Notes 1b Flashcards
Chronic optic neuritis
- Features: persistent visual loss, color desaturation, persistent APD
- will eventually lead to optic atrophy with shrunken and pale disc
Benedikt’s Syndrome
midbrain stroke in ventral mesencephalic tegmentum
- ipsilateral third nerve palsy with contralateral involuntary movements such as tremor and choreoathetosis
Claude’s Syndrome
midbrain stroke in midbrain tegmentum (more dorsal than Benedikt)
- ipsilateral CN III palsy and contralateral ataxia and tremor
- As compared to Benedikt;s, they have more ataxia bit no involuntary choreoathetotic movements
Weber Syndrome
midbrain stroke with
- ipsilateral CN III pasy with contralateral hemiplegia
SPARCL trial
studied benefit of atorva 80 in reducing overall incidence of stroke and CV events
Regions involved in ASPECTs score
Score less than __ is bad?
4 deep structures (caudate, IC, lentiform nucleus, insular region)
and 6 cortical regions
Score less than 7 assoc with increased dependence and death
indications for revascularizing extracranial ICA
70-99% = should be revascularized
50-69% + symptomatic (stroke, TIA, visual sx all count) = revascularized
<50% = medical therapy alone
Moyamoya syndrome
Most commonly presents in children
presents with ICH, headaches, seizures, movement disorders, cognitive loss
on Angio: bilateral stenosis of carotids, MCA, ACA with extensive collateral circulation at the base of the brain appearing like a “puff of smoke” (on the R)
Dejerine Roussy Syndrome
thalamic pain syndrome
Anterior choroidal arteries arise from? Posterior?
ICA
PCA
Vertebral artery segments
- The V1 segment extends from the subclavian artery to the transverse foramen of C5-C6.
- The V2 segment runs within the transverse foramina of the cervical vertebra from C5-C6 to C2.
- The V3 segment extends from the transverse foramen of C2 and turns posterolaterally around the arch of C1, between the atlas and the occiput. This segment is extracranial.
- The V4 segment begins where the vertebral artery enters the dura at the foramen magnum and joins the contralateral vertebral artery to form the basilar artery —> gives off PICA and anterior spinal artery
In patients with stroke or TIA caused by ICAD, what is recommended
ASA 325 daily
If within 20 days, can use plavix 75mg for 90 days in addition to ASA
Know the venous drainage of the skull including the weird ones like ophthalmic, galen, trolard, labbe
Vein of Trolard/Labbe
- The vein of Trolard is a large anastomotic vein that connects the Sylvian vein to the superior sagittal sinus
- The vein of Labbe is a large vein traveling over the temporal lobe convexity connecting the Sylvian vein to the transverse sinus.
CADASIL: defect and characteristic finding
NOTCH3 on chromosome 19
characteristic finding: blood vessel with a thick wall containing basophilic granular material
Origins of the R/L common carotids and R/L verts
- Right common carotid artery arises from the innominate artery that originates from the aortic arch.
- right vertebral artery originates from the right subclavian artery, which arises from the innominate artery
- left common carotid artery originates directly from the aortic arch (A small percentage of the population have what is called a “bovine aortic arch,” in which the left common carotid has the same origin with the innominate artery, and in some cases the left common carotid will originate from the innominate artery)
- left vertebral artery arises from the left subclavian artery which originates from the aortic arch
Most frequent locations for intracranial aneurysms are
ACOM (30%), PCOM (25%)
carotid cavernous fistula
tear in the cavernous segment of the ICA allowing AV shunting to the cavernous sinus, therefore inc pressure in the sinus with drainage to the superior ophthalmic vein and impaired drainage in the eye
causes ophthalmoplegia, chemises, proptosis, inc IOP, retinal ischemia and vision loss.
Treated with endovascular embolization.
RCVS
more common in men/women
sx?
risk factors
imaging shows?
tx
women
- headaches with or without other neurologic sx, with vasoconstriction of cerebral arteries that resolved spontaneously within 12 weeks
- May develop focal neurologic sx and seizures (transient)
- May be complicated by IPH, SAH, strokes (permanent)
- Associated with PRES
- Risk factors: vasoactive drugs including amphetamines, cocaine, cold medicines with decongestants, triptans, ergot alkaloid derivatives, and other adrenergic and serotonergic drugs. Patients also may report triggers such as strenuous activity, sexual activity, Valsalva, and/or stressful or emotional situations.
- Vessel imaging will show “beading” pattern
- tx: vasodilators such as calcium channel blockers and Mg sulfate
CREST Study
CEA vs stenting of the carotids
stenting: lower rates of MI, inc risk of periop stroke
stenting recommended in patients <70
CEA recommended in patients >70
also reasonable to stent patients that are more high risk surgical candidates
Know the CSF flow
Foramen of Monro connects
lateral and third vent
Cerebral aqueduct connects
3rd and 4th vent
roof of 4th vent is made by? floor?
cerebellum
pons and medulla
CSF leaves the ventricular system through the (2)
lateral foramen of Luschka
Midline foramen of Magendie
CSF is reabsorbed at the
arachnoid granulations
BUZZWORDS: ipsilateral 3rd nerve palsy and contralateral hemiplegia
Weber Syndrome (midbrain lesion)
BUZZWORDS: ipsilateral 3rd nerve palsy and contralateral involuntary movement
Benedikt Syndrome
lesion in ventral portion of the mesencephalic tegmentum
BUZZWORDS: ipsilateral 3rd nerve and contralateral ataxia and tremor
Claude’s Syndrome
lesion in the distal portion of the mesencephalic tegmentum
BUZZWORDS: ipsilateral 7th nerve palsy with contralateral hemiplegia
Millard Gubler Syndrome
lesion in the pons
BUZZWORDS: Limited upward gaze, convergence retraction nystagmus, light-near dissociation, lid retraction, skew deviation of the eyes
Parinaud Syndrome
lesion affecting the quadrigeminal plate
BUZZWORDS: Quadriplegia, inability to speak, limited horizontal gaze, preserved consciousness, vertical gaze and blinking
Locked in Syndrome
BUZZWORDS: Contralateral hemibody sensory loss with subsequent development of pain, allodynia, paresthesia. Results from a thalamic lesion
Dejerine-Roussy Syndrome
BUZZWORDS: finger agnosia, right-left disorientation, agraphia, acalculia
Gerstmann Syndrome
BUZZWORDS: Normal variant with vascular supply to both medial thalami
Artery of percheron
BUZZWORDS: Deep branch of ACA that supplies anterior limb of IC, inferior head of the caudate, anterior globus pallidus
Recurrent artery of Heubner
BUZZWORDS: caused by chronic HTN, associated with the pathogenesis of lacunar strokes
liphyalinosis
BUZZWORDS: Infarct in the posterior circulation causing behavioral abnormalities, altered LOC, abnormal ocular motion
Tip of the basilar syndrome
BUZZWORDS: Dilated thin-walled vessels, with no smooth muscle or elastic fibers, and no intervening brain parenchyma. Popcorn appearance on MRI
Cavernous malformation
BUZZWORDS: thin walled venous structure with normal intervening brain tissue
venous angioma
BUZZWORDS: abnormally dilated capillaries, normal intervening brain tissue.
Capillary telangiectasia
BUZZWORDS: nidus, with arteries and veins communicating without an intervening normal capillary bed in between
AVM
BUZZWORDS: assoc with Charcot Bouchard Aneurysms
Hypertensive ICH
BUZZWORDS: Congo Red positive, apple-green birefringence with polarized light
Cerebral Amyloid Angiopathy
Types of edema (3)
Interstitial, vasogenic, cytotoxic
Interstitial edema: mechanism and seen in?
Seen in acute hydrocephalus, CSF is forced by hydrostatic pressure to move from the ventricles to the interstitium of the brain parenchyma
Vasogenic edema: mechanism and seen in
extracellular accumulation of fluid 2/2 BBB disruption → extravasation of fluid from intravascular space.
Tumors, PRES
Cytotoxic edema: mechanism and seen in?
intracellular accumulation of fluid (hypoxia-ischemia) that leads to a lack of energy to the cells, leading to depletion of ATP and failure of Na/K ATPase, causing alteration in the selective permeability of the cellular membrane
Strokes, anoxic injury
Evidence for hypothermic therapy?
32-34C for V-fib
Evidence is limited in non-VF rhythms, including PEA or asystole
Complications of hypothermic therapy?
- coagulopathy
- arrhythmias
- electrolytes abnormalities
- risk of infections.
Uncal herniation:
What is it
CN most commonly affected?
Features?
mass effect on ipsilateral midbrain
CN3
- Mass effect causes compression of parasympathetic fibers = mydriasis
- Contralateral hemiparesis
- unconscious (disturbance in ascending arousal system)
Weird way that uncal herniations can cause ipsilateral hemiparesis?
pressure can lead to displacement of the midbrain against the contralateral Kernohan’s notch, resulting in compression of the contralateral corticospinal tract = ipsilateral hemiparesis.
Risk of hemorrhage and infection for intraventricular catheters?
6
22
Hyperventilation to lower ICP therapy typically lasts for? risk?
10-20 hours
Can cause rebound increase in ICP
Normal ICP?
5-15
Interventions to reduce ICP?
- Hyperventilation (lasts for 10-20 hrs)
- Osmotic agents (mannitol: given in boluses of 0.5 to 1.5g/kg)
- Hypertonic solutions
- Steroids
- CSF drainage
- Decompression
- Barbiturate coma (in refractory cases, reduced cerebral metabolic activity)
- Pharmacological paralysis
- Hypothermia
Complication of mannitol (2)?
- hypotension/ hypovolemia (causes diuresis, serum osmolarity should be checked at regular intervals, should be not higher than 320)
- depletion of K, MG and phosphorus
Side effects of propofol
- hypotension
- respiratory depression
- hypertriglyceridemia
- infections
- propofol infusion syndrome
Propofol infusion syndrome
- lethal complication, seen in high doses for long period of time and manifests with
- hypotension
- bradycardia
- lactic acidosis
- hyperlipidemia
- rhabdomyolysis.
Side effects of barbituate coma
- hypotension
- myocardial depression
- hyperlipidemia
- hypothermia
Vasospasm from SAH can occur between what days? when is the peak?
3-15 days
6-8 days
Diffuse axonal injury: mechanism
seen in?
macroscopic findings?
microscopic findings?
disruption of intracerebal axons and is caused by effect of angular forces and shear injury, but not from direct contusion or penetrating trauma
seen in severe head injuries such as MVCs where brain is subject to rotational or stretching forces.
Macro: small hemorrhages in the corpus callosum, superior cerebellar peduncle, deep nuclei, hemispheric white matter
Micro: evidence of swollen “bulb-like” and disconnected axons throughout the brain.
In basal skull fractures, what should be avoided? What should be started
NG tubes
Also should start ppx antibiotics since there is potential external access to the CSF
Apneustic breathing
respiratory pause at full inspiration and occurs from bilateral pontine strokes (Pontine respiratory group in the pons is responsible for cessation of inspiration)
Cheyne Stokes breathing?
periodic breathing in which hyperventilation alternates with apnea and depth of breathing increases and decreases gradually → forebrain impairment in the setting of an intact brainstem
Ataxic breathing?
irregular pattern (gasping respiration) seen with lesions damaging the respiratory rhythm generator in the upper medulla.
Antidote for dabigatran (pradaxa)?
ibarucizimab (Praxbind)
Antidote for apixaban and rivaroxaban?
Andexanet alfa (Andexxa)
Critical illness myopathy?
common cause of failure for patients to wean off the vent
primary myopathy with loss of thick myosin filaments and varying degrees of necrosis.
Somatosensory evoked potentials with median nerve stimulation showing bilaterally absent N20 responses at days 1 and 3 accurately predict poor outcome post cardiac arrest
just know
Apnea test is performed how?
- patient should be pre-oxygenated for 10min with an FiO2 of 100%.
- A baseline ABG should be obtained with a pCO2 between 35-45
- Patient is then disconnected from the ventilator but should receive ventilation at a rate of 6L/min
- Patient is then observed for 10min for any chest or abdominal rise suggesting an inspiratory attempt
- After 10min, ABG is obtained, if pCO2 > 60 then the test is positive and patient can be turned brain dead
- To perform apnea test, patient should not be hypotensive or hyper/hypo thermic
Other ways besides apnea testing to confirm brain death?
EEG showing no activity >30 mins
Transcranial dopplers showing no flow signal
Angiogram showing no flow in circle of willis
Decorticate rigidity cause and mechanism?
hemispheric dysfunction or a lesion above the red nuclei
disinhibition of the red nuclei with facilitation of the rubrospinal tracts (involved in flexor tone in UE)
Decerebrate rigidity cause and mechanism?
- lesion in the brainstem or below the superior colliculi and the red nuclei but above the vestibular nuclei
vestibular nuclei are intact → enhancing the extensor tone without the influence from the red nuclei
Lesion below the vestibular nucleus?
Will knock out red-flexor and vestibular-extensor connection, usually assoc with flaccid limbs
Formula for CPP
CPP = MAP-ICP
Malignant hyperthermia
Mechanism
Cause
presents with?
tx?
- Autosomal dominant disorder
- There is an excessive release of calcium from the sarcoplasmic reticulum in skeletal muscles in response to halogenated inhaled anesthetic and depolarizing muscle relaxants (succinylcholine)
- Associated with mutation in ryanodine receptor gene and patient with central core disease (myopathy resulting from mutation in the ryanodine receptor gene)
- Initially presents with rise in the end tidal partial pressure of CO2 during anesthesia, muscle rigidity, hyperthermia, altered consciousness and autonomic instability
- Rhabdomyolysis occurs, leading to renal failure
- Dantrolene should be administered early on
NMS vs Serotonin Syndrome
NMS: febrile, muscle rigidity, AMS, autonomic instability
SS: AMS, hyperthermia, muscle rigidity, autonomic hyperactivity, hyperkineses, clonus
Terson’s Syndrome
intraocular hemorrhage secondary to SAH/SDH. Caused by rapid increase in ICP leading to ocular bleed.
Assoc with worse prognosis
Foster-Kennedy Syndrome
Tumor in optic nerve or frontal lobe causes contralateral papilledema (due to inc ICP and atrophy of unilateral optic nerve), can also cause anosmia
rhinorrrhea lacrimation, sinus pressure, nasal congestion, and conjunctival injection frequently coexist with migraine because of?
CN 5 cross activation of the parasympathetics by stimulation of the superior salivatory nucleus of the facial nerve.
migraine criteria?
5 HAs, each lasting 4-72 hours
with 2/4 of: Unilateral, pulsatile, severe intensity, aggravated by routine activity
and also: nausea OR vomiting/photo + phonophobia
Migraine with brainstem aura criteria
Migraine criteria + at least 2 attacks with a fully reversible aura consisting of sensory, visual, speech, language sx and at least 2 of the following:
- Dec LOC
- Diplopia
- Dysarthria
- Tinnitus
- Hyperacusis
- Vertigo
- Ataxia
Chronic migraine criteria?
Migraine criteria for >15/mo for more than 3 months.
Types of TACs?
- cluster headache
- paroxysmal hemicrania
- hemicrania continua
- short-lasting unilateral neuralgiform headache attacks
- SUNCT: short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing
- SUNA: short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms
Difference between retinal migraine and migraine w aura
retinal migraine presents with monocular vision disturbance
Tension HA criteria
10 HAs, each lasting between 30 mins and 7 days.
2/4 of the following: bilateral location, pressing/tighthening (nonpulsating) quality, mild or moderate pain intensity, it should not be aggravated by routine physical activity.
- Neither nausea or vomiting is present
- Only one of either photophobia or photophobia can be present
Pathophysiology of headaches
- Activation of central generator (cortex vs brainstem vs both)—> cortical spreading depression —> meningeal blood vessel dilation —> release of vasoactive neuropeptides (calcitonin gene-related peptide (CGRP), substance P …) —> neurogenic inflammation —>worsening dilation and inflammatory response causing more pain —> pain signals reaching the trigeminal nucleus caudal (TNC) (in brainstem)—> continuous TNC firing leads to central sensitization (allodynia) if activated pathways are not stopped (triptan has minimal to no effect at this stage)
MOA of triptans?
agonists of serotonin receptors 5HT-1B and 5HT-1D
New daily persistent HA
- begins abruptly and patient charactistically recall the exact date it started, must be present for more than 3 months
Criteria for hemicrania continua
- continuous one-sided headache for at least 3 months with moderate to severe exacerbations
- At least one autonomic sign on the side of the headache: conjunctival injection, lacrimation, facial sweating or flushing, rhinorrha, congestion, sense of ear fullness, partial Horner’s (ptoisis and/or miosis) or eyelid edema
- Very responsive to indomethacin (patient must respond completely to indomethacin)
Criteria for hemicrania continua
- continuous one-sided headache for at least 3 months with moderate to severe exacerbations
- women>men
- At least one autonomic sign on the side of the headache: conjunctival injection, lacrimation, facial sweating or flushing, rhinorrha, congestion, sense of ear fullness, partial Horner’s (ptoisis and/or miosis) or eyelid edema
- Very responsive to indomethacin (patient must respond completely to indomethacin)
Cluster HA criteria
- Duration 15- 180 min
- More common in men (in contrast to HC and PH)
- At least 5 attacks of severe unilateral temporal, orbital, and/or supraorbital pain
- Presence of either agitation or restlessness and/or at least one autonomic sign (check HC part)
- Can occur up to 8 times per day
Paroxysmal hemicrania criteria
- At least 20 attacks of severe unilateral temporal, orbital, and/or supraorbital pain lasting 2-30min
- At least one autonomic sign
- Very responsive to indomethacin (patient must respond completely to indomethacin)
Trigeminal neuralgia criteria
tx?
- Not associated with autonomic features
- At least 3 attacks of unilateral facial pain in trigeminal nerve distribution, with no radiation outside the boundaries of this territory
- Pain characterization (should have 3/4): lasts 1 sec - 2min, severe intensity, shooting/electric shock-like/stabbing or sharp, precipitated by stimuli to affected area
- Most commonly V2 and V3
- 1st line tx: carbamazepine
What disorders should come to mine when there is bilateral trigeminal neuralgia?
MS, Lyme, Sarcoidosis, stuff like that
SUNCT and SUNA criteria?
Difference between the 2
- More common in males
- At least 20 attacks of mod to sev unilateral head pain in the temporal, orbital, supraorbital and/or other trigeminal distribution
- Duration 1-600 sec
- At least 1 autonomic sign
- Difference between SUNA and SUNCT: SUNCT requires both conjunctival and lacrimation, whereas SUNA requires only one or neither of conjunctival injection and lacrimation
Hypnic headache
- “alarm clock headache”
- More common in women
- Recurrent headaches developing only during sleep and causing the patient to wake up
- Must occur 10 or more days/months for at least 3 months
- Lasts between 15min and 4 hrs after waking
- Begins after the age of 50
Characteristics of HA in patients with Chiari Malformations
occipital area
precipitated paroxysmally by cough, bending forward, valsalva
Low pressure headache features
positional HA in nature
Common after LPs, neurosurgery procedures, dural tear
Most common location of spontaneous CSF leaks?
T spine
MRI findings in dural leaks/low pressure HAs?
- pachymeningeal enhancement
- downward displacement of the brain and crowding of the posterior fossa due to the sagging and traction of intracranial structures and dura, which may mimic Chiari I malformation
- subdural hematomas or hygromas
- engorgement of cerebral venous sinuses
- pituitary enlargement
- flattening of the optic chiasm
- increased anteroposterior diameter of the brainstem
- decrease in the size of cisterns and ventricles
How to diagnose a dural leak?
MRI myelography with fat suppression
Treatment for dural leak
bedrest, hydration and caffeine
If doesnt work → blood patch
Which triptan has a long half life and is not ideal for abortive tx?
Frovatriptan
How long do you anticoagulate for CVST?
3 months, unless hypercoag panel is positive than lifelong.
Familial hemiplegic migraine type 1
chromosome 19p13 (CACNA1A gene), resulting in a defect in P/Q calcium-channel subunit
Familial hemiplegic migraine type 2
Chromosome 1q23 (ATP1A2 gene) resulting in a defect of A1A2 sodium potassium ATPase.
Familial hemiplegic migraine type 3
Linked to chromosome 2q24 (SCN1A gene), resulting in defects of pre and post synaptic voltage gated sodium channels
Findings in idiopathic cranial pachymeningitis on imaging? CSF? biopsy?
prominent leptomeningeal enhancement
CSF with lymphocytic pleocytosis
leptomeningeal biopsy may show perivascular inflammation
Association with women who have migraine with aura and inc risk of stroke
higher in women <45yo
even higher with smoking and estrogen containing OCPs
