nutritional deficiency is it associated with? What is Rumination Disorder?
Asymmetric facial anatomy and midface hypoplasia with a noted tilt of the head in a patient may be indicative of what CN pathology?
4th nerve palsy, specifically a chronic problem.
Chronic 4th nerve palsy is often congenital.
What items should be on the differential for a 6th cranial nerve palsy?
Where does the right medial longitudinal fasciculus begin in the brainstem, and where does it terminate?
Note that an individual muscle weakness in the eye, such as medial rectus, would likely be a problem with the PPRF or MLF.
The above condition would be called an internuclear ophthalmoplegia.
Why would a restrictive or fibrotic right lateral rectus cause left gaze diplopia?
What acronym is used to screen for depression symptoms?
What acronym is used to characterize the symptoms of Persistant Depressive Disorder?
What acronym is used for the differential diagnosis of spinal nerve root, plexus or peripheral nerve lesions?
