Term
| increase in volume of one compartment in a closed space... |
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Definition
| leads to compensatory decrease in volume of other compartments. Decompensation is often rapid and dangerous. (Monroe-Kelly Doctrine) |
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Term
| Brain and Spinal Cord Edema--think of the different types |
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Definition
Cytotoxic-anoxic, infectious, toxic, neurons and glia swell leading to decreased ECF and increased ICF
Vasogenic-Transudation from plasma deading to increased ECF
Perineoplastic, inflammatory |
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Term
| treatment of Brain and Spinal Cord Edema |
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Definition
| diuretics like mannitol, furosemide, hypertonic saline if traumatic or treat with steroids if perineoplastic or inflammatory |
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Term
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Definition
| produced at constant rate by choroid plexus (there is no excess production unless there is a rare choroid plexus papilloma) (no reduction in production except in neonatal meningitis) THIS IS NOT PRESSURE CONTROLLED |
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Term
|
Definition
-Treat with ventricular drainage, shunt or LP
-Can be obstructive or communicating |
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Term
| Vasodilation from increased pCO2 and drugs |
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Definition
| hyperventilation can decrease pCO2 and exceed effect to overly vasoconstrict and cease cerebral blood flow (CBF) |
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Term
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Definition
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Term
| Venous outflow Obstruction |
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Definition
| elevate head of bed, clear venous compression |
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Term
| Volume associated with any pathology (what can cause increased volume in head and spinal cord?, and what are some treatments?) |
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Definition
tumor, cysts, abscesses, hematoma, contusion, cerebral infarction, radiation necrosis
treatment: surgical removal or aspiration of mass or craniectomy to decompress |
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Term
|
Definition
visualized with MRI, The more active an area, the greater the need for high CBF, autoregulation matches flow to need.
-CBF usually excees demand by a lot so O2 extraction is low, aka high reserve capacity
-If CBF is too low, the brain will first increase the extraction ratio
-As MAP varies b/t 50 and 150 mmHg, CBF stays relatively constant
Hypercapnia (excess CO2) (produced locally w/ normal brain cell activity) leads to increased CBF
Hypocapnia leads to decreased CBF
HTN pushes physiologic CBF curve to the right
The avg CBF for the brain is 50mL/100g/min
at 25 EEG changes occur
Below 20, reversible dysfunction occurs in conjunction with a rising risk of infarction over time. (the lower under 20 the sooner the likliehood of infarction)
CPP=MAP-ICP, so as CPP decreases brain will try to compensate by increasing blood pressure (MAP)
Testing this vicious cycle= as ICP increases, CPP decreases-->infarction-->edema-->increased ICP |
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Term
| Rostro-Caudal Decay-Focal Expaning Mass/Lesion-Progressive Damage |
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Definition
Focal distortion and local hemispheric dysfunction-->effacement of local sulci and gyri
-compression of lateral ventricles
Midline shift and subfalcial herniation-->cingulate gyrus herniates beneath the sharp edge of the falx cerebri--agitation and headache
Temporal Lobe herniation
1)Uncus herniates through the tentorium cerebelli into the incisura tentorii where the cerebral peduncles lay
2)impinged cerebral peduncles leads to contralateral weakness (hemiparesis)-->can also get paradoxical worse weakness on ipsilateral side due to kernohan's (tentorial) notch (severe cerebral peduncle compression)
3)lead to compression of CN III
-ipsilateral unilateral dilation of pupil due to loss of PSNS input first to go
-ipsilateral loss of most extraocular movements next
Obliteration of basal CSF cistern--CSF circulation impaired-->hydrocephalus
Midbrain infarction (prognosis worsening now, the next 5 things occur simultaneously)
1)both oculomotor nuclei affected-->bilateral pupil dilation
Duret hemorrhages--small areas of bleeding in ventral and paramedian parts of midbrain and pons as scraped against forament magnum (coning)
Progression from flexor to extensor posturing
1)flexor bias=midbrain reticular formation is okay
2)extensor posturing=midbrain RF is lost/damaged, pontine and medullary reticular formations are OK, flaccidity
Loss of brainstem reflexes
1)occulocephalic-Doll's eye maneuver
-if reflex is lost, eyes follow rotation of head
-if reflex is preserved, the eyes move contralateral to head rotation
2)Corneal- blinking to aversive stimuli
Medullary compression syndromes=respiratory reflexes, vasomotor responses with increased systolic BP and bradycardia (Cushings Triad increased ICP, HTN, bradycardia (and/or irregular respiration) |
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Term
| Signs of Diffuse Increased Intracranial Pressure (like pseudotumor cerebri) |
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Definition
headache
nausea/vomiting-worse in morning from venous pooling from lying down all night
papilledema
1)increased ICP on ganglion cell layer of retina impinges on nerves, axonal transport disrupted
2)causes optic disc to bulge forth and swell, loss of sharp margins
3) CSF outflow from eye obstructed
4)CN VI palsy-diplopia on far vision, lateral rectus weakened-->a false localizing sign in increased ICP
5)obscured vision-- often transient, during peaks of ICP |
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Term
| Ventriculomegaly syndrome (IE normal pressure hydrocephalus) |
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Definition
ventricular enlargement w/o increased ICP
cortical afferents and efferents coursing near ventricles affect first and worst gait apraxia, incontinence, confusion = "wet, wacky, wobbly"
May progress to combine with increased ICP |
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Term
| Epidemiology of Head Injury |
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Definition
500K to >1 million cases /year
1) most are mile ~20 % mod-severe
2)Half of 150K trauma deaths are from head injury
3)5.3 million disabled by head injury (mostly veterans) |
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Term
|
Definition
Occurs at impact
1)Diffuse axonal injury: contusion and intracerebral hemorrhage, subarachnoid, subdural, and epidural hemorrhages
2)Skull fracture, cranial nerve injury, arterial dissection, dura/arachnoid injury with CSF leak |
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Term
|
Definition
1)Cell death due to decreased CBF and O2
2)Inflammation, excitotoxicity (increases metabolic deman), Ca2+ influx, ion pump dysfunction, free radicals
3)Lots of emergent care focuses on limiting this-->prevent hypotension, maintain CPP, and CBF, control ICP |
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Term
|
Definition
Airway, breathing, Cerebrum (ABC)
Breathing, bleeding, brain, bowel, bladder, bone (BBBBB)
Cervical spine immobilization until cleared clinically and radiologically |
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Term
| Mini Neurological Assessment-Glasgow Coma Scale |
|
Definition
Eye Opening
1)Spontaneous=4, speech=3, Pain=2, No respons=1
Verbal Response (5)
Oriented (5), Confused (4) Inappropriate 3, incomprehensible 2, none 1
Best motor response (6)
Obeys command 6
localizes pain 5
withdraws 4
flexor posture 3
extensor posture 2
None 1
Best score=15
Worst=3
Monitor ICP at 8 or Less |
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Term
| Initial Evaluation in head injury/multiple trauma |
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Definition
ABCS
Pupils
Spinal level
Toxins: drugs, EtOH
CT head and neck and any other injured area (faster than MRI, shows blood) |
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Term
|
Definition
Primary brain injury causing axonal shear
1)Anoxic/hypoxic/bleeding injuries can be super-imposed
2)Presents as scattered brain injury with lack of localizing signs
Stain for degenerating axons
1)Nerve cells are intact
2)clusters of disrupted axons
3)Small balloons of proteins from the axonal transport form at the point of the shear/damage (end balls)
4)Increased signaling in white matter on later MRI indicates disruption of axons in frontal Lobe |
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Term
Case: 36 yr old woman in MVA on icy road, found unresponsive hours later, intubated and sedated in ambulance, flexes on right, localizes on left (injury is worse in left hemisphere), ICP is high normal, initial CT "normal", slow recovery in ICU.
Patient is agitated, obeys commands, recognizes family, tracheostomy needed at 2 weeks, at 6 months she is in offic for f/u with dizziness, unsteady gait, spastic right arm, left sided intention treamor, and slow deliberate speech |
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Definition
| Patient has lingering symptoms that are not localize-able-- multiple punctate lesions |
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Term
|
Definition
Located between skull and dura
bright white biconvex lens on early CT
often due to middle meningeal artery (high pressure, expanding lesions)
trauma-temperoparietal locus
Craniotomy to prevent secondary injury |
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Term
| 10 year old boy struck w/ baseball, seems dazed at first, lies down, found stuporous later, difficult to rouse, positive right drift test, annoyed by exam/speaking, CT shows hematoma and lateral ventricle , tx with mannitol or hypertonic salin +intubation w/ low CO2 + craniectomy to relieve ICP, seizure en route to OR treated w/ diazepam and dilatin, develops dilated left pupil (temporal herniation), flexes to pain on left, extends on right |
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Definition
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Term
|
Definition
Located btw the dura and arachnoid
Appear crescent-shaped on CT
1)Often a chronic process whrein blood liquefies and appears like CSF
2)May seem ok but slowly develop confusion and clumsiness
3)More common in the elderly b/c brain parenchyma atrophy, more space for blood |
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Term
| Old guy, hits his head on a locker, forgets about it, wife brings him to the Dr. b/c he isn't acting right... |
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Definition
| treat with a surgical burrhole to remove blood, pt has a subdural hematoma |
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Term
| Meningitis as Delayed Complication of frontal Smash injury |
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Definition
Intermittent clear fluid drain from nose (CSF!) after facial fracture-->drainage stops b/c of herniation of brain into the tear
2)patient presents again 3 mos later w/ fever and stiff neck following symptoms of sinusitus
-The poor membranes, no bone and healing surgical wounds permitted the infection to enter the meninges |
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Term
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Definition
55yo male found down w/ bruise on forehead, combative and confused in ER, resists exam, no focal deficit, pupils appear equal
Bifrontal brain contusions after assault
-Leads to lack of socially appropriate behavior
-Thought and emotional spasticity-irritability, etc
Contusions appear as bright reactive areas on CT, evolve over time, often incorporating edema over time |
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Term
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Definition
| 71 yo man found down after a fall, unresponsive, localizes left, extends right, CT shows blood in right temporal lobe and sylvian cistern (subarachnoid hemorrhage), surgery dependent on degree of swelling and hydrocephalus |
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Term
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Definition
| Paroxysmal event caused by abnormal brain electrical activity |
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Term
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Definition
| chronic condition char. by recurrent 2+ unprovoked seizures |
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Term
|
Definition
| single seizure lasting 30 minutes or serial seizures over a 30 minute period w/o full recovery b/t episodes |
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Term
| Differential diagnosis of paroxysmal events with neurologic manifestations |
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Definition
epileptic seizures
nonepileptic seizures
syncope, panic attack, migraine, TIA/stroke, cataplexy |
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Term
| Epidemiology of Seizures and epilepsy |
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Definition
Can develop at any age, but MC in:
kids-genetics and brain tumors
elderly-strokes and brain tumors
181,000 seizures and epilepsy/year
2.7 million epilepsy in the US
2-5% of population will have at least 1 non-febrile seizure during lifetime
(I know this notecard sounds weird but it's how his lecture notes were written) |
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Term
|
Definition
majority=idiopathic 2/3
stroke=mc 2nd ~11%
Also congenital>trauma>neoplastic>degenerative>infxn |
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Term
|
Definition
Family Hx in 1st degreee relative
Febrile seizures, head injury, MR
Brain infxn, or lesions (tumor, malformations, stroke)
Acute symptomatic seizure
Dementia MS |
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Term
| Clinical Features of a seizure |
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Definition
Abn Mental state
1)unresponsive, confused
2)inappropriate vocalization-screaming, laughing NOT CRYING
Abnormal movements
1)tonic stiff; clonic-jerks
2)Dystonic posturing
3)Myoclonic jerks- DDx metabolic, anoxic, JME
Automatisms-common in partial epilepsies
1)oralimentary-lipsmackin, chewing, etc
2)Manual-fumbling, fidgenting
Abnormal Sensations
1)Tingling
2)Pain
3)Visual Spots
4)Tinnitus
5)Abnormal Taste
6)Deja Vu |
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Term
| Classification of Seizures |
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Definition
Partial -begins in one part of hemisphere
1)simple-preserved consciousness
2)Complex Impaired Consciousness
Generalized-involves both hemispheres
1)secondary evolves from simple or complex partial seizure
2)primary- begins in both hemispheres simultaneously |
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Term
|
Definition
Temporal Lobe Onset-consciousness impaired
1)premonitory aura (knows to get in bed), motionless staring
2)single UE dystonic posturing-contralateral to seizure onset
3)Manual and oroalimentary automatisms
4)Wipes Mouth/nose with hand-hand used is ipsilateral to seizure
5)+/- postical aphasia
1)Right temporal lobe onset=no aphasia
2)Left temporal lobe onset=aphasia due to affected language centers |
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Term
|
Definition
Onset in 1 Hemisphere
1)open eyes, motionless
2)Slow, aversive head deviation-away from seizure
-eyes look away from seizure!
-in destructive lesions ex strokes, the eyes will look toward the damage
-grunting vocalization
-flexion posturing of UE contralateral to onset
-generalized tonic followed by clonic activity |
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Term
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Definition
-Brief pause during conversation-appear to stare off a thousand miles away
-some hand automatisms
-No postictal phase
-can occur 100s of times during a day |
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Term
|
Definition
| sterotyped, abrupt onset and end, open blank staring eyes, grunting, rhythmic synchronous movements, shor duration, common to injure self, partial or complete amnesia, no secondary gain (does not get something from this) |
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Term
|
Definition
variable-- gradual buildup and prolonged resolution, usually closed eyes, emotion crying sobbing, and grunting vocalization, asynchronous, side-to-side, head shaking, pelvic thrusting, no tonic phase, head arching back, variation in amplitudes of movements, unresponsiveness, prolonged duration, rare to injure self, indifference to memory of event, secondary gain may be identifiable (get something from the seizure)
-Can be precipitated and aborted by suggestion
-Can be a form of conversion disorder, often females with high incidence of sexual abuse, rape |
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Term
| Basic approach to dealing with a seizure |
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Definition
1) Are events epileptic? (diff. from nonepileptic paroxysmal attacks) If so what type of seizures (partial, generalized, etc.
2)Is there an associated epilepsy syndrome (JME, LGS, etc)?
3) What are the treatment options? (depends on seizure type and epilepsy syndrome) |
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Term
| Diagnostic Tools for Seizures |
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Definition
1)History
2)Physical Exam
3)Basic Tests- Interictal EEG, MRI/CT, routine labs
4)Advance tests-video EEG monitoring, PET (evaluates abnormal brain function, particularly glucose utilization, ictal SPECT, fMRI, MEG
5)MRI evaluates abnormal brain anatomy such as scars, tumors, etc.
-detects mesial temporal sclerosis, cavernous hemangiomas
-this last thing has high cure rates with surgery |
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Term
| Partial Seizure treatments |
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Definition
Use whatever you like-phenytoin, carbamazepine, etc, valproate aka Depakote (DON"T USE WITH ANY POSSIBILITY OF PREGNANCY!!!!!! SEVERE BIRTH DEFECTS), oxcarbazepine, topiramate, lamotrigine, phenobarbitol
Adjunctive theraphy=any monotherapydrug, gabapentin, tiagabine, zonisamide, levetiractam, pregabalin |
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Term
| Absence Seizure treatments |
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Definition
Ethosuximide
DON'T USE ANY PARTIAL SEIZURE MED=precipitate more absence seizures
Absence w/ GTCS valproate, topiramate, lamotrigine, levetiracetam |
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Term
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Definition
| With antiepileptic drug ~47% became seizure free with first AED, 13% more after 2nd, 4% with addition of 3rd, 38% intractable (did not achieve 1 year seizure freedom) |
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Term
| Treatment for intractable epilepsy |
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Definition
Vagal nerve stimulator=pacemaker for atonic seizures and comorbid depression
Surgery
corpus callostomy-can help prevent partial seizures from generalizing
lesionectomy
anteromedial temporal lobectomy
neocortical resection
multiple subpial transections
functional hemispherectomy |
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Term
|
Definition
| the mental process of knowing, includes aspects of awareness, perception, reasoning, and judgement |
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Term
|
Definition
| The origination and development of a disease |
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Term
|
Definition
A shift from the disease metaphor to the vision of well being.
focusing on factors that support human health and well-being, rather than on factors that cause disease |
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Term
| Who needs a mental status exam? |
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Definition
| Everyone in an altered state of consciousness |
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Term
|
Definition
Important part of every neurological exam
- Evaluation of awareness
- consciousness
- behavior
- emotional state
- content and stream of thought
- cognitive capacity
- orientation
- memory
- calculation
- language
- judgement
- reasoning
- presence of hallucination or delusions
- Praxis (ability to carry out imagined acts)
- Constructional ability
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Term
| Altered states of consciousness |
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Definition
Dementia Coma- No response even to pain'-check their blood for drugs and metabolic abnormalities - check for narcotic antagonist
Thiamine levels- glucose levels
- examine all of the body
- ABG
- CMP
- CBC
- Body Temp
- Stupor-responds only to pain
- Obtundation/lethargy- responds to vigorous movement/shaking or loud voices
- Catatonia-awake but not moving or responding
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Term
| Wernicke's encephalopathy |
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Definition
- Alcoholics only given glucose will develop b/c glucose utilization depletes their small thiamine reservoir leading to micro-hemorrhages and severe memory problems
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Term
|
Definition
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Term
|
Definition
Mental disturbance marked by clouding of consciousness
-may be accompanied by lethargy
-Restlessness
-Fluctuating levels of impairment
-Medical emergency b/c DZ or drug intoxication to which it is secondary may be fatal if untreated
-May also be from fever, alcoholic withdrawal, anoxia, anemia, infxns, etx
-can also be from atropine, barbiturates, bromides, chlorodiazepoxide, chlorohydrate, clonidine, cocaine, diazepam, digitalis, alcohol, ethanol, haloperidol, lithium, PCP, Phenytoin, Prednisone, Propranolol
-Tricyclic Antidepressants |
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Term
|
Definition
- Frontal lesions of sylvian fissure-motor
- non-fluent aphasia with agrammatism, repitition failure, and relatively retained comprehension
- AKA telegraphic speech
- often accompanied by right hemiparesis and oral apraxia
- Comprehension for grammatical relationships is impaired, but not individual word meanings
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Term
|
Definition
- Posterior lesions of Sylvian fissure
- Fluent or sensory aphasia with impaired comprehension and circumlocution
- full sentences with lots of mistakes
- poor repetition, reversals, reading, and rhyming
- May have alexia
- very long circular speech
- patient is unaware of the disturbances
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Term
|
Definition
- Lesions interrupting frontal and posterior regions of sylvian fissure (interrupting the pathways between the two)
- poor repetition
- A lesion in the arcuate fasciculus
- [image]
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Term
|
Definition
- Phoenemic-literal.. shammer for hammer
- Semeantic... pliers for hammer
- Neologism... humdup for hammer
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Term
|
Definition
- Both broca's and wernicke's
- totally non-fluent, but understand emotional intonation and facial expression, speech comprehension is usually impaired
- usually with sever right hemiparesis
- rge lesion in the perisylvian area of the frontal, temporal and parietal lobes of the brain causing an almost total reduction of all aspects of spoken and written language.It involves a "left side blowout" which includes Broca's area, Wernicke's area and the Arcuate fasciculus
- [image]
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|
Term
| Primary progressive Aphasia |
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Definition
- Fluent or non-fluent
- Difficulty finding words to point of difficulty to speak
- Semantic dementia- fluent progressive aphasia, a form of fronto-temporal dementia
- Can progress to frontotemporal dementia or Alzheimer's
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|
Term
|
Definition
- Disturbance in execution of learned movements other than those caused by co-existent weakness or sensory loss
- Ideational dyspraxia
- Movements of affected body parts suffer a lack of basic plan although individual familiar movements can be carried out
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Term
|
Definition
- Treats famiiliar stimuli as unfamiliar or misnames them for other stimuli
- loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss
- depending on where the lesion is depends on which type of agnosia you get
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Term
|
Definition
- Cognitive deterioration sufficient to interfere with social occupational functioning including memory, orientation, abstraction, ability to learn, visuospatial perception, and constructional abilities and language
- should be suspected wherever mental changes or insidious onset emerge and gradually interfere with daily living activities that are appropriate for age and background
- Patients are alert
- always accompanied by memory impairment
- Performs similar tasks at inappropriate times- draws a circle correctly, then keeps drawing a circle instead of a house
- Clinical state with loss of function in multiple cognitive domain
- Not during the course of a delirium
- diagnosis
- check lab tests (b12, thyroid fxn tests, CBC, electrolytes, enzymes, complete history)
- medical and neuro exam
- neuroimaging
- neurosyphillis
- HIV/AIDS dementia
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Term
|
Definition
- Frontotemporal Dementia
- Severe atrophy of frontal and temporal poles
- spared motor and sensory cortex
- diffuse loss of neurons and gliosis
- associated with chromosome 17 mutations in Tau gene, which encodes a MT-associated protein (MAP)
- Inclusions (pick bodies contain Tau deposits)
 |
Term
|
Definition
- Dementia with parkinsonisms, fluctuations, hallucinations, and delusions
- 30-80% of PD may become demented over 10-15 years
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|
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Term
|
Definition
- New variant CJD-Bovine spongiform encephalopathy-->Mad cow disease
- Chronic Wasting Disease
- Gerstmann Straussler Sheinker disease
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|
Term
| Vascular Cognitive Impairment--> |
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Definition
| Multi-infarct dementia, vascular dementia |
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Term
| Main Cases of Treatable Dementia |
|
Definition
- Drug FX-polypharmacy
- Depression
- Normal Pressure hydrocephalus (incontinence, gait instability, dementia)
- Metabolic toxic conditions- Korsakoff (alcoholics with thiamine deficiency), pellagra, niacin, and tryptophan deficiency, vitamin B12 deficiency (DON'T GIVE FOLATE!)
- Hypo or Hyperthyroidism
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Term
|
Definition
- Rate is vastly increasing b/c of our aging population
- Symptoms- Deficits in:
- recent memory
- language/word finding
- judgement, decision making
- route finding, visuospatial fxns
- mood, personality, social behavior
- Pathology
- Neuritic plaques-extracellular amyloid-Bdeposits, appears as fibrils, protofibrils, oligomers, and monomers
- neurofibrillary tangles-->intracellular MAP Tau deposits
- Cerebral Amyloid Angiopathy-->can lead to hemorrhages in brain vasculature
- Has activated microglia, cytokines, and reactive oxygen species
- Amyloid precursor protein is broxen down to produce the smaller A protein with small intermediate-soluble oligomers in the aggregation process can confer synaptic dysfunction, whereas large, insoluble deposits might function as reservoirs of the bioactive oligomers
- There is a misfolding of the GCSF protein, no protein folding pathway exists for the amyloid protein
- Alzheimer Physiology
- APP expression and trafficking
- APP cleavage
- AB aggregation and toxicity
- Ab Degradation
- AB clearance from brain to blood
- This is a very Chronic disease
- GENETICS OF ALZHEIMERS
- 60-70% risk is genetic
- Codominant ApoE4 allele on chromosome 19 increases risk. RIsk varies between ethnic groups
- <1% of early onset due to AD genetics
- Chromosome 21-APP changes in DS begin early in life with increased CSF Ab in childhood, C-11 B is increased in early life in healthy middle aged controls, mid-life cognititive performance predicts late-life dementia
- Chromosome 14-Presenilin 1
- Chromosome 1- Presenilin 2
- Totoal >160 rare but highly penetrant mutations
- Protective factors
- Non Modifiable:young age, apoE-e3 and apoE-e3 alleles, (-) family Hx of dementia, (-) mild cognitive impairment, male
- Modifiable: high education and occupational achievement, vigorous part. in mental and physical activities, pediatricians helping families develop goog habits early on.
- Avoidance of:
- Cardiac Dz, HTN, DM
- High fat diet, obesity, smoking
- head injury, alcoholism
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|
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Term
|
Definition
Acetylcholinesterase inhibitors
Inhibitors fo excitotoxicity from NMDA-type glutamate receptors |
|
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Term
|
Definition
Brain biopsy or autopsy is required for definitive diagnosis
Exclusion diagnosis 80-90% accurate when all other things excluded |
|
|
Term
| Amyloid Plaque Formation (not something we necessarily have to know, but I liked this picture) |
|
Definition
 |
Term
| Stress, Aging and Neurodegenerative Disease |
|
Definition
- Ageing challenges proteome homeostasis b/c of decreaseing proteostasis capacity and increasing protein damage
- Proteostasis- the control of the concentration, conformation, binding interactions, and location of individual proteins making up the proteome
- Graceful aging depends on the cell's ability to encounter the effects of stress by maintaining protein folding, which in turn permits appropriate protein function
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|
Term
| Systems with functional and structural decline during aging |
|
Definition
- CNS
- PNS
- Vision
- Audition
- Skeletal
- Gastrointestinal
- Hepatic
- Renal-genitourinary
- Cardiovascular
- Hematologic
- Endocrine
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|
Term
| Activity Depression Cycle |
|
Definition
Depression leads to inactivity which leads to depression which leads to inactivity.... and so on
-Apathy is a prominent feature of depression (anhedonia) |
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|
Term
Steps of the Neuro Exam that matter in Neuromuscular Disorders |
|
Definition
- Motor-- Strength, bulk, ton, fasciculations, abnormal movements
- Increased tone-->UMN process
- Decreased tone-->LMN process
- MRC scal of strength-->0 to 5
- Sensory--pain/temperature, light touch, vibration, proprioception, Romberg
- Reflexes--DTR, etc
- Abn Babinski reflex-->toe goes up
- Hoffman reflex-->when flicking finger to induce a stretch no reflex should be seen, in abnormal--induced stretch reflex and flexion of thumb
- Clonus--rhytmic muscle contraction, hyperreflexia
- Biceps and Brachioradialis-C5/C6
- Triceps C7
- Patella--L4
- Ankle S1
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|
Term
| Basic Differential (think of the sunshine vitamin..) |
|
Definition
V- Vascular/ischemic (stroke, vasculitis)
I-infection
T-Trauma
A- Autoimmune/inflammatory
M-Metabolic/systemic
I-Inherited/congenital
N-Neoplastic
D-Drugs/toxins |
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|
Term
Mononeuropathy (MN)
Carpal tunnel
cubital tunnel
Peroneal MN
Radial N palsy
Meralgia paresthetica
Bell's Palsy |
|
Definition
- Carpal tunnel syndrome-- median nerve compression at wrist
- cubital tunnel syndrome--ulnar nerve compression at elbow
- Peroneal MN from compression at fibular head (person with a cast on bottom of leg)
- Radial Nerve Palsy--Wrist Drop, think of cast around middle of humerus (humeral shaft), crutches can compress
- Meralgia paresthetica-- lateral femoral cutaneous MN from compression at inguinal ligament, usually b/c of tight belt, causes numbness, tingling, or burning sensation in anterolateral aspect of thigh.
- Bell's palsy--facial nerve MN CN VII
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|
|
Term
|
Definition
- symmetric and distal
- both sensory and motor
- LMN signs--diminished/absent reflexes, distal atrophy, fasciculations
- axonal or demyelinating, sensory or motor or autonomic or mixed, etc
- Toxic--hyperglycemia (DM2), EtOH, chemotheraphy (alkaloids), heavy metals
- Claw hand
- shield sign
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Term
| Red Flags of neuromuscular disorders |
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Definition
- Sudden distal symmetric onset, rapidly ascending
- UMN and LMN
- sphincter involvement
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Term
|
Definition
- Asymmetric/atypical--red flags!
- irregular, uneven progression
- pure motor or pure sensory
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Term
|
Definition
- lesion of a particular nerve root
- radicular (shock-like) pains radiating down extremity in particular dermatome
- paresis in particular myotome
- depressed reflexes
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Term
|
Definition
- Lesion of a particular trunk/cord of plexus causing sensory disturbances, weakened muscles, and decreased reflexes in a common distribution
- Lower trunk: medial arm pain, numbness, intrinsic hand mm weakness w/o reflex change
- Erb's palsy: damaged brachioradialis, deltoid, bicep leading to pronated, flexed hand to the back. Upper trunk
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Term
| Neuromuscular Junction Disorders |
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Definition
Act. via nicotinic cholinergic receptors snare proteins grab vesicles and dump for release. Botulism weakens snare proteins.
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Term
|
Definition
damage to nACHRs
- present with weakness
- fine motor control affected early
- EOM, facial, laryngeal, pharyngeal
- myasthenia gravis: Abs to receptor
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Term
|
Definition
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Term
|
Definition
- Symmetric, proximal weakness
- Inherited or acquired
- myalgias and cramping occaisonally, but no SENSORY deficits
- structural protein problems: DMD, BMD, FSHD, LGMD, OPMD
- Metabolic myopathies
- myotonic myopathies: Dystrophic:myotonic dystrophy; nondystrophic myotonia congenita, periodic parlyses
2. Acquired Muscle disorders
- polymyosistis: inflammatory, progresses over months
- Dermatomyosists:polymyositis with a rash
- Inclusion body myositis:>50 years. Slowly progressive myopathy
- Toxic myopathies: statins, steroids, ethanol, colchicine
- Ishemic (compartment syndrome)
- infectious
- Others
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Term
| Duchenne Muscular Dystophy (DMD) |
|
Definition
- Presentation, clumsy kid falls down a lot
- walks on toes with waddling gait
- Gower's sign--rises from floor butt-first, walking his hands up his thighs to stand upright
- proximal weakness and large doughy calves
- elevated CK
- Defect in dystrophin gene causes gradual degeneration of muscles
- X-linked 1/3 are new mutations
- DMD is more severe than Becker
- DMD--Loss of ambulation before 12
- BMD loss of ambulation before 16
- Tx with corticosteroids to slow progression
- Death due to respiratory failure
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Term
| Inherited Metabolic Myopathies |
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Definition
McArdle's-deficiencty in myophosphorylase
Pompe's--acid maltase deficiency |
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Term
|
Definition
- Toxic Myopathies
- statins, steroids, EtOH, colchicine
- statins are MC Cause of Myopathies
- Ischemic-compartment syndrom
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Term
| Nerve Conduction Studies: Surface electrode |
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Definition
i. Motor Nerve Conduction
o Measured in mV with latency in msec
o Compound muscle AP
ii. Sensory Nerve Conduction
o Measured in mV with latency in msec
o Sensory nerve action potential
iii. Tests largest (thickest), fast fibers
o Axonal damage/loss—reduced amplitude
o Demyelinating—reduced velocity
o Small fiber polyneuropathies can appear normal |
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Term
|
Definition
Needle places electrode inside mm to record resting and activated mm
i. Normal—normal amplitude and duration in triphasic morphology
o Inactive muscles should be silent
o Active mm should reveal a number of motor units firing near the tip of the needle
ii. Denervation—abnormal spontaneous activity
o Fibrillations, positive sharp waves, fasciculations
iii. Re-innervation
o Surviving more units responsible for more muscles
o Higher amplitude, longer duration, and complex waveforms
iv. Reduced recruitment
o Defined by rapid firing of a reduced number of motor units
o Very severe in post-polio or spinal muscular atrophy
Makes a loud roaring sound
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Term
| Lab Testing for Neuropathy |
|
Definition
Serology
i. Serology
o Metabolic—DM is MC; thyroid
o Nutritional—B12
o Inflammatory—ANA, RF, ESR, CRP, CSF protein level
o Toxic—heavy metals, EtOH in urine and serum
o Infectious—Lyme, West Nile virus
o Biopsy—rarely indicated: sural nerve
May demonstrate inflammation, segmental demyelination, or small vessel vasculitis |
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Term
|
Definition
i. Serology—CPK, TSH
ii. Biopsy—stain for enzymes
Used to differentiate neuropathic from myopathic and/or inflammatory from non-inflammatory. May be only means of definitive diagnosis.
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Term
|
Definition
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Term
| Lambert-Eaton Myasthenic Syndrome |
|
Definition
- Presentation--Sx progress gradually and improve with activity
- Transient diplopia, blurred vision, dysarthria, dysphagia, dry mouth
- Symmetic proximal weakness, ptosis, reflexes trace but improve with strength testing
- Normal sensation
- Shows anticholinergic properties as well
- Autoimmune IgG directed against voltage-gated Ca2+ channels responsible for aiding vesicular fusion with presynaptic membrane
- Better at night b/c gets better with effort
- 2/3 are paraneoplastic
- small cell lung CA is MC
- lymphoproliferative disorders, pancreatic, breast, ovarians CAs
- May preced tumor Dx by 3-4 years
- Prognosis related to malignancy
- Other 1/3 are autoimmune
- [image]
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Term
|
Definition
|
|
Term
| Amyotrophic Lateral Sclerosis |
|
Definition
- Fasciculations, painless progressive muscle weakness
- Atrophy distal >proximal paresis (wasting of hand and wrist mm)
- brisk reflexes in weak muscles
- UMN and LMN dysfxn in same limb
- Present abnormal reflexes-babinski and HOffman
- Begins in one extremeity and spreads to contralateral limb before other areas
- Progressive loss of anterior horn cells and lateral corticospinal tracts (chronic)
- UMN and LMN findings: bulbar dysfxn, brisk or absent reflexes, extensive planar response (babinski: corticospinal infection)
- 100% mortality in 3-5 years
- survival decreased the more proximal the onset >~worse
- Bulbar (brainstem and Cervical)>thoracic>lumbar/sacral
- Electrodiagnostic testing
- Show signs of denervation, reduced recruitment, and re-innervation
- EMG is abnormally large unusual (helps determine denervation and reinnervation
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|
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Term
|
Definition
- Proximal
- symmetric upper and lower extremity weakness
- DTRs are normal 2+
- Dysphagia, dysarthria, myalgias, dysphonia
- difficulty climbing stairs and BRUSHING HAIR
- Dysphagia, dysarthria, myalgias, dysphonia
- difficulty climbing stairs and brushing hair
- CPK >20,000 (normal is 190)
- 30-60 yo females mostly; NEVER kids
- MC acquired myopathy
- Cancer risk (9%)
- Immune system attacks mm directly
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Term
|
Definition
- Same as polymyositis and accompanied with volacious heliotropic rash
- females>males; children and adults
- skin lesions preced muscle signs
- immune system attacks vessels which then cause ischmia to mm
- Perifascicular muscle fiber degeneration from ischemic vasculitis process
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Term
|
Definition
- Presentation
- Long slow progression over 5+ years
- disproportionate weakness and atrophy of forearm flexors and knee extensors
- Difficulty rising from chairs, climbing stairs, gripping things
- No SENSORY Disturbances
- Proximal arms normal
- Mildly diminished vibration in feet, otherwise normal sensation
- Males>>>females;<50 yo
- CK normal to mildly elevated
- Dx made clinically and supported with muscle Bx
- Eosinophilic cytoplasmic inclusions and muscle fibers with rimmed vacuoles lined with granular material
- NOT RESPONSIVE TO IMMUNOSUPPRESSION
- usually takes > 5 years to diagnose
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Term
| Guillain-Barre Syndrome (Acute Inflammatory Demyelinating Polyradiculopathy, AIDP) |
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Definition
[image]
a. Presentation
i. Rapidly-progressive weakness
o Day 0—tingling in feet, ‘off-balance’
o Morning, Day 1—too weak to walk
o Afternoon, Day 1—intubation due to respiratory failure
ii. Score of 1 on MRC strength test in UE, 0 in LE
iii. Alert, oriented
iv. Areflexic, loss of vibratory sense below knees
v. Individual otherwise healthy develops a viral/bacterial infect (campylobacteria)
vi. VERY ACUTE
b. Nerve conduction studies: increased latency, speed of impulse decrease, slow
c. Immune-mediated attack on PNS and ANS
i. Destroys Schwann cells myelinating the axons
ii. Distal symmetric weakness and sensory disturbances
iii. Spreads proximally over days
d. CSF reveals albuminocytologic dissociation
i. Elevated protein without WBCs
e. 40-60% preceded by URI, GI infection, or nonspecific febrile illness
i. Commonly Campylobacter jejuni
f. IVIG or plasmapheresis hastens recovery
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Term
| What Substance is secreted by the pineal gland? |
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Definition
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Term
| Stages of sleep are considered slow wave sleep? |
|
Definition
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Term
|
Definition
- Reduction in muscle tone with the exception of extra-ocular muscles which are engaged in rapid eye movements in bursts behind closed eyelids; EEG becomes desynchronized with low voltage, high frequencey, background with alpha bursts; autonomic functions variable: Fluctuating respirations, pulse and nocturnal tumescence; vivid dreaming
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Term
| How is the first half of sleep distinguished from the second half of sleep? |
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Definition
| The first half of sleep is slow wave predominant and the second half is more REM |
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Term
| Describe the age related changes in sleep architecture |
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Definition
- Over the life cycle, a a gradual decrease in sleep occurs
- Babies sleep 1 hours a day, 1/2 in REM, the hypotonia may contribute to SIDS
- By early adolescence, REM is down to about 20% and remains there proportionally through remaining lifespan
- The elderly show increased sleep latency, reduced slow-wave sleep, decreased REM latency, reduced total REM, frequent awakenings, decreased sleep efficiency
- These changes may be due to age-associated neuronal loss in the SCN
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Term
| Primary Idiopathic Insomnia |
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Definition
One month or more of poor quality sleep
§ Idiopathic- more common in elderly
§ Inadequate sleep hygiene – bad habits
§ Sleep state misperception
§ Psychophysiological insomnia
§ Treatment depends on cause |
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Term
| Circadian Rhythm Sleep Disorder |
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Definition
§ Delayed vs. advanced
§ Jet-lag type
§ Shift work type
§ Treatment
· chronotherapy- gradual or sudden shift
· phototherapy- bright blue light when sleepy
· melatonin- when trying to go to bed not tired |
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Term
|
Definition
§ Obstructive -1-8% adult males
· Bipap and Cpap
· Mouthpiece to keep lower jaw from sagging
· Surgically only tracheotomy proven effective
§ Central
· Extremely rare due to lower medullary lesions
· Nocturnal ventilation and sleep alarms during day |
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Term
|
Definition
§ Diagnosed by presence of cataplexy or sleep onset REM in multiple sleep latency test
§ Stimulants for sleep attacks
§ Noradrenergic antidepressants or sodium oxybate for cataplexy |
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Term
|
Definition
Idiopathic or post-viral
Kleine-Levin:self-limited condition common on teenagers, can lose entire years of their lives |
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Term
| Non-REM movement Disorders |
|
Definition
§ Restless Leg Syndrome (RLS)
· Dopamine agonists- but not levodopa due to initial exacerbation
· Gabapentin
§ Benign Nocturnal Myoclonus
§ Bruxism
· Mouthguard/ aerobic exercise
· Clonazepam
§ Rhythmic Movement Disorder (headbanging)
§ Periodic Limb Movements of Sleep (PLMS) |
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Term
| Non-REM arousal disorders |
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Definition
Self Limited
§ Sleep terror disorder (night terrors)
· During first 100 minutes of sleep
· Fear behaviors with autonomic arousal
· Non-responsive and amnestic
· Nightly for days to weeks
· Benign Rolandic Epilepsy ?
§ Sleepwalking
· Peak incidence around age 8 |
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Term
|
Definition
| Distinguishable from night terrors by lack of amnesia and confusion when awakened |
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Term
|
Definition
- Older men most commonly, associated with Lewy body diseases
- Treatment with REM suppression, dopaminergics or as nightmares
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Term
|
Definition
- Inappropriate REM atonia during wakefulness
- Increased in probands of narcoleptics
- reassurance sufficient
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Term
| Last year sleep Guy stuff, so we probably don't need to know, but it made sense |
|
Definition
1. Structure of Sleep and Functions
a. In a typical 8 hour period there are 4-6 cycles of NREM sleep followed by REM sleep
i. 5% in NREM1 (i.e. drowsiness)
ii. 50% in NREM2
iii. 20% in NREM3—deep, restorative
iv. 25% in REM
b. Most slow-wave (NREM) sleep is at beginning of sleep cycle
i. Common parasomnia—sleepwalking
c. Most REM sleep is at end of sleep cycle
i. Common parasomnia—nightmares
d. Approximately 25% of sleep is REM from puberty to end of life
i. Percentage is conserved as people age
e. In the elderly, there is:
i. Decreased nocturnal total sleep time
ii. Increased awakenings
iii. Decreased slow-wave sleep
f. Possible functions include:
i. Memory and learning (and unlearning!)
ii. Body repair, immune competence, energy conservation, etc.
2. NREM and REM and Polysomnograms
a. NREM Sleep Physiology
i. Physiology
o Decreased HR, BP, tidal volume, skeletal muscle tone, and CBF
o Regular ventilation, except NREM1
ii. NREM1
o Low-amplitude spiked frequency
iii. NREM2
o Sleep spindles and K complexes
iv. NREM3
o Slow waves
b. REM Sleep Physiology
i. Tonic Phenomena
o Desynchronized cortical EEG
o Voluntary muscle atonia
o Impairment of thermal regulation
o Dreams, increased CBF
o Erections, clitoral engorgement
ii. Phasic Phenomena
o Irregularly accelerated HR and RR
o Muscle twitches, REMs
o Ponto-geniculo-occipital (PGO) and sawtooth waves
3. The NREM and REM Sleep Centers and the
a. NREM Sleep Center—Ventral Lateral Preoptic Nucleus (VLPO)
i. Projects to and inhibits:
o Ascending ACh and monoamine arousal neurons
o Hypocretin neurons in lateral hypothalamus
ii. Receives inhibitory inputs from the ascending monoamine arousal neurons
b. REM Sleep Center
i. Sleep-on cells in subcoeruleus region in pontine tegmentum
o Transmits excitatory signal (Glu, ACh) to ventromedial medulla which transmits an inhibitory signal (Gly, GABA) to anterior horn of spinal cord
o Causes muscle paralysis/atonia
ii. Sleep-off cells in locus coeruleus (NE) and raphe nucleus (5-HT)
4. The Wake Promoting Systems
a. Ascending Arousal Systems
i. Acetylcholine System
o Originates in pontine tegmentum
o Projects to thalamus
o Facilitates transmission of sensory information to cortex
ii. Monoamine System
o Originate in locus coeruleus, raphe nuclei, periaqueductal gray (DA), and tuberomamillary nucleus (hist.)
o Project to lateral hypothalamus (hypocretin), VLPO (GABA), and cerebral cortex
o Activates the cortex to facilitate thalamic inhibition of VLPO
b. Alertness Stabilizing System
i. Hypocretin/Orexin System
o Originates in posterolateral hypothalamus
o Projects to cerebral cortex and ascending monoamine and cholinergic neurons
o Stabilizes wake state—functions in supervisory role
§ Strengthens arousal signals, thereby enhancing inhibition of VLPO sleep signals
§ Activated VLPO inhibits both hypocretin and arousal signals, inducing sleep
ii. Narcolepsy is deficiency of hypocretin
5. Control Mechanisms of Sleep
a. Homeostatic Control
i. Proportional increase in sleep drive with increased duration since last sleep period
o Increases throughout the day until quenched by sleep
ii. Due to increasing adenosine in VLPO
o Caffeine is adenosine receptor antagonist, inhibiting VLPO-adenosine-regulated sleep homeostasis
b. Circadian Regulation
i. Located within suprachiasmatic nucleus of hypothalamus
ii. Genetic Control
o Per and Tim genes produce auto-inhibitory proteins against their transcription, providing molecular oscillation over a circadian cycle
o AD mutation in similar human gene causes familial advanced sleep phase syndrome
iii. Drive to wakefulness varies rhythmically
o Susceptibility to sleepiness is most apparent from 2-8AM and 2-5PM
o These periods will be more intense during periods of sleep deprivation
6. Effects of Sleep Deprivation
a. Fatigue and sleepiness
b. Impaired short term memory
c. Decreased speed of data perception
d. Impaired information processing and decision making
Mood changes—irritability and decreased energy |
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Term
|
Definition
| Abrupt development of a focal neurological deficit due to a vascular cause |
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Term
|
Definition
- same clinical syndrome as a stroke, but resolves completely <24 hrs
- without permanent brain injury (old definition)
- with modern imaging, most events>several hours=infart
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Term
| Epidemiology of Strokes in US |
|
Definition
- 750K new strokes each year
- 3rd leading cause of death
- Leading cause of serious disability in adults
- 4.5 million stroke survivors
- COST $45 BILLION/year
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Term
| Aftermath of Stroke and Risks |
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Definition
- in ~25% the stroke progresses during hospitalization
- mortality 30 days 8-20%
- 1 year 15-25%
- 5 years 40-60%
- complete or partial dependence (disability) about 25-50%
- 35 % have persisting dementia @1yr-risk factor for Alzheimer's
-
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After TIA
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After Stroke
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30 days
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4-8%
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3-10%
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1 yr
|
12-13%
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5-14%
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5 yr
|
24-29%
|
25-40%
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Term
| Annual Risk of Stroke or Vascular Death |
|
Definition
i. Symptomatic carotid stenosis
o Stroke—16.2%
o Vascular death—2.9%
ii. Major Stroke, Minor Stroke
o Stroke—9%, 6.1% respectively
o Vascular death—3.5%, 3.2% respectively
iii. TIA
o Stroke—3.7%
o Vascular death—2.3%
iv. Transient monocular blindness
o Stroke - 2.2%
o Vascular death – 3.5%
v. Asymptomatic stenosis
o Stroke - 1.3%
o vascular death – 3.4%
vi. General elderly population
o stroke – 0.6%
o vascular death – 1.0% |
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Term
| Causes of mortality at 5 years in stroke pts |
|
Definition
- 18% stroke, 39% CV condition
- Consider atherosclerosis as a central heart DZ with slerosis radiating
- carotids become atherosclerotic before femoral arteries
- if femoral arteries have atherosclerosis there is ~100% chance of carotids having it
- Cornary artery disease, cerebrovascular disease, and peripheral arterial disease
- Typically if you have one, you have another one that coexists
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Term
|
Definition
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|
Term
|
Definition
o hemorrhage into the substance of brain
o Basal ganglia (esp. lateral putamen) is MC site (40%) > cerebral hemispheres = thalamus (20% each) > pons = cerebellum (10% each)
o HTN is MC cause
o Other causes:
§ Anticoagulants
§ Amyloid angiopathy—dementia, increasing age, Alzheimer’s
§ AVMs—young pts
§ Venous sinus thrombosis, cerebral mets, trauma
§ Cerebral metastases
§ Trauma
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Term
|
Definition
| Caused by a variety of things, but it's where there isn't enough blood flow to an area |
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|
Term
|
Definition
o AFIB is MC embolic cause
§ 2nd MC ischemic stroke
o PFO and ASD is found in 40% of young (<45 yo) pts with cryptogenic stroke
§ Associated with migraines, more in women
§ Closure touted as a cure for both stroke and migraine
o Aortic atherosclerosis is cause of 30% of cryptogenic stroke
o Acute anterior wall MI, endocarditis, myxoma, etc. |
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|
Term
| Atherosclerotic Large Vessel 20% |
|
Definition
o Acute plaque rupture and thrombotic occlusion à hypoperfusion à ischemia or artery-to-artery embolism à ischemia or combination of hypoperfusion and impaired washout of emboli
o Carotid atherosclerosis—MC cause in USA
o Intracranial atherosclerosis
§ African American, Asian > Caucasian
§ Women > men
§ DM > non-DM
o Hypercoagulable states, dissection |
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|
Term
| Lacunar or Small Vessel Stroke |
|
Definition
o Lipohyalinosis—small penetrating arteries < 200 micron diameter
§ MCA and basilar artery perforators à disorganization and disruption of lumen with hyaline material à occlusion à ischemia à necrosis à “lacune”
o HTN is biggest risk factor
§ Increased in African Americans |
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|
Term
| Misc. Causes of Ischemic Strokes |
|
Definition
o Drugs, pregnancy, hypercoagulable states, venous thromboses, migraine, oral contraceptives, trauma, etc. |
|
|
Term
|
Definition
i. Large vessel ischemia
o Embolic—sudden
o Thrombotic—maximal at onset
ii. Small vessel ischemia—progression over minutes or stuttering over hours
iii. Intracranial hemorrhage
o Intracerebral hemorrhage—steadily progressive over minutes-to-hours
o SAH—instantaneous Sx and maximal at onset |
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Term
| Patent Foramen Ovale and ASD and Strokes |
|
Definition
i. general population 25-30% remain probe patent
ii. stroke lifetime risk 1:6 ~17%
iii. Associated with Migraine (females = 18%, Males 6%)
iv. closure touted as cure for stroke and migraine
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|
Term
|
Definition
a. Sx onset
i. large vessel ischemia
o embolic --> sudden onset
o thrombotic -->sx maximal at onset or stuttering over minutes/hours
ii. small vessel ischemia -->progression over minutes or stuttering over hours
iii. intracranial hemorrhage:
o intracerebral hem. --> steadily progressive over minutes/hours
o subarachnoid hem.--> sx instantaneous and maximal at onset
iv. sx variable in type/intensity depending on vessel. brain region involved
o BOTH Large and SMALL vessel: weakness, paralysis, or incoordination; numbness or tingling; ataxia, gait instability, vertigo; double vision
o Large vessel only: visual loss (transient monocular is called amaurosis fugax; binocular = hemianopsia); cognitive dysfnx including aphasia and neglect; decreased level of consciousness; agitation or confusion; memory loss
o Hemorrhage: sudden headache with nausea and vomiting
b. Carotid Territory Stroke Pattern (NOT SPEC. MENTIONED IN STUDY GUIDE)
i. Paralysis and numbness
o Face and arm > leg
§ MCA > ACA
ii. Higher Cortical dysfxn
o Aphasia—dominant hemisphere
o Neglect—non-dominant hemisphere
§ Anosognosia—pt is unaware of disability
§ Asomatognosia—pt does not recognize disability in body
§ Difficulties with visuospatial reasoning, music appreciation
§ Aprosody—emotional context of speech is lost
iii. Visual loss
o Homonymous hemianopsia
o Amaurosis fugax—transient monocular blindness due to severe ipsilateral ICA stenosis
c. Typical L ICA Territory Stroke—MCA or ICA Occlusion
i. Aphasia—mute
ii. Right homonymous hemianopsia
iii. Right face and arm weakness and numbness > leg
iv. Forced gaze deviation to the left
o Eyes look toward stroke lesion!
§ Right FEFs drive eyes left
§ Dysfxn of left FEFs cannot drive eyes right
d. Typical R ICA Territory Stroke—MCA or ICA Occlusion
i. Left hemineglect
ii. Left homonymous hemianopsia
iii. Left face and arm weakness and numbness > leg
iv. Forced gaze deviation to right
o Dysfxn of right FEFs cannot drive eyes left
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|
Term
| Vertebro-Basilar Territory Ischemia (know this!!!!!) |
|
Definition
- Transient loss of consciousness (very rare without other neurological signs)
- most of these episodes are actually cardiovascular
- croosed motor-sensory Sx
- Ataxia, gait instability, vertigo
- Diplopia- b/c CN III, IV, and VI abnormalities due to midbrain and pons dysfxn
- Bulbar dysfxn--slurred speech due to loss of control of lips/face
- Memory loss
- Isolated homonymous hemianopsia or cortical blindness
- Bilateral occipital lobe dysfxn
- decreased level consciousness
- dysfxn of ascending reticular arousal systems
- sudden headached with nausea and vomiting
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Term
| Middle Cerebral artery Stroke |
|
Definition
- Most of lateral cortex of cerebral hemispheres
- areas involved in speech, language, and swallowing
- Broca's area, wernicke's area, Heschl's gyrus, angular gyrus
- Corpus Striatum=esp. internal capsule
- Left middle cerebral artery=aphasia and apraxia
- right MCA=left side neglect, prosopagnosia (inability to recognize faces), cognitive problems (including agnosia)
- either MCA=hemiplegia or hemiparesis, as well as contralateral hyposthesia
- damage to internal capsule=UMN dysarthria and dysphagia
- Damage to either MCA=hemianopsia (loss of sight in one half of the visual field. Blindness affects contralateral aspect of both visual fields)
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|
Term
|
Definition
- Aphasia-mute
- R. Homonymous Hemianopsia
- R. Face and arm weakness>Leg
- Forced Gaze deviation to left
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|
Term
|
Definition
- Left hemineglect-- complete Left inatention
- left homonymous hemianopsia
- Left. face and arm weakness>leg
- Forced Gaze deviation to Right
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|
Term
| Higher Cortical Dysfunction |
|
Definition
- Aphasia- Dominant (left) hemisphere- Language Disturbance (not dysarthria)
- Broca's
- Wernecke's
- Mixed
- Neglect- Nondominant (right) hemisphere
- anosogonsia
- Asomotognosia
- Extinction
- Complete hemineglect
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|
Term
Lacunar Syndromes (KNOW THIS!!!!)
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|
Definition
a. Pure Motor Stroke/Hemiparesis
i. Most Common lacunar syndrome
ii. Hemiparesis/hemiplegia affects face, arm, and leg equally or face and leg to lesser extents
iii. Transient sensory Sx (but not signs)
iv. Dysarthria and dysphagia
v. Lacune is usually in posterior limb of internal capsule carrying the descending corticospinal and corticobulbar tracts, or basis pontis
b. Ataxic Hemiparesis
i. 2nd MC lacunar syndrome
ii. cerebellar and motor sx
iii. Ipsilateral weakness and clumsiness
iv. Affects leg > arm
o “Homolateral ataxia” or “crural paresis”
v. Onset over hours to days
vi. Frequently infarcts are in posterior limb of internal capsule, basis pontis, and corona radiata
c. Dysarthria and Clumsy Hand
i. variant of ataxic hemiparesis
ii. Lesion in the pons
iii. Weakness in hand most prominent with writing
d. Pure Sensory Stroke
i. Persistent or transient numbness or paresthesias on one side of body
ii. Occasionally complaints include pain, burning, or unpleasant sensations
iii. Infarct is in thalamus usually
e. Mixed Sensorimotor Stroke
i. Hemiparesis or hemiplegia noted with ipsilateral sensory impairment
ii. Infarct in thalamus and adjacent posterior internal capsule (carotid and vertebrobasilar territories)
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|
|
Term
|
Definition
- Mass lesions-cancers, mets, abscesses, etc
- subdural hematoma
- somatization-psychiatry issue: MC
- Migraine, seizure
- Hypo and hyperglycemia
- Fever and infection in elderly wit prior brain injury (esp UTIs)
- Demyelination MS, acute disseminated encephalomyelitis
- Transient Global amnesia
- Encephalitis-HSV-1
- Cerebritis- Lupus
- Inherited metabolic derangements- Mitochondrial encephalopathies
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Term
| Treatment of stroke- The basics |
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Definition
a. Treatment Strategies
i. Early recognition, evaluation, and Dx
ii. Rapid initiation of reperfusion therapy
iii. Neuroprotectants
iv. Life-saving surgery for hematomas and malignant cerebral edema
b. Therapeutic Options
i. Antithrombotics—aspirin is effective and safer than heparin
c. Prevention Strategies
i. Try to lessen HTN, hyperlipidemia, DM
ii. Lifestyle changes—smoking cessation
iii. AFIB awareness
o Warfarin with INR 2-3 is standard of care unless a contraindication exists (GI or intracerebral bleeds)
§ Reduces stroke risk by 60-70%
o Lone AF can be tx with aspirin
d. Therapeutic options Ischemic Stroke- Standard approach = Antithrombotics
i. Heparin – unproven value acutely
o relatively contraindicated in first week post-op
o increases risk of hemorrhagic conversion
ii. Aspirin = SAFE, proven but small benefit
e. A Fib = most common cause of embolic stroke
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Term
Carotid Stenosis Treatments |
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Definition
a. Extracranial Carotid Stenosis
i. Carotid endarterectomy—remove intima and media with atherosclerotic plaque
o Patient must be otherwise healthy
o Significant risks of perioperative stroke and death
ii. Carotid artery stenting
o For medically ill pts with high-surgical risk
o Does not require general anesthesia; shorter hospitalization
o Lower risk of MI and re-stenosis
o No risk of cranial nerve injury
b. Intracranial Carotid Stenosis
i. Tend to be younger than other strokes
ii. Stenosis location:
o Basilar Artery = Middle and Proximal >> Distal;
o ICA = terminal, cavernous, petrous
o MCA = M1
o VA= V4
iii. Differential Dx includes vasculitis, dissection, recanalized embolism, moyamoya arteriopathy, radiation arteriopathy
iv. Aspirin 1300mg is as effective and safer than warfarin
v. Angioplasty and stenting are emerging therapies for Tx
o Reduce risk of stroke by remodeling vessel stenosis = improve flow and ↓ embolization
o investigation except in patients who fail medical therapy
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Term
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Definition
a. Presenting manifestations are catastrophic
i. Ipsilateral severe headache precedes or occurs with stroke
ii. SAH is common with intracranial dissection
b. Risk factors include:
i. Trauma
ii. Fibromuscular dysplasia
iii. Collagen disorders—Ehlers-Danlos, Marfan’s, etc.
iv. Chiropractic manipulation
v. Migraine
c. mechanism
i. unknown
ii. elevated serum elastase activity increased in migraine
o matrix degradation
d. Typically have excellent prognosis and vessels heal completely (spontaneous)
e. DZ of younger patients
f. ICA dissection-->ipsilateral Horner’s, aphasia or neglect (L or R, respectively), contralateral paralysis
(could not find this in our notes)
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Term
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Definition
i. First CT the brain
o If (+) à CT angiogram/digital subtraction angiography (DSA)
o If (-) à LP
§ If (-) à DSA
ii. Treat HTN to systolic < 140mmHg
iii. Remove intracranial components causing increased ICP
o Ventriculostomy
o Decrease BP
iv. Maintain Cerebral Perfusion
v. Monitor for Cerebral Vasospasm
o major cause of morbidity – causes ischemic stroke
o Triple “H” therapy = hypertension, hypervolemia, hemodilution
o Nimodipine q 2 hr
o TCD
o Frequent neurological assessment
o multimodal monitoring
vi. Monitor for hydrocephalus and meningitis
vii. Clipping
o For non-moribund pts with various aneurysms
§ MCA, Pcom, Acom, etc.
o Fusiform and wide-necked aneurysms
o Large Hematomas
viii. Coiling
o For moribund pts—less complications with coiling
o Vertebrobasilar and ICA aneurysms – Pcom and Acom |
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Term
| Acute Treatments of Ischemic Stroke |
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Definition
i. Focus on time of onset—duration of ischemia is crucial to minimize
o ischemia < 5 mins rarely = infarct
o ischemia >15 mins almost always = INFARCT
ii. Physical (NHSS at minimum)
o Look for Horner’s
o Listen for Bruits and Funduscopic exam; Cardiac Exam
o Vascular – pulses and pressures
o Skin/Extremities
iii. Order a CT without contrast
o Differentiates ischemic and hemorrhagic stroke
o Very fast
o NEVER INITIATE TX WITHOUT CT!!!
iv. MRI
o Benefits—superior by providing vascular anatomy and differentiates irreversible brain injury from salvageable, non-functioning tissue
o Drawbacks—takes a long time, not as readily available, may not be tolerated by pts
v. Follow ABC &Ds and then:
o Manage increased ICP, severe HTN, dysphagia/nutrition status, and body temp
o Isotonic fluids without dextrose are preferred to avoid brain swelling/edema and injury from (avoid hypotonic fluids)
o Must monitor blood glucose—brain is intolerant of hypo- and hyperglycemia
o A = Airway = intubate if patient is comatose
o B = Breathing = Immediately initiate O2
o C = Circulation
vi. Monitor for decreased level of consciousness, ipsilateral papillary changes, contralateral hemiparesis, posturing (too late)
vii. Optional imaging studies
Mandatory analysis in all strokes (couple of slides – not indicated on study guide, but for completion if you so desire) |
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Term
| CT w/o Contrast pros and Cons |
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Definition
i. this is a requisite in all stroke/TIA patients
o complete within 30 minutes
ii. differentiates between ischemic and hemorrhagic strokes
iii. never initiate any therapy without a CT (except ABCD’s)
iv. excludes intracranial tumors and vascular malformations, which are contraindications to most revascularization therapies |
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Term
| Pros/COns MRI angiography |
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Definition
i. Benefits:
o superior in diagnosis (esp. ultra-acute)
o gives vascular anatomy
o differentiates areas of irreversible brain injury from salvageable but non-functioning tissue
ii. Cons:
o not as rapid as CT and not as readily available |
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Term
| What happens with increased Intracranial Pressure |
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Definition
a. 2 bad things happen:
i. cerebral blood flow and oxygen delivery are reduced (ischemia)
ii. displaced volume mechanically damages the brain (brain tissue shift) |
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Term
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Definition
- Limits Ischemic damage and is neuroprotective
- Proven by several studies
- Hypothermia has significantly decreased infarct volume and extended time required for damage to occur ("window")
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i. decreases metabolic demand, Ca2+ influx, and formation of free radicals
ii. limits lipid (membrane) peroxidation
iii. decreases inflamm. response
iv. preserves endothelium/ BBB
v. limits reperfusion injury
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Term
| Other Neuroprotective Agents |
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Definition
- Preserves Neural tissue despite continued Ischemia
- May expand tx window for reperfusion Tx
- Usually pharmacological agents
- Primarily NMDA/Ca2+ inhibitors
- Et-Oh and Caffeine most potent known agents
- works great in rats, does not work in human (intolerable side effects)
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