amaurosis fugax is a marker of what disease?
what is usually seen on physical exam?
carotid artery disease
How do you differentiate between traumatic lumbar puncture and subarachnoid hemorrhage?
traumatic lumbar puncture = absent
SAH = present (due to hemoglobin breakdown)
acoustic neuromas are derived from what kind of cells?
schwann cells (myelinization of peripheral nervous system axons)
patient w/ history of NHL presents w/ pain that wraps around the abdomen along with weakness/difficulty walking and paresthesias in the lower extremities
what should you get next? (2)
consider epidural spinal cord compression; which will ultimately lead to bladder/bowel dysfunction
high dose corticosteroids (to reduce edema around tumor tissue) + MRI spine (confirm + plan definiitve therapy)
elderly p/w forgetfulness interferering w/ ADLs and unsteady gait
what would her labs typically show?
B12 deficiency (causes subacute combined degeneration - affects dorsal spinal colum and lateral corticospinal tract)
unlikely alzheimers dementia since motor ∆s are late manifestation
increased indirect bilirubin, elevated LDH, low haptoglobin (erythroid cells do not mature normally and subsequently die in the bone marrow)
territories affecting the:
posterior communicating artery vs posterior inferior cerebellar artery
posterior communicating artery (PCA) - CN III palsy (ptosis and anisocoria), diplopia
posterior inferior cerebellar artery (PICA) - ataxia and bulbar dysfunction
How is lewy body dementia diagnosed?
what features would suggest lewy body dementia over other forms of dementia?
need 2 of 3:
- cognitive fluctuations
- visual hallucinations
- parkinsonism (bradykinesia, rigidity, gait abnormalities)
differs from other dementia:
- prominent fluctuation of cognitive symptoms
- vivid dreams
- neuroleptics (i.e. haloperidol) and dopamine agonist hypersensitivity (i.e. worsening parkinsonism, confusion, autonomc dysfunction, worsening visual hallucinations)
patient p/w with disordered gait, slowed thought process/speech, chronic cognitive decline, and abnormal findings on mental status exam.
labs indicate macrocytic anemia, hyponatremia
what 3 things should you screen for initially?
hypothyroidism (can cause hyponatremia, macrocytosis, slowed thought speech/process)
vitamin B12 deficiency
CT vs MRI head (if the above three are ruled out)
acute vs preventative treatment for cluster headaches
acute: 100% oxygen via mask
preventative: verapamil (ADR: heart block, bradycardia)
rapidly progressive weakness of the lower extremities following an URI, accompanied by sensory loss and urinary retention is characteristic of:
how does this differ from guillain-barre syndrome?
transverse myelitis - inflammation that extends the entire width of the spinal cord, resulting in damage to nerve fibers and subsequent decreased electrical conductivity in the CNS
60% idiopathic, 40% associated with autoimmune disorders such as MS, neuromyelitis optica, SLE, Sjogren’s syndrome and sarcoidosis among other
diagnosis: MRI of spine
treatment: 3-5 days of high dose steroids
Guillain-barre syndrome - also presents w/ flaccid paralysis and hyporeflexia after history of URI, BUT sensory level and bladder/bowel dysfunction after URI makes transverse myelitis a more likely diagnosis
progressive ascending flaccid paralysis and areflexia after recent URI or GI infection
What bugs mediate this phenomenon?
Guillain-Barre Syndrome - acute inflammatory demyelinating ascending polyneuropathy that results in bilateral, symmetric weakness and/or flaccid paralysis progresses rapidly to involve the upper extremities, cranial nerves, and eventually the muscles involved in respiration
Hx of URI vs GI infection 2/2 to campylobacter, CMV, EBV, or HSV infection
Most of spontaneous remission, but for those who have severe/progressive GBS, give plasmapheresis and/or IVIG
triad of normal pressure hydrocephalus
gait disturbance (wide based, magnetic "feet stuck to the floor") followed by impaired cognition and urinary inciontinence
undergo lumbar drainage of CSF. If there is a drastic change in gait speed, stride length, verbal memory, and visual spatial attention before/after removal of 30-50cc CSF, would benefit from definitive treatment with VP shunt placement.
narcolepsy: modafinil (stimulant, primarily a dopamine reuptake inhibitor), scheduled naps, good sleep hygiene
cataplexy: venlafaxine (SNRI), SSRI, or TCA
diagnostic test in a patient presenting w/ monocular vision loss accompanied by eye pain that worsens w/ eye movement as well as distal sensory loss
these patients often experience painful muscle spasms. treatment?
consider multiple sclerosis exacerbation (optic neuritis + transverse myelitis)
get MRI of the brain/spine - should see ovoid peri-ventricular WM lesions
Lumbar puncture - should see oligoclonal bands and elevated IgG index performed in aytpical cases to confirm the diagnosis; not required for diagnosis
acute treatment: IV steroids (oral steroids associated w/ increased risk of recurrent optic neuritis)
maintenance treatment: ß interferon, glatiramer acetate (disease modifying drugs)
muscle spasms: baclofen
late-life depression (occring after age 65) is a significant risk factor for the development of ... in the years that follow?
dementia (vascular or Alzheimer)
major features of PIck's disease
speech abnormalities (logorrhea, echolalia, aphasia, mutism)
impaired executive functioning (initiation, goal setting, planning)
hyper-oral behavior (licking lips, etc)
symmetric atrophy of frontal/temporal lobes
pathology: neuronal loss, neuronal swelling w/ pick bodies (cystoplasmic inclusions)
what differentiates between Wernicke's Encephalopathy and Wernickse-Korsakoff Syndrome?
Wernicke's Encephalopathy - ophthalmoplegia (paralysis of muscles within the eye), horizontal nystagmus, and cerebellar ataxia
Wernicke-Korsakoff - addition of memory loss and confabulation
myasthenia gravis is a disease of ...
there is an association between myasthenia gravis and...
neuromuscular junction - autoantibodies against the ACh receptor.
thymoma (tumor of epithelial cells)
vertigo triggered by certain provocative positions
benign paroxysmal positional vertigo
tx: canalith repositioning procedure
initial treatment for parkinson disease symptoms
dopamine agonists (pramipexole, bromocriptine)
levodopa is reserved for later use, as it may hasten the destruction of substantia nigra cells and worsen symptoms long-term
patient w/ a drinking problem presents with confusion, tremors, and ataxia. Which of these should you give first?
FIRST - give thiamine, as Wernicek's encephalopathy is due to thiamine deficiency.
then glucose (if you give glucose before thiamine, it can preciptate korsakoff's syndrome, brain MRI will show abnormal enhancement of mammillary bodies)
T/F patients who experience febrile seizures have a higher risk of recurrence.
they're also at a slight increase risk for subsequent development of epilepsy
patient w/ large pituitary mass w/ partial field defect, mild erectile impotence, and low FSH/LH
treat w/ dopaminergic receptor agonist (bromocriptine and cabergoline) - even large prolactinomas will shrink
physical exam findings
predominant cause of death
AD vs de novo mutation of TSC1/2 gene
- derm: hypopigmented/ash leaf spots, angiofibromas of malar region, shagreen patches
- neuro: CNS lesions (cortical tubers/hamartoma), epilepsy, cognitive disability/behavioral problems
- cardio: rhabdomyomas
- renal: angiomyolipomas
diagnosis: cutaneous exam, funduscopy, brain MRI, EEG (if abnml, give anti-epileptic therapies), CTAP (to evaluate for angiomyolipomas)
- if diagnosis is uncertain, then genetic testing can be done, but it is not done as part of the initial evaluation
cause of death: epilepsy/uncontrollable seizures
patient on phenytoin develops horizontal nystagmus and blood levels indicate phenytoin level of 20 (normal is 10-20mcg/mL). What should you do?
patient has phenytoin toxicity, as the earliest sign is the presence of nystagmus on far lateral gaze.
reduce dose, but do not stop it completely (to prevent seizure relapse)
patient found unconscious in bed, AFVSS, unrespnosive to verbal and tactile stimuli. Irrigation of the R ear w/ COLD water causes a transient conjugate slow deviation of the gaze to the right, followed by saccadic correction to the midline.
oculovestibular testing is NORMAL (transient conjugate slow deviation of gaze to the side of the stimuli (brainstem mediated) followed by saccadic correction to the midline (cortical correction) is normal.
transection of hypoglossal nerve can cause tongue deviation..
to the side of the injury (weakness on the side of the injury cannot overcome the forces from the muscles of the stronger side)
Patient presents w/ inability to raise eyebrow or close the eye, drooping of the mouth corner, and disappearance of the nasolabila fold.
Would would be suggestive of an intracranial lesion (warranting brain imaging to evaluate for ischemia or tumors)?
Bells Palsy (idiopathic neuropathy of CN VII)
serum ELISA is indicated only if patient has a travel history to an endemic area, erythema migrans, or bilateral facial palsy.
forehead muscle sparing (i.e. preservation of forehead and brow movements) would warrant brain imaging
BP goals for patient w/ acute ischemic stroke s/p tPa
BP goals for patient w/ acute ischemic stroke who did not receive tPa
acute ischemic stroke s/p tPa ≤ 185/105 but ≥ 140/90 (maintains adequate perfusion of ischemic pneumbra but avoids hemorrhagic transformation)
acute ischemic stroke who did not receive tPa ≤ 220/120
sudden onset of severe (occipital) headache
diagnosis / diagnostic tests?
SAH - commonly due to ruptured sacculary (berry) aneurysm, WHOML, N/V, focal neurological deficits
diagnostic tests: non-con CT, lumbar puncture to exclude SAH definitively in patients w/ suspected SAH and negative non-con CT (would show elevated opening pressure, xanthochromia), cerebral angiography (to identify bleeding source)
50F p/w 6 mo history of periodic involuntary closure of R eye that is provoked by bright light or cigarette smoke.
diagnosis and treatment?
dx: blepharospasm (form of focal dystonia)
tx: botox injections
dominant parietal lobe lesions
non-dominant parietal lobe lesions
what are the typical presentations of each?
Dominant parietal lobe lesions (usually LEFT) = speech, language, difficulty w/ performing simple math, inability to name things/fingers, impaired writing, inability to tell L vs R side of body
Non-dominant parietal lobe lesions (usually right) = construction apraxia (difficulty w/ drawing lines), dressing apraxia (struggles with wearing clothes), confusion
dominant temporal lobe lesions
non-dominant temporal lobe lesions
what are the typical presentations of each?
Dominant temporal lobe lesions (usually LEFT) = visual disorder (homonymous upper quadrantanopia), Wernicke's
Non-dominant temporal lobe lesions (usually right) = visual disorders (homonymous upper quadrantanopia), impaired perception of complex sounds (auditory agnosia)
Argyll Robertson pupils
normal pupillary constriction with accomodation but not with light
Ocular symptoms of Argyll-Robinson Pupil, take the first letter of each word and read it forwards/backwards .
Forward: ARP - Accommodation Reflex Present.
Backwards: PRA – Pupillary Reflex Absent.
symptoms of late neurosyphilis
- degeneration of posterior spinal colums -> impaired vibration/proprioception, sensory ataxia, instability druing Romberg test
- degeneration of nerve roots -> diminished pain/temperature sensation, areflexia, lancing pain (brief shooting/burning pain)
argyl robertson pupils
- normal pupillary constriction w/ accomodation, but absent w/ light
- ARP - Accommodation Reflex Present
- PRA - Pupillary Reflex Absent
the cremasteric reflex corresponds to which level of the spinal cord?
what is the hungry bone syndrome?
caused by sudden withdrawal of parathyroid hormone in patients w/ severe hyperparathyroidism (i.e. after parathyroidectomy), resulting in in in an increased influx of calcium from the circulation into the bone. Calcium levels nadir between 2-4 days post-op
patient undergoing opioid withdrawl
opioid (methadone, buprenorphine) or non-opioid (clonidine)
prefer methadone over buprenorphine due to worse withdrawals from buprenorphine
prefer methadone over clonidine if patient is already on a methadone regimen
prefer clonidine over metahdone to reduce level of autonomic arousal and discomfort if patient is non-compliant w/ methadone program
21M p/w progressive difficulty w/ ambulation x1 day and paresthesias in lower limbs followed by sense of fatigue and weakness in lower extremities and arms
Symptoms developed during camping/hiking. Diagnosis? Treatment?
neuro-toxin secreting tick - symptoms develop 5-6 days after a female tick attaches to the patient.
typical presentation: progressive ascending paralysis that occurs over hours-days; AFEBRILE (i.e. if the patient has a history of fever or prodromal illness, then this diagnosis is unlikely)
treatment: remove the tick!!
when is window in which tPA should be used?
< 4 hours
65M w/ new severe onset L sided HA w/ ipsilateral miosis and ptosis
consider Horner syndrome 2/2 carotid artery dissection
- classically presents w/ ptosis, miosis, and anhidrosis, but not anhidrosis is NOT always present because the sweat nerve fibers travel along the external carotid artery.
- symptoms result from the disruption of sympathetic nerves that travel along the carotid artery to innervate the face/eye
- get CT angiography of H&N, if negative but carotid dissection is still suspected, get MRA or cathether angiograph (gold standard)
Treatment: anti-thrombotic therapies
Potential complication: stroke
Wallenberg Syndrome is due to occlusion of which artery?
posterior inferior cerebella artery OR vertebral artery
EEG shows bilateral polyspike and slow discharge
diagnosis: juvenile myoclonic epilepsy (JME) - starts w/ myoclonic jerks in the upper extremities within the first HOUR of waking. Generalized tonic-clonic seizures occur later.
diagnositic test: EEG
treatment: valproic acid
What imaging study should you get if a child has suspected cerebral palsy (commonly presents w/ upgoing Babinski reflex and hyperreflexia, premature birth, gross motor + cognitive delay)?
MRI brain - identify etiology and for prognostic purposes
major ADR of carbamazepine
neutropenia/bone marrow suppression
elderly folks are also at risk for SIADH