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Flashcards in Neurology Deck (143):

Diabetic CN III Neuropathy

- Ischemic deficit (not compression) affecting somatic fibers only.
- CN III has both somatic and parasympathetic fibers which have different blood supplies.

Somatic fibers: innervates superior, inferior, and medial rectus, inferior oblique, and levator palpebrae

Parasympathetic fibers: innervates the sphincter of the iris and ciliary muscle -----> fixed, dilated pupil and loss of accomodation

Symptoms: "down and out" gaze, ptosis (unopposed action of the lateral rectus and superior oblique)
- Intact pupillary response and accommodation.

- Compression neuropathy affects all functions.


Todd's palsy

preceded by a focal motor seizure


Carotid artery thrombosis

- Most commonly affects the middle cerebral a. ---> contralateral hemiparesis and hemianesthesia


Lacunar stroke - pure motor hemiparesis

- Lacunar infarction in the posterior limb of the internal capsule

Presentation: unilateral motor deficit (face, arm, and to a lesser extent leg), mild dysarthria
- No loss of sensory, visual, or higher cortical function


Lacunar stroke - pure sensory stroke

- Stroke in the ventroposterolateral nucleus of the thalamus.

Presentation: unilateral numbness, parasthesias and hemisensory deficit involving the face, arm, trunk, and leg


Lacunar stroke - ataxic hemiparesis

Lacunar infarction of the anterior limb of the internal capsule

Presentation: weakness that is more prominent in the lower extremity, along with ipsilateral arm and leg incoordination


Lacunar stroke - dysarthria-clumsy hand syndrome

Lacunar stroke at the basis of the pons

Presentation: hand weakness, mild motor aphasia
- NO sensory abnormalities


Migraine treatment and prophylaxis

Antiemetics: prochlorperazine, chlorpromazine, and metaclopramide

- NSAIDS or triptans if started early into the headache.

Prophylaxis: amitriptyline, propranolol


Basal ganglia hemorrhage

Symptoms: contralateral hemiparesis and hemisensory loss, homonomyous hemianopsia, gaze palsy


Cerebellar hemorrhage

- Usually NO hemiparesis
- Facial weakness, ataxia, nystagmus, occipital headache, and neck stiffness


Thalamic hemorrhage

Symptoms: contralateral hemiparesis and hemisensory loss, non-reactive miotic pupils, upgaze palsy, eyes deviate towards hemiparesis


Cerebral lobe hemorrhage

Symptoms: Contralateral hemiparesis (frontal lobe), contralateral hemisensory loss (parietal lobe), homonymous hemianopsia (occipital lobe), eyes deviate away from hemiparesis, high incidence of seizures


Pons hemorrhage

Symptoms: deep coma and total paralysis within minutes, pinpoint reactive pupils


Essential tremor

- Bilateral action tremor of the hands, usually without leg involvment
- Possible isolated head tremor without dystonia(involuntary repetitive movement)
- Relieved with alcohol
- no other neurologic defecits.

Treatment: propranolol; second-line: primidone and topiramate


Parkinson's disease tremor

- resting tremor (4-6Hz) that decreases with voluntary movement
- Usually involves legs and hands
- facial involvement less common
- May progress to involve other areas of the body

Tetrad: resting tremor, rigidity, postural instability, and bradykinesia

- Tremor worsens when performing mental tasks and disappears with movement
- Due to progressive loss of dopaminergic neurons in the basal ganglia.


Cerebellar tremor

- Usually associated with ataxia, dysmetria (lack of accuracy during voluntary movement), or gait disorder
- Tremor increases steadily as hand reaches its target

-Can see postural, action, or intention tremors



- Low amplitude (10-12Hz), not visible under normal conditions
- acute onset with sympathetic activity (drugs, hyperthyroidism, caffeine)
- Usually worse with movement and can involve the face and extremities


Brain death

- Absent cortical and brainstem function
- Spinal cord may still be functioning, so DTR can still be present.
- HR becomes invariant due to loss of vagal control.


Status epilepticus

- single seizure lasting longer than 30 mins
- Brains that have seized for >5 minutes are at risk of permanent injury due to excitatory cytotoxicity ----> cortical laminar necrosis


Neurofibromatosis type 2

- mutation in tumor suppressor gene on chromosome 22
- Subcutaneous neurofibromas, cafe-au-lait spots, deafness due to acoustic neuromas

severe variant - Wishart - framshift or nonsense mutations
milder variant - Gardner - missense or splice-site mutation


Primary sclerosing cholangitis

Clinical features: fatigue, pruritis
- 90% of pts have underlying IBS, mainly ulcerative colitis

Labs: Aminotransferases


Ascited Fluid Characteristics

Neutrophils: 250 peritonitis (secondary or spontaneous)

Total protein: >or= 2.5 (high-protein ascites) - CHF, constrictive pericarditis, peritoneal carcinomatosis, TB, Budd-Chiari syndrome, fungal

or=1.1 (indicates portal hypertension) - cardiac ascites, cirrhosis, Budd-Chiari syndrome


Blood supply of the brain

Common carotids ---> internal carotids ---> opthalmic artery and then anterior and middle cerebral arteries
Subclavian arteries ---> vertebral a. ---> posterior inferior cerebellar a., then anterior spinal a., then basilar a. ---> anterior inferior cerebellar a., then pontine a. ---> superior cerebellar a., then posterior cerebral a. which connect to circle of willis vis posterior communicating a.


Middle cerebral artery supply

lateral surface of the frontal, parietal, and upper temporal lobes, genu and posterior limb of internal capsule, majority of the basal ganglia, proximal parts of the visual radiations as they emerge from the lateral geniculate nucleus of the thalamus and course in Meyer's loop


Anterior cerebral artery supply

medial surface of the frontal and parietal lobes (motor and sensory areas for pelvis and lower limbs), superior inch of the frontal and parietal lobes, anterior 4/5 of corpus callosum, anterior limb of internal capsule


Posterior cerebral artery supply

inferior temporal lobe and occipital pole


Anterior cerebral artery occlusion deficits

spastic paresis and anesthesia of contralateral lower limb

Note: if bilateral, urinary incontinence can occur
- if anterior corpus callosum is involved, a transcortical apraxia of the left limbs may occur (disconnection of left hemisphere's (language dominant) from motor cortex of right hemisphere)



Inability to perform particular purposive actions


Middle cerebral artery occlusion deficits

- spastic paresis of the contralateral lower face and upper limb and anesthesia of the contralateral face and upper limb
- Aphasia can occur when left MCA is affected and left-sided neglect can occur when right MCA is affected
- Contralateral superior quadrantanopsia w/ occlusion of the branches supplying Meyer's loop.


Vertebral a. course

through transverse processes of upper 6 cervical vertebrae; enters posterior fossa after passing through foramen magnum


Anterior spinal a. supply

ventrolateral 2/3 of cervical spinal cord and ventromedial part of medulla


PICA supply

cerebellum and dorsolateral medulla


Labyrinthine a. supply

branch of the basilar a. that follows the course of CN VIII; supplies the inner ear


AICA supply

part of pons, anterior and inferior cerebellum


Superior cerebellar a. supply

rostral pons and superior cerebellum


Pontine branches supply

pons via paramedian and circumferential branches


PCA supply



Midbrain CNs

III and IV


Upper pons CNs



Lower pons CNs



Upper medulla CNs



Medial medullary syndrome

Occlusion of the vertebral a. or anterior spinal a.
Localizing sign
- CN XII - ipsilateral paralysis of half the tongue w/ atrophy (tongue deviates towards the lesion)
Affected nerve tracts
- medial lemniscus - contralateral deficit of proprioception and touch, pressure, and vibratory sensation in limbs and body
- pyramid (corticospinal tract) - contralateral spastic hemiparesis of both limbs


Lateral medullary syndrome (Wallenberg)

Occlusion of PICA
Localizing CNs
- vestibular or cochlear parts of CN VIII - may produce nystagmus, vertigo, N/V (w/ vestibular nystagmus, the fast component will be away from the side of the lesion)
*Lesions of the cochlear nucleus or auditory nerve produce an ipsilateral sensorineural hearing loss.
- CN IX - diminished or absent gag reflex
-CN X - dysphagia or hoarseness, palate will droop on affected side and the uvula will deviate away from the side of the lesion
- spinal nucleus and tract of CN V - loss of just pain and temperature on ipsilateral side of half the face (touch and corneal blink reflex will be intact)
Affected nerve tracts
- spinothalamic tracts - pain and temperature deficit in contralateral limbs and body
- descending hypothalamic fibers - ipsilateral Horner syndrome
* If solitary nucleus is affected, taste sensations may be altered


Medial Pontine Syndrome

occlusion of the paramedian branches of the basilar a.
- CN VI - internal strabismus of the ipsilateral eye (diplopia on lateral gaze to the affected side)
- Corticospinal tract - contralateral spastic hemiparesis of both limbs
- Medial lemniscus may be affected - contralateral deficit of proprioception and touch pressure and vibratory sensations in the limbs and body.
- CN VII may be affected if it extends laterally

- Long tract signs are the same as in medial medullary syndrome but the CN signs localize the lesion


Upper motor neuron

Due to spinal cord lesions


Myesthenia gravis

- AutoAbs against acetylcholine receptor on post-synaptic membrane
Signs and symptoms:
- extraocular muscle weakness (ptosis and diplopia), bulbar muscle weakness (jaw fatigue with chewing and dysarthria with talking).
- symmetrical proximal weakness of the extremities (upper more than lower), neck (flexors and/or extensors), and bulbar muscles (dysarthria/dysphagia)

- Normal reflexes, muscles bulk/tone, sensory function and autonomic function.

Diagnosis: CPK is normal differentiating it from primary muscle problem
- Associated with the presence of a thymoma ---> always order CT of the chest bc thymoma can sometimes be invasive.
- Sometimes associated with thyroid disease ----> ultrasound can be helpful.


Amyotrophic lateral sclerosis

- Affects distal muscles more
- sensory abnormalities and ocular deficits are usually absent



- Affect both motor and sensory function of single nerve


Multiple sclerosis

- Autoimmune CNS demylenating disease
- Upper motor neuron signs
- Oligoclonal IgG bands in the CSF with normal opening pressure, protein, and cell count.

Treatment of acute exacerbations:
- IV steroids in symptoms are severe.
- Mild sensory symptoms do not require steroids.
- Steroids do not prevent future attacks or prevent progression.

Reduce frequency of acute exacerbations:
- interferon, plasmapheresis, cyclophosphamide, IV immunoglobulin, glatiramer acetate



- in diabetes mellitus
- vitamin B12 deficiency
- Guillain-Barre syndrome
- Chronic inflammatory demyelinating polyneuropathy

Signs and symptoms: reduced or absent reflexes, parathesias, motor and sensory symptoms of both upper and lower extremities, but not usually bulbar symptoms


Exertional heat stroke

Risk factors: obesity, certain medications (anticholinergics, antihistamines, phenothiazines, tricyclics)

Clinical manifestations: core temperature >104F AND CNS dysfunction (altered mental status, seizure, confusion, irritability)
- Additional organ or tissue damage (renal/hepatic failure, DIC, ARDS, coagulopathic bleeding)

Other possible signs and symptoms: dry or sweaty skin, hypotension, tachycardia, hyperventilation, diarrhea, cramps, ataxia
Management: rapid cooling: ice water immersion preferred, fluids, electrolyte correction, no role for antipyretic therapy

- Evaporative cooling is preferred in nonexertional heat stroke (elderly patients with comorbidities).


Heat exhaustion

>104 F, but no CNS dysfunction


Multiple system atrophy (Shy-drager syndrome)

Degenerative disease

- Parkonsonism
- autonomic dysfunction
- widespread neurological signs (cerbellar, pryamidal, LMN)

- Accompanied by bulbar dysfunction and laryngal stridor.

Treatment: anti-Parkinsonism drugs are ineffective; treated w/ intavascular volume expansion w/ fludrocortisone, salt supplementation, alpha adrenergic agonists, and constrictive garments on the lower body


Idiopathic orthostatic hypotension

- Degeneration of postganglionic sympathetic neurons
- Solely autonomic dysfunction.


Familial dysautonomia (Riley-Day syndrome)

Autosomal recessive condition found in Ashkenazi Jews
- autonomic dysfunction with severe orthostatic hypotension.


Chemotherapy-induced peripheral neuropathy

-symmetrical parasthesias of the fingers and toes, early loss of ankle jerk reflexes, loss of pain and temperature sensation, occasional motor neuropathy

- Commonly due to platinum-based meds (cisplatin), taxanes (paclitaxel), and vinca alkaloids (vincristine)



Perception of a normally innocuous stimulus as painful


Benign essential tremor

- action tremor


Alzheimer's disease

Pathophysiology: selective loss of cholinergic neurons

Early findings:
- anterograde memory loss
- visuospatial deficits
- language difficulties
- cognitive impairment with progressive decline

Late findings:
- neuropsychiatric
- dyspraxia (difficulty performing learned motor tasks)
- lack of insight regarding deficits
- noncognitive neurologic deficits (pyramidal and extra-pyramidal motor, myoclonus, and seizures)
- urinary incontinence

- two or more areas of cognitive deficits
- progressively worsening memory and other cognitive function
- no disturbance of consciousness
- onset after 60
- absence of other systemic or neurologic disorder causing progressive cognitive deficits

- first-line: cholinesterase inhibitors (donepizil, galantamine, rivastigmine).
- Moderate to severe: memantine


Stroke due to endocarditis

- commonly occurs in the MCA
- Antibiotics reduce the risk of septic emboli in patients with endocarditis.


Guillain-Barre syndrome

associated with Campylobacter jejuni, Herpes viruses, Mycoplasma, and H. influenza as well as certain vaccines (influenza)

Cause: antibodies directed against Schwann cells

Clinical features: symmetric ascending muscle weakness with absent or depressed DTRs
- bulbar symptoms (dysarthria and dysphagia)
-Facial nerve palsy
- Albumino-cytologic dissociation (elevated protein and normal cell count)

Diagnosis: nerve conduction studies which show demyelination

Treatment: IVIG or plasmapharesis
Miller-Fischer variant: begins with cranial nerve deficits (uncommon)


Malignant hyperthermia

-affects genetically susceptible patients who have anesthesia with halothane or succinylcholine



- sleep loss
- emotions
- alcohol withdrawal
- flashing light

Clinical clues:
- aura
- can occur with sleeping/sitting position
- head movements
- tongue biting
- rapid, strong pulses

- delayed return to baseline
- usually sleepy and confused afterward (postictal state)


Syncope (vasovagal)

- upright position
- emotions
- heat
- crowded places

Clinical cues:
- symptoms of presyncope (lightheadedness)
- unlikely to occur with sleeping/sitting position
- rarely, several clonic jerks can occur with prolonged cerebral hypoperfusion as well as urinary incontinence
- pallor and diaphoresis
- weak, slow pulses

- immediate spontaneous return



- weakness
- fatigue
- muscle cramps
- flaccid paralysis
- hyporeflexia
- tetany
- rhabdomyolysis
- arrhythmias

ECG findings:
- broad flat T waves
- U waves
-ST depression
- premature ventricular beats

Can lead to:
- torsades de pointes
- V fib
- A fib


Deep brain stimulation

Used to treat Parkinson's disease, dystopia, or essential tremors; blocks faulty nerve signals that cause tremors, rigidity, etc.




Used to treat bipolar I disorder and epilepsy (partial-onset seizures, generalized seizures of Lennox-Gastaut syndrome, and primary generalized tonic-clonic seizures)

Risk: serious skin rash - greater risk in pediatric pts

Metabolic inhibitor of OCT2

Mechanism: triazine derivative which inhibits the release of glutamate and inhibits voltage-sensitive Na channels, stabilizing neuronal membranes
- weak inhibitor of 5-HT3 receptor
- inhibits dihydrofolate reductase


Lennox-Gastaut syndrome

Severe seizures in childhood
-presentation usually before 8 yrs (typically 3-5)
-may evolve from other epilepsy syndromes

Defining criteria:
- multiple seizure types, particularly tonic and atypical absence seizures, but also atomic and myoclonic seizures. Periods of nonconvulsive status epilepticus occur in most cases at some stage.
- slow (less than 2.5 Hertz) spike wave pattern on the interictal EEG that is generalized and usually has highest amplitude in the frontal region
- mental retardation with or without other neurologic abnormalities.

- no drug is highly effective
- kerogenic diet and VNS




Use: myoclonic seizures (juvenile myoclonic epilepsy), partial-onset seizures, and primary generalized tonic-clonic seizures

Off-label: status epilepticus, in setting of subarachnoid hemorrhage to prevent seizures

Side-effects: high BP, behavioral problems,

Mechanism: unknown



acetyl-cholinesterase inhibitor used to treat Alzheimer's



- Key factor in differentiating between this and Alzheimers disease is the awareness of problems.


Relapsing-remitting MS treatment

Interferon-beta slows the progression


Progressive MS treatment

Methotrexate, cyclosporine, mitoxantrone


Trigeminal neuralgia

Treatment of choice: carbamazepine (second-line treatment: gabapentin and lamotrigine)
- In cases resistent to medical therapy, treat with surgery to relieve pressure.



- Inflammation of the carotids and the vagus

Diagnosis: clinical, but sometimes requiring MRI


Burning mouth syndrome

- caused by a virus

Symptoms and signs: reddened mucosa with significant pain
- aggravated by dryness

Treatment: supportive care


Huntington's chorea CT findings

- atrophy of the caudate nucleus seen as enlargement of the lateral ventricles.


Atrophy of the lenticular nucleus

- seen in Wilson's disease


Pick's disease

Ct findings: atrophy of the fronto-temporal cortex



- inability to recognize sensations and hence identify things.


Creutzfeldt-Jakob disease

Probable diagnosis:
- Rapidly progressive dementia
- 2 out of 4 clinical features:
- myoclonus
- akinetic mutism
- cerebellar or visual disturbance
- pyramidal/extrapyramidal dysfunction (hypokinesia)
- Periodic sharp wave complexes on EEG (bi or tri-phasic)
- Positive 14-3-3 CSF assay

Definitive diagnosis includes above features in combination with
- brain biopsy findings (gold standard)
- demonstrated PRNP gene mutations

- Lack of inflammatory response
Other symptoms: insomnia, apathy, behavioral changes, and impaired vision


Normal pressure hydrocephalus

Additional symptoms: slow, broad-based, shuffling gait
- Fecal incontinence may be seen in severe disease.
- Memory loss w/o focal neurologic deficits

Diagnosis: Enlarged ventricles on CT or MRI along with normal opening pressure on LP

Treatment: sequential CSF removal (serial large volume LPs)
- Ventriculoperitoneal shunt may be placed if the patient responds to LP.


Herpes encephalitis

Cause: most commonly HSV-1

Symptoms and signs: acute onset (


Dominant optic atrophy

Kjer's optic atrophy

Synopsis: affects the optic nerves, causing reduced visual acuity and blindness beginning in childhood

Clinical presentation:
2 forms:
1. Isolated bilateral optic neuropathy (non-syndromic)
2. Extra-ocular signs (syndromic)

Pathophysiology: optic nerve fiber loss due to mitochondrial dysfunction

Treatment: none


Orthostatic tremor

-Postural tremor thought to be a variant of essential tremor.
- Occurs in the legs upon standing and is relieved by sitting down
- High frequency (14-18 Hz) without other clinical symptoms.


Large fiber peripheral neuropathy

- Can present with action or postural tremors due to impaired proprioceptive input.


Metastatic brain cancer

Lung > breast > unknown primary > melanoma > colon

Primarily solitary brain mets: breast, colon, renal cell carcinoma

Multiple brain mets: lung cancer, malignant melanoma

Rare brain mets: prostate cancer, esophageal, oropharyngeal, hepatocellular carcinoma, non-melanoma skin cancers


Intracerebral hemorrhage

Characteristics: acute focal neurologic deficits that gradually worsen over time ---> elevated intracranial pressure

Risk factor: hypertension


Central cord syndrome

Cause: hyperextension injuries frequently in elderly patients with pre-existing degenerative changes in the C-spine

Mechanism: selective damage to the central portion of the anterior spinal cord, specifically the central corticospinal tracts and the decussating fibers of the lateral spinothalamic tract

Signs and symptoms: weakness more pronounced in the upper extremities
- May have loss of pain and temperature sensation in the arms due to damage to the spinothalamic tract


Anterior (ventral) cord syndrome

- Bilateral spastic motor paresis distal to the lesion

Cause: occlusion of the anterior spinal artery or burst fracture of the vertebra


Brown-Sequard syndrome

- Hemisection of the cord (most often due to a penetrating injury).

- Ipsilateral: weakness, spasticity, loss of vibration sense and proprioception
- Contralateral: loss of pain and temperature sensation.


Posterior (dorsal) cord syndrome

- Bilateral loss of vibratory and proprioceptive sensation , often with weakness, parasthesias, and urinary incontinence or retention.

Causes: most commonly MS and vertebral artery dissection


Primidone side effects

- Is converted to phenylethylmalonamide and phenobarbital

- Can participate acute intermittent porphyria: abdominal pain, neurologic and psychiatric abnormalities.

diagnosis: test urine for porphobilinogen


Parkinson's disease

Treatment: amantadine (dopamine agonist)



Inflammatory cells in the anterior chamber of the eye


Anterior spinal artery occlusion

- Bilateral signs commonly seen at mid-thoracic levels with sparing of the dorsal columns.

- Affects the corticospinal tracts and spinothalamic tracts ---> spastic paresis and loss of pain and temperature.


Miller-Fischer test

- Assessment of gait and cognitive function both before and after a large-volume lumbar puncture to assess for normal pressure hydrocephalus


Meniere's disease

classic triad: episodes of dizziness lasting 30 minutes to several hours, unilateral tinnitus, and fluctuating hearing loss

-Thought to be due to an increase in the volume of endolymph ---> permanent damage of the vestibular and cochlear appartuses

Treatment: symptomatic with meclizine and scopalimine



- Descending motor weakness


Allergic conjunctivitis

Treatment: frequent attacks - antihistamine and mast cell stabilizing properties (ketotifen - H1 antagonist , mast cell stabilizer and eosinophil inhibitor)


Tenting at the junction of the optic nerve and the globe

Expanding of the retrobulbar space causing the globe to stretch the optic nerve


Vitamin A deficiency

night blindness, xerosis and anemia


Retinitis pigmentosa

progressive peripheral vision loss and night vision loss leading to central vision loss

Physical exam: mid-peripheral retinal hyperpigmentation and optic nerve waxy pallor


Pseudotumor cerebri

1) MRI to r/o other intracranial processes
2) lumbar puncture to establish diagnosis
3) acetazolamide to treat


Acute angle-closure glaucoma

Treatment: cholinergics, epinephrine, alpha-adrenergics,
emergency treatment: carbonic anhydrase inhibitors, mannitol, and topical beta-blockers


Viral conjunctivitis

Symptoms: clear discharge, preauricular adenopathy

- No treatment necessary, usually resolves in 5-7 days


Progressive multifocal leukoencephalopathy

Symptoms: diplopia, gait ataxia, altered mental status

Diagnosis: CT scan of the brain showing diffuse lesions of the white matter

Treatment: initiate HAART therapy


Central retinal artery occlusion

- Sudden, painless unilateral loss of vision

Opthalmoscopy: pale retina and cherry red spot at the fovea


Epidural abscess

- Most commonly due to S. aureus, but also gram negative rods, Streptococci, and coagulase negative Staph.


Periventricular leukomalacia

Leads to cerebral palsy, specifically spastic diplegia (more commonly of the lower extremities)


Athetoid cerebral palsy

due to damage of the basal ganglia

Causes: kernicterus, asphyxia, or genetic/metabolic diseases

Symptoms: hypotonia with later rigidity and dystonic movements


Cotard's syndrome

Mental disorder in which patients complain of having lost their possessions, status, strength, and even inner organs


Dementia pugilistica

post-traumatic dementia occurring after blunt-force trauma to the head

Symptoms: decreased attention, slowed information processing, increased distractibility, and problems with memory. Behavioral changes include impulsivity, depression, aggression, and personality changes


beta-2 transferrin test

test to confirm leakage of CSF
- specific for CSF fluid, but can also be found in vitreous humor and the serum of newborns.

Signs of CSF leak: orthostatic headache and tinnitus, neck pain or stiffness, nausea and vomiting, anorexia, vertigo, dizziness, and change in vision

- Defects in anterior cranial fossa ---> leakage through the nose; defects in middle cranial fossa ---> leakage through the ears

Complications: meningitis (most commonly with Strep pneumonae - most common cause of meningitis in adults)


Reflex sympathetic dystrophy

- Pain and swelling of one extremity (commonly a hand), associated with skin atrophy.
- Thought to be due to vasomotor instability.


Sebaceous cell carcinoma

- Often mistaken for recurrent chalazion
- Diagnosed via biopsy


Polycythemia vera

Treatment: phlebotomy along with hydroxyurea
- Add in aspirin unless contraindicated.
- Interferon A is used in patients who have refractory pruritis or don't respond to other treatment.



- Used to manage patients with thrombocytosis who are refractory to other forms of treatment.

Risks: heart failure and orthostatic hypotension in elderly with CV disease



- Used to treat CLL and non-hodgkin's lymphoma


Cluster headache

- May be triggered by alcohol
- Thought to be involve the hypothalamic nuclei that regulate circadian rhythm.
- Pain and vasomotor symptoms probably mediated by seritogenic pathways


Noncommunicating syringomyelia

- Associated with trauma



fluid-filled cavity in the medulla

Symptoms: dysphagia, nystagmus, phyrangeal and palatal weakness, asymmetric weakness and atrophy of the tongue, and loss of pain and temperature in the trigeminal nerve distribution.


Non-proliferative diabetic retinopathy

small-vessel disease in the eye
- Occlusion, dilation and increased permeability of the small vessels in the eye ---> microaneurysms
- Serous fluids and lipoproteins leak ---> hard exudates
Small vessel ischemia ---> microinfarctions of the nerve fiber layer ---> cotton wool spots


Macular edema treatment

lasar photocoagulation


Proliferative diabetic retinopathy

- Prolonged ischemia and neovascularization
Treatment: lasar photocoagulation to prevent blindness



- Followed closely until functional visual impairment results
- Surgery removes the cataract, leaving the posterior lens capsule. if the capsule opacifies, it can be removed with laser (ultrasonic fragmentation of the lens nucleus).



Bladder-selective cholinergic agent that helps increase bladder contractility



Anticholinergic used to treat urine loss


Age-related macular exudative degeneration

Progression: age-related maculopathy ('drussen') ---> atrophic (dry) or exudative (wet) degeneration ---> no therapy has been proven to treat dry form, but lasar photocoagulation of the subretinal neovascular membranes may delay wet form


CMV retinitis

Symptoms: scotoma, visual field deficits, floaters or flashing lights

Management: perform a fundoscopic exam to r/o retinal detachment ---> treat with IV foscarnet or gancyclovir


Acute dystonia

- Includes torticollis
- Can be due to drugs used to treat Parkinson's disease (dopamine receptor blockade)

Treatment: dopamine agonst (carbidopa/levadopa), anticholinergic/antihistamine (diphenydramine, benztropine, trihexphenidyl), muscle relaxant or benzos
- Focal dystonias can be trated with botox


Toxic labrynthitis

Vertigo caused by alcohol or medications (commonly aminoglycosides)


Pronator drift

Sign of upper motor neuron problem - supination is weaker than pronation


Mononeuritis multiplex

Painful, asymmetric, asynchronous sensory and motor peripheral neuropathy involving damage to > or = to 2 nerves

-Seen in patients with systemic vasculitides



- Commonly seen in hepatitis B and C

Deposition of antibody-antigen complexes in small and medium sized arteries

Symptoms: palpable purpura, arthralgias, peripheral neuropathy, and hypocomplementemia


corticosteroid-induced myopathy

-Lower extremity weakness and proximal muscle atrophy

Diagnosis: normal muscle enzymes and EMG results

Treatment: taper the steroids and wait for improvement (3-4 weeks)


Type I spinal motor atrophy (Werdnig-Hoffman disease)

Degenerative disease of motor neurons that begins in fetal life and progresses during infancy
- Progressive denervation of muscles with following atrophy ; no DTRs with fasciculations of the tongue

- Death occurs in early infancy to 2 years old

Diagnosis: muscle biopsy showing perineural denervation, or genetic tests



serotonin agonist that is used to treat migraines


Hypoxic-ischemic encephalopathy

- most common cause of neonatal seizures

Treatment: benzos


Tuberous sclerosis

Symptoms: hypopigmented ash-leaf lesions (more visible under UV light), infantile spasms and seizures ---> mental retardation

Cause: seizures are thought to be caused by excess CRH which causes excess excitability

Diagnosis: EEG showing hypsarrhythmia (high voltage, asynchronous chaotic slow wave activity)

Treatment: ACTH which suppresses CRH


Wernicke's encephalopathy

Cause: thiamine deficiency

Classic triad:
1. encephalopathy w/ disorientation and indifference
2. oculomotor dysfunction (nystagmus, lateral rectus plasy and conjugate gaze palsies)
3. Gait ataxia due to combined polyneuropathy, cerebellar involvement, and vestibular paresis

Treatment: give magnesium, thiamine and glucose
- magnesium is needed for thiamine transport into neurons
- give thiamine before glucose because glucose will use up pyruvate dehydrogenase for which thiamine is a cofactor, making the problem worse


Delerium tremens

Treatment: benzodiazipines and haloperidol (for agitation)


Carotid artery dissection signs

Horner's syndrome: miosis, anhydrosis, and ptosis