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IPAP JUNIOR SEM. > Neuro Last Test > Flashcards

Neuro Last Test Flashcards

1
Q

Define vertigo

A

A sense of rotational motion. Indicates a dysfunction with the vestibular pathways

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2
Q

Define disequilibrium

A

Being “unsteady”
About to fall
And is often associated with some type of abnormal gait

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3
Q

Define light headed es

A

The sensation that one is about to faint

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4
Q

Define presyncope

A

Presyncope: used to describe a transient cerebral hypo perfusion. Often a prodrome to a true syncopal event

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5
Q

What is benign disequilibrium of aging

A

Multiple-sensory-defect dizziness :

Elderly when walking

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6
Q

Define syncope

A

A transient decrease in blood flow to the brain, resulting in a loss of consciousness.

Characterized by sudden loss of consciousness, and postural collapse, with spontaneous recovery.

Will be experienced by at 30% of the adult populations and accounts for about 3% of ER visits

So…..anything that decreases blood flow and decreases O2 to the brain can cause syncope

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7
Q

What are the 3 types of Syncope

A

Neurally mediated

Orthostatic HOTN

Cardiac Syncope

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8
Q

What are the two types of Neurally mediated syncope

A

Vasovagal and reflex

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9
Q

Define Vasovagal Mediated Syncope

A

Provoked: fear, pain, anxiety, intense emotion, sight of blood, unpleasant sights and odors, orthostatic stress

Sympathetic withdrawal – vasodilation

Increased parasympathetic activity – bradycardia

They account for nearly 1/2 of all syncopal episodes

Often present with a prodrome – seconds to minutes before\
Diaphoresis, pallor, nausea, yawning

Rare in the supine pt

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10
Q

Refine reflex mediated syncope

A

specific localized stimuli that provoke the reflex vasodilation and bradycardia that leads to syncope

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11
Q

A pt presents with a LOC, first had TachyHR and now is Brady,
Has an ashen-grey color
(pallor in the conjunctiva)

Has a threads pulse and may have clonic jerks of the face and hands

They quickly regain consciousness with a brief ep of confusion

What type of syncope event is this

A

Vasovagal

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12
Q

A solider just passed out in formation from a Vasovagal syncopal event

What is the Tx

A

Place the patient in the supine position with feet slightly elevated

Feel improved pulse

Consciousness should gradually return

Treat underlying causes

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13
Q

Define Carotid Sinus Hypersensitivity

A

Caused by increased pressure on carotid sinus baroreceptors

Is a reflex syncope

Typically occurs after shaving, wearing a tight collar or simply turning the head to one side

Usually in men > 50 yo

S/S: Sinur arrest, AV blocks, vasodilation, mixed response

Cause; Afferent nerve fibers activate the efferent sympathetic nerve fibers in the heart and blood vessels

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14
Q

Define Situational syncope

A

A type of reflex syncope

Cause by an abnormal autonomic control

May involve a:

  • Cardio-inhibitory response
  • Vasodepressor response
  • or both

Can be from cough, deglutition, micturition, defecation

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15
Q

Define glossopharngeal neuralgia

A

Likely involves activation of afferent impulses in the glossopharyngeal nerve that terminate in the nucleus solitarius of the medulla

Less likely to have a benign origin: vascular compression, MS, or tumors.

Many cases are idiopathic.

More prevalent in elderly

Symptoms – bradycardia, hypotension, fainting, and asystole

Pain very similar to Trigeminal Neuralgia

Sharp, repetitive pain precipitated by:
Swallowing 
Chewing
Talking
Yawning
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16
Q

What is the Tx approach to Glossopharyngeal Neuralgia

A

Start with:
-Carbamazepine (anti-epileptic drug)

If meds fail consider surgical intervention

Microvascular decompression if vascular compression is evident

Rhizotomy of Glossopharyngeal/Vagal fibers

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17
Q

Define Ortho HOTN

A

systolic blood pressure drop of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg within 3 min of standing

Common causes:
Polypharm
Diabetes, Dehydration, being weak

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18
Q

What is the Tx approach to Ortho HOTN

A

1st: remove causes
(meds if applicable)

2: mitigate risk

3: if unable to still control
Consider: with fludrocortisone acetate and vasoconstricting agents (midodrine, L-dihydroxyphenylserine, and pseudoephedrine )

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19
Q

A Pt presents with syncope without any prodrome, asso with exertion or post exertion

What type of syncope is high on the DDx

A

Cardiac Syncope

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20
Q

What is the likely cause of syncope when it occurs when the pt is lying down

A

CV

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21
Q

A pt presents with Impulsion, oscillopsia, N/V, and gait ataxia

Think

A

Vertigo

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22
Q

What is the DIx-Hallpike maneuvaer

A

This test is performed by rapidly moving the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side.

Test for Vertigo causes

This is performed initially for the posterior semicircular canals.

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23
Q

What are saccades and pursuits of the eye

A

Saccades – fast eye movements

Pursuit – slow eye movements

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24
Q

A pt presents with long episodes of iunchanging dizziness

Not affected by head position or movement

+nystagmus

With hyper reflexia, ataxia, and dysarthria

Is this central or peripheral vertigo

A

Central

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25
Q

A pt presents with intense short lived epidsodes of dizziness, typically effected by head position, with HORIZONTAL nystagmus without vertical nystagmus, with inner ear sxs, and hearing abNML

What kind of vertigo is this?
Peripheral or central ?

A

Peripheral

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26
Q

Describe vestibular neuronitis

A

Usually a single attack, with paraoxysmal vertigo

Has preserved auditory function

Lasts several days to weeks

May be related to viral illness

+nystagmus

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27
Q

What is the Tx for Vestibular neuronitis

A

Most Pts recover spontaneously
Glucocorticoids may improve outcome
—if given in first 3 days

Vestibular Suppressant meds
—Diazepam (benzodiazepine) 5 to 10 mg every twelve hours
—Meclizine (antihistamine) 25 to 50 mg every eight hours

Vestibular therapy if not completely resolved over time

No proven benefit to Antivirals !

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28
Q

Describe labyrinthitis

A

Same S/s as vestibular neuronitis WITH hearing loss

Cause unknown
Hearing loss can be perm.

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29
Q

What is the Tx approach to Labrythitis

A

TX:
ABX
-If febrile
-Signs of infection

Vestibular suppressants in acute phase

  • Diazepam
  • Meclizine
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30
Q

What is the major diff between vestibular neuronitis and labrynthitis

A

Hearing loss is not preserved in labrythitis

Treatment for Vestibular involves steroid (glucocorticoids)

And Labrythinitis does not

Both treatments involve Diazepam and/ or meclizine

Labrythitis can get ABX if fever

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31
Q

What is the MC cause of vertigo following a concussion

A

Labyrinthine Concussion- Traumatic Vertigo

Sx usually diminish after several days

If associated with basilar skull fracture:

  • Severe vertigo
  • Lasting several days to weeks
  • Deafness in affected ear

Chronic Post-traumatic may result from cupulolithiasis

  • This causes excessive cupular deflection with head movement
  • Causing episodic positioning vertigo
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32
Q

A pt presents with labrynthitis s/s following a head concussion

What is the tx appraoch

A

Supportive care
Vestibular suppressants
-Diazepam (benzodiazepine)
-Meclizine (antihistamine)

Vestibular therapy

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33
Q

What is the Triad of Menieres Dz

A

TRIAD

  1. Unilateral deafness
  2. Episodic/paroxysmal vertigo
  3. Unilateral Low freq. tinnitus
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34
Q

A pt presents with vertigo lasting from minutes to days, unilateral deafness, and unilateral low freq tinnitus

What is the likely pathology

A

This is the triad of Menieres Dz

Pathology: thought to be 2ndary to excess fluid in the inner ear

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35
Q

For a pt with fluid found in the middle ear and the triad of Menieres dz what must you submit the pt for

A

DX: Audiometry for all patients!

Consider Vestibular testing and MRI.
- Sometimes can only be made for certain on pathologic examination of a gross-section of the cochlea (biopsy)

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36
Q

What is the Tx approach to Menieres Dz

A

Change Diet: avoid high salt, caffeine, alcohol, nicotine, and MSG

Reduce Stress,
Diuretics to remove excess fluid
(HCTz/ Triamterine)

N/V: Meclizine, scopolamine, and diazepam

+/- Hearing aids

Last stage: SRGRY or middle ear injection with ABX (genta)

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37
Q

What causes a perilymphatic fistula

A

Caused by
Leakage of perilymphatic fluid from the inner ear that drips into the tympanic cavity

Most cases are caused by:
Physical injury:
-Blunt head trauma or a Hand slap to the ear
Extreme barotrauma: Air flight or Scuba diving
Vigorous Valsalva maneuvers: Weight lifting or Cough/Sneeze
After middle ear surgery

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38
Q

What is the Tx for perilymphatic fistula

A

Conservative Management: bed rest, head elevation, and avoidance of straining

Failure to resolve after several weeks of conservative therapy is an indication to consider a surgical patch of the oval or round window

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39
Q

A pt presents with benign paroxysmal postional vertigo

What are the common S.s

A

Brief, sudden episodes of severe vertigo

Typically w/ nausea & vomiting

Occur with change in head position/posture

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40
Q

What is the management of BPPV (vertigo)

A

Meclizine q 4-6 hrs
Valium 5mg TID
+/- scopalamine patch

+ Epley maneuver

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41
Q

Define acoustic neuroma

A

Benign tumor arising from the sheath of CN VIII in the internal auditory canal

AKA, Acoustic schwannoma
Arises from the Schwann cells
(Dip in the 4000 MgHrtz)

MC to CN VIII
Can be in CNV or VII

Presents with insidious onset hearing loss; also tinnitus, HA, vertigo, facial weakness

Unilateral Sensorineural hearing loss on exam

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42
Q

What is the presentation, Dx and Tx of Acoustic Neuroma

A 
Presentation
May be asymptomatic
Loss associated with the affected CN
Hearing loss
Vestibular symptoms
Facial paresthesia
Pain

Imaging: MRI with contrast

TX
If symptomatic, non-compressible, and < 3 cm
Stereotactic radio surgery – gamma knife

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43
Q

What is the best test to find a Acoustic Neuroma

A

MRI with contrast

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44
Q

Define Vestibular migraine

A

Episodic vertigo

Temporarily related to HA

Lasts from minutes to hours

Have have a positioning component

Disequilibrium may last days to weeks

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45
Q

Define central disorders that cause vertigo

A

Central vertigo is due to a disease originating in the CNS

Lesions within the brain itself
—Cerebellum
—Pons

Disorders present with ataxia, vertigo and often with nystagmus
(Central S/s)

Symptoms present slowly over several months

Little or no change in symptoms with head movement

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46
Q

A tumor in the cerebellum would present with

A

Incoordination

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47
Q

A tumor that is in the basal ganglia would present with

A

Impaired postural reflexes

Basal ganglia: are the caudate nucleus, putamen, and globus pallidus in the cerebrum

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48
Q

A tumor that is in the sensory tracts would present with

A

ABNML proprioception

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49
Q

What are the causes of chronic central vertigo

A

MS
ETOH induced
Hypothyroid
Congenital

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50
Q

What are the 5 common causes of central vertigo

A
  • Vertebrobasilar Ischemia/Insufficiency
  • Vertebrobasilar TIA or Stroke
  • Tumors
  • Multiple Sclerosis (demyelination) (p
  • Neurodegenerative conditions that include the vestibulocerebellum
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51
Q

A pt presents with vertigo plus Diplopia
Dysarthria
Ataxia
Numbness

Think:?

A

Central Vertigo cause

Vertebrobasilar Ischemia/Insufficiency

Order an MRI (ischemic infarct)
and send to higher level of care

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52
Q

Describe a TIA or Stroke

A

Caused by infarcts into the medial branch of the PICA

Sudden onset
Difficulty maintains posture
Infarct or hemmorghe

Order a CT/ MRI

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53
Q

How do you manage a TIA or Stroke

A 
Workup
R/O
Anemia
Pregnancy
Glucose derangement
MRI preferred modality to detect:
Infarction
Hemorrhage
Tumor
White matter lesions of MS

Intra-arterial angiography to Dx:
Occlusions
—This getting supplanted by CT angiography, noninvasive
MR angiography, and Doppler US

Central causes: Referral to higher care

Wernicke’s = Thiamine replacement
MS flare – Prednisone burst

Avoidance of offending agents.

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54
Q

What do you treat wernickes stroke with

A

Thiamine replacement

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55
Q

What do you treat a MS flare with

A

Presdnisone

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56
Q

What are the drugs that can cause central vertigo

A

Gentamycin
Salicylates
Quinine
Cis-platinum

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57
Q

Define SZR

A

Seizure: transient occurrence of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.

Aura: brief symptoms that may precede the onset of some seizures

Epilepsy: group of disorders characterized by recurrent seizures

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58
Q

What are the three Etiologies of SZR

A

Primary CNS dysfunction

Underlying systemic disease

Drug induced

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59
Q

What are the 5 physiological conditions that can lead to SZR

A

HOgl (if glucose less than 30)
HONa+ ( is less than 120)
Hyperosmolar (Non Keto Hypergl)
HOCa2+ (less than 9.2, with or without tetany)
Uremia (greater than 19, or rapid decline in KD function)

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60
Q

What is the approach to evaluating a SZR

A
  1. Real or not?
  2. Clues to predisposition
    (Head truama, Stroke, tumor)
  3. Precipitating fxs
    (Sleep deprivation, drugs, alcohol)
  4. Infection? Systemic illness?
  5. Truama?
  6. Complete Neuro Exam
  7. Order Labs, glucose, calcium, BMP, ESR, BUN, Cr, LFTS
  8. Initial SZR imaging is a MUST!
    (MRI is superior to CT)
    (In ER CT non con is sometimes best)
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61
Q

What does a FTA-ABS lab test

A

Syphillis

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62
Q

Focal vs gen SZRs

A

Focal Seizures:

  • Originate within networks limited to one brain region
  • Previously called partial seizures

Generalized Seizures:
- arise within and rapidly engage networks distributed across both cerebral hemispheres

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63
Q

Describe a focal SZR with INTACT awareness

A

Motor manifestations
Tonic: muscles stiffen

Myoclonic: extremely brief (<1sec) muscle contraction

Clonic: rhythmical muscle contractions

Two Named Versions
-Jacksonian March
seizure activity over a progressively larger region of motor cortex
-Todd’s Paralysis
localized paresis for minutes to hours in the involved region following the seizure

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64
Q

What is Jacksonian March

A

Jacksonian March:

seizure activity over a progressively larger region of motor cortex

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65
Q

What is Todds Paralysis

A

Todd’s Paralysis:

localized paresis for minutes to hours in the involved region following the seizure

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66
Q

Describe Focal SZR with IMPAIRED awareness

A

Transient impairment

Unable to maintain nl contact w/ environment

Unable to respond appropriately

Impaired recollection of the ictal phase
-Aura
-Automatisms
—involuntary, automatic behaviors that have a wide range of manifestations
—chewing, lip smacking, swallowing
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67
Q

Describe an absent SZR

A

Sudden, brief lapses of consciousness

Lasts for seconds

No postictal concussion

No loss of postural control

Onset childhood/early adolescence

100s X per day

“Daydreaming”, Decline in school performance

Electro physiologic hallmark (typical)
Generalized, symmetric, 3-Hz spike-and-slow-wave discharges that begins & ends suddenly, superimposed on a nl EEG background

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68
Q

What is the most common SZR type in a metabolic derangement

A

Gen Tonic Clonic SZR

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69
Q

What are the three phases of a GEn Ton Clon SZR

A

Tonic phase to Clonic Phase to Postictal phase

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70
Q

What is the Tonic phase of a Gen Ton Clon SZR

A

Tonic Phase: extension of body

Lasts about 10-20 seconds

May have apnea
Tongue biting

EEG: progressive increase in generalized low-voltage fast activity, followed by generalized high-amplitude, polyspike discharges

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71
Q

What is the clonic phase of a Gen Ton Clon SZR

A

Clonic Phase: alternating muscle contraction and relaxation

Lasts no more than 1 minute

EEG: high-amplitude activity is typically interrupted by slow waves to create a spike-and-slow-wave pattern

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72
Q

Describe the postictal phase of a Gen Ton Clon Phase

A

Postictal Phase:
Unresponsiveness & muscular flaccidity

Excessive salivation

Bladder or bowel incontinence may occur at this point

Postictal confusion for minutes to hours

EEG: diffuse suppression of all cerebral activity, then slowing that gradually recovers as the patient awakens

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73
Q

Describe an Atonic SZR

A

Sudden loss of postural tone

Lasts 1-2 seconds

Consciousness is briefly impaired

Zero postictal confusion

EEG: brief, generalized spike-and-wave discharges followed immediately by diffuse slow waves that correlate with the loss of muscle tone

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74
Q

Describe a Myoclonic SZR

A

Cause sudden jerking in the muscles

May involve one part of the body or entire body

Normal common form (physiologic form) is sudden jerking movement and when falling asleep

Pathologic form is associated with metabolic disorders, degenerative CNS disease or anoxic brain injury

EEG: bilaterally synchronous spike-and-slow-wave discharges

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75
Q

What is the main type of SZR in epilepsy

A

Gen Clon Ton SZR

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76
Q

What is the pt education for Epilepsy

A

No heavy machinery or at heights,

No swimming alone

Patients with epilepsy are generally undereducated and underemployed for their level of function

Issue of driving must be addressed: most states require a 3-18 month seizure-free period before pt may resume driving

Medical Providers are responsible to
warn patients of danger to themselves or others when driving with uncontrolled seizures

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77
Q

What is the gen appraoch to SZR treatment (epilepsy)

A

Underlying cause!
Avoid triggers
Alcohol or stress, sleep deprivation

Rx is the mainstay

Always watch for new rash/ Steven Johnsons syndrome!

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78
Q

What is are the Rx options for Absence SZRs

A

Valproic acid

Ethosuximide (Zarontin)
—May cause bone marrow suppression

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79
Q

All anticonvulsants have what side effects

A

All anticonvulsants may lead to hematologic or hepatic toxicity

CBC and LFTs at 2 weeks, 1 month, 3 months, 6 months, and every 6 months

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80
Q

What are the Rx options for Focal SZRs

A

1st line

Lamotrigine (Lamictal)
SE/AR: Stevens—Johnson Syndrome

Carbamazepine (Tegretol)
SE/AR: leukopenia, aplastic anemia, heptotoxic

Oxcarbazepine (Trileptal)
SE/AE: less risk of the above

Phenytoin (Dilantin)
Awful Cosmetic SE/AR: Gingival
Hypertrophy (AVOID IN YOUNG PTS)

Levetiracetam (Keppra)
No known drug-to-drug interactions, great for elderly !!

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81
Q

What are the Rx options for Gen Clon Ton SZRs

A

First Line
—Lamotrigine (Lamictal)
SE/AR: Stevens—Johnson Syndrome

—Valproic acid
Laboratory testing is required to monitor toxicity because valproic acid can rarely cause reversible bone marrow suppression and hepatotoxicity.

—Levetiracetam
No known drug-to-drug interactions, great for elderly

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82
Q

When can you step down Tx for SZRs

A

Seizure free x 1-5 years (typically 2)

Single Seizure type

NML Neuro Exam
No FMHx of Epilepsy
NML EEG

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83
Q

Define Status Epilepticus

A

Prolonged seizure activity lasting 5 minutes or more

Continuous seizure

Discrete, recurring seizures with unconsciousness during ictal period.

Is a medical emergency: -Cardiorespiratory dysfunction, hyperthermia, and metabolic derangements can develop

Mortality rate for adults with first episode of status epilepticus: 20%.

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84
Q

What are the common causes of Status epileticus

A

Anticonvulsant withdrawal/noncompliance
Metabolic disturbances
Hypoglycemia
Drug toxicity

CNS infection
CNS tumors
Refractory epilepsy
Head trauma

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85
Q

What are the Rx options to treat status epilepticus

A

First Line
Lorazepam, or Midazolam, or Diazepam

Followed by
Phenytoin or Fosphenytoin

If fails, then general anesthesia w/ ventilatory support

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86
Q

If a pt has recurrent SZRs despite RX tx,

What is the approach ?

A

Determine serum level of drug

MRI to rule out structural lesion

Evaluate lifestyle factors that may be contributing

Change to a second drug

Referral to neurologist if seizures are not controlled within three months

Treating refractory seizures: surgical excision, vagus nerve stimulation

If first drug achieved partial control, consider adding a second drug:
-referral

Best addressed with neurology consultation

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87
Q

What are the 3 most important pieces of HPI

A

Baseline Function

Time of Onset
—slow
—step wise
—acute?

Current meds

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88
Q

A pt presents (child) with sig high fever

What derm condition is indicative of meningitides

A

Skin rash of the lower extremities

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89
Q

What is the ABN number of a mini mental status exam

A

Less than 24 requires addition testing

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90
Q

What are the essential elements of a mental status exam

A 
Comprehension
Repetition
Fluency
Naming
Reading
Writing
Speech
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91
Q

What are the 5 types of aphasia

A

Global!
Conduction!

Transcoritcal motor
Transcoritcal sensory

Subcortical

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92
Q

What is global aphasia

A

Fluency is impaired, repetition is impaired, comprehension is impaired, may have a associated severe Right hemiparesis, caused by a large lesion in the Left hemisphere

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93
Q

What is conduction aphasia

A

Fluency is preserved, comprehension is preserved, but repetition is severely impaired . Naming and writing are also impaired.

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94
Q

Describe working memory

A 
<30 seconds
7 bits of information (+/- 2) 
Vulnerable to distraction
Anatomically related to the RAS, Prefrontal cortex, and Parietal lobe.
Tested with “repeat after me”
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95
Q

What is episodic memory

A

Lasts for minutes to many months or even years

Binds information about “What,” “Where,” and “When”

“Lay down” significant memories throughout the day which allows them to move through life connected to previous experiences.

Anatomically related to Hippocampus, Dorsomedial nucleus of the thalamus.

This is affected in thiamine deficiency.

Tested with word recall @ 3-5 min, or by asking of trivial events of the day – “What did you have for breakfast?”

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96
Q

Describe lasting memory

A

Lifelong – related to new protein synthesis and creation of new synapses

Lt. Anterior temporal lobe
And
Frontal lobe

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97
Q

What is the term Mental activities involved in planning, initiating, and regulating behavior.

A

Executive function

98
Q

Define delirium

A

Typically acute in onset
Responds to at least some stimuli appropriately
Can appear sleepy, disoriented, and inattentive
Level of consciousness may be impaired

Any age
Typically reversible

99
Q

define dementia

A

Typically chronic in onset with worsening over time
Usually appear “normal” but confused
Normal level of consciousness
Impairment in the content of consciousness

Typically more elderly (but not always!)
Irreversible

100
Q

What is the hallmark description of delirium

A

Hallmark description is waxing and waning levels of consciousness.

101
Q

What happens to GABA when a long term drinker stops drinking?

A

Decrease GABA

102
Q

A pt presents with anxiety, tachyHR, and agitation

PHx is +ETOH abuse
+delirium tremens

What is the D/o and Tx?

A

Withdrawal;

Treat with Benzo
upcoming Tx options Gabapentin

103
Q

What is the MC found vit deficiency in ETOH abuse

A

Thiamine deficiency Most Commonly in the chronic alcoholics

Leading to wernickes encephalopathy

Characteristic clinical triad of: -Ophthalmoplegia/ Nystagmus

  • Gait Ataxia
  • Global Confusion

Requires prompt Thiamine replacement

104
Q

A pt presents with Ophthalmoplegia/ Nystagmus, Gait Ataxia, and Global Confusion

What is this a classic triad of

A

Wernickes encephalopathy from Thiamine deficiency

105
Q

all patients with undiagnosed altered mental status, oculomotor disorders, or ataxia should receive …

A

Parenteral Thiamine

106
Q

What is Korsakoffs psychosis

A

Deficits in learning and memory may follow wernickes encephalopathy (Korsakoff’s psychosis) characterized by gaps in memory, confabulation, and disordered temporal sequencing.

107
Q

What is the main risk factor for dementia

A

Age, followed bu FMHx and Risease Risk

108
Q

A fall of 1.5 standard deviations below normal on standardize memory test is Dx of

A

Mild cognitive impairment

109
Q

Does Dementia impact function?

A

No

110
Q

What are the risk factors for Cognitive impairment leading to Dementia

A

Memory deficit >1.5 SD from the norm

Presence of Apolipoprotein ε4 allele

Small hippocampal volume & low CSF

FHx of dementia

111
Q

What are the 3 steps of Alzheimer’s disease (typical)

A

1st memory impairment
2nd Language/visuospatial deficits
3rd Executive dysfunction

112
Q

What are the risk fx for Alzheimer’s

A

Risk Factors for AD:
Age > 70
(+) FMHx of AD

Diabetes increase risk of AD by 3x

The major genetic risk:
ε4 allele of the apolipoprotein E (ApoE) gene

113
Q

Define Alzheimer’s pathology

A

neuritic plaques of AB42 amyloid and neurofibrillay tangles

114
Q

What is the diff of Cognitive Impairment and Alzheimer’s

A

AD impaires function and MCI retains function

115
Q

What are the Tx approaches to Alzheimer’s

A

Behavior MGMT

Rx:
Drugs:
Cholinesterase Inhibitors 
-Donepezil 10mg daily target dose
-Rivastigmine 6mg twice daily
-Galantamine ER 24mg daily

N-Methyl-D-aspartate (NMDA) receptor antagonist
-Memantine 10mg twice daily

116
Q

What are the findings in End Stage Alzheimer’s

A

Physically: Rigid, mute, incontinent, bedridden

Hyperactive DTRs, myoclonic jerks

Death
Most common aspiration
Malnutrition, 2ndary infxn, PE, CAD

Typical duration of symptomatic AD is 8-10 years

117
Q

Define Vascular Cognitive Impairment/ vascular dementia

A

strongest Rsk fx AGE (70)

Dementia arising from a vascular insult/ cerebrovascular dz

(Infarcts)

118
Q

Describe Frontotemporl Dementia

A

Most common behavioral variant

Has three variants ;
behavioral
Primary Progressive Semantic
No fluent/ Agrammatic variant

Group of Clinical Syndromes
Frontotemporal lobe degeneration
Presents in 5th to 7th decade of life

EARLY behavior decline
(Alzheimer’s is Late behavioral decline)

119
Q

What is the gross hallmark of FTD pathology

A

Atrophy of frontal and/or temporal cortex on MRI

Microscopically:
misfolded tau protein

120
Q

Are the any Txs for FTD?

A

NO, sadly sadly NO

121
Q

Define Dementia with Lewy Bodies

A

Dementia syndrome characterized by

  • Visual hallucinations
  • Parkinsonism
  • Fluctuating alertness
  • Sleep behavior disorder

Delusions common

Microscopically
-Lewy bodies throughout the brain

122
Q

What is the Tx approach to Dementia with Lewy Bodies

A

Cholinesterase Inhibitors

Excercise and Antidepressants

123
Q

What are the three most common reversible causes of Dementia

A

Depression
hydrocephalus
ETOH dependence

124
Q

Define psuedo dementia

A

Depression is most commonly mistaken for dementia.

Both show mental slowness, apathy, self-neglect, irritability, difficulty with memory, etc…

All patients with suspected dementia must be screened for depression and anxiety.

125
Q

Define Dementia vs Depression

A 
Dementia: 
Pt unaware of deficits 
No c/o memory loss 
Few sedative symptoms 
Worse at night 
AbNML Neuro Exam
AbNML Labs possible

Depression:
They are aware of deficits
With C/o memory loss
Not worse at night

126
Q

What is the Tx approach to Psuedodementia

A

TX the depression

SSRI, SNRI
CBT

127
Q

What is the classic triad of NML pressure hydrocephalus

A

Cognitive decline (dementia)

Urinary Incontinence or Urinary Urgency

Gait difficulty

128
Q

What is the managment Tx for normal pressure hydropcephalus

A

Shunt

129
Q

In a pt that has a thiamine deficienty and low glucose

Which should be replaced 1st

A

Thiamine

130
Q

Define basal ganglia

A

Central processing center of the brain

Movements
Cognition
Emotions
learning

131
Q

Define essential tremor

A

Goes away during sleep
And goes away with ETOH ingestion

Rhythmic oscillatory movement characterized by its relationship to voluntary motor activity

Increases with stree

132
Q

Define Chorea

A

Dancing, flailing type tremor

Decreased grasp “milkmaid”

Often falls

Irregular speech

Irregular gait
“Dancing gait”

133
Q

Define Hemiballismus

A

Unilateral chorea

Most often due to vascular Dz or stroke.

Tx: dopamine depleting/ blocking agents

Severe: pallidotomy

134
Q

Define Athestosis

A

Restless

Slow, sinuous involuntary

Can lead to dystonia

135
Q

Define Dystonia

A

Sustained muscle contractions frequently with twistings and repetitive movements

Not present during sleep

Focal:

  • Torticollis
  • Blepharospasm
  • Writers cramp

Generalized:
Cerebral Palsy
Acute Dstonia

136
Q

Define Tardive dyskinesia

A

Involuntary movements of the face or tongue

After antipsychotics drugs or Reglan

137
Q

Define Myoclonus

A

Sudden rapid twitch like muscle contractions

Can be generalizes, fovcal, multi focal
Or segmental

138
Q

Define TIcs

A

Brief, rapid, recurrent, purposeless moments

Can be motor or phonic
Simple or complex
Tourette’s- COmplex

139
Q

Coprolalia

A

Profanity

140
Q

Echolalia

A

repetition of sounds

141
Q

Define Parkinsonian tremor

A

4-6hz tremor

Most copious at rest

Increased with stress

Improves with activity

142
Q

Define cerebral tremors

A

Result from stroke, tumor, or disease (MS)

Often with dysarthria, nystagmus, and gait problems

143
Q

Define a psychogenic tremor

A

Functional tremor

Assoc with conversion D/o
SUDDEN ONSET

Decreased with distraction

144
Q

Define orthostatic tremor

A

Rhythmic muscle contractions
Occurs in legs or trunk
Most notably after standing

“Unsteadyness”

Decreases with sitting, or walking

145
Q

Physiologic tremor

A
146
Q

What is the gene mutation associated with the most common tremor

A

Essential tremor is the most common tremor

Gene: EMT1 and 2

147
Q

Acute dystonia and tx

A

Remove any offending agents plus diphenhydramine and baclofen

148
Q

Drugs that are assoc with Dystonia RXNs

A

Anti psych drugs
Phenytoin
] Phenothiazines- eg. chlorpromazine (Thorazine); Fluphenzaine (Prolixin)
Haloperidol (Haldol)

Atypical antipsychotics (fewer side effects/extrapyramidal symptoms)
Eg. Olanzapine (Zyprexa), Resperidone (Risperdal)

Phenothiazine anti-emetics (also act as dopamine antagonists)
eg. Promethazine (Phenergan), Prochlorperizine (Compazine)

Cocaine, LSD
Tricyclic antidepressants - eg. Amitriptyline
Lithium
Anticonvulsants: Phenytoin, Carbamazepine

149
Q

Tx approach to acute dystonia Slide 30 lecture 8

A
150
Q 
4 core symptoms:
An urge to move the legs with or without sensations
Worsening sx’s with rest
Improvement with activity
Worsening in the evening or nights

What is this

A

RLS

151
Q

Define Tourette Syndrome

A

Effects Boys more than girls
Chronic and life long

Multiple motor and verbal tics

assoc: OCD and ADD

Dx: prior to age 21

152
Q

What is the Tx approach to Tourette’s

A

Ed and counseling

Haloperidol to reduce tics
Clonidine reduces tics
Also
Fluphenzaine and Botulinum Toxin A

153
Q

Define Parkinsonism

A

Any clinical syndrome that relates to Parkinson’s Dz

4 causes: 
Neuroleptic Drug Exposure 
Cerebrovascular Dz 
Methyl-phenyl-tetrahydropyridine 
Encephalitis lethargica 
Any combination or presentation of 
Tremor
Rigidity 
Bradykinesia 
Postural instability 
Cognitive impairment
154
Q

define Parkinson’s Dz

A 
A complete combination of all 4: 
Resting tremor 
Cogwheel Rigidity 
Bradykinesia 
Gait impairment
155
Q

What is the pathophysiology of Parkinson’s Dz

A

Damage to the Substantia Nigra with cell loss in basal ganglia

Dopamine exerts an inhibitory effect on release GABA

Without dopamine, GABA output increases

156
Q

What are the late features of Parkinson’s Dz

A

Disregulation of autonomic sys

Ortho instability
Dementia
Skin greasiness, seborrhea

157
Q

What are the Tx approaches to Parkinson’s Dz

A

Dopamine Agonist
(Pramipexole, Ropinirole)
And Dopamine replacement

Anticholinergics can reduce gritos and tremor
(Benzotropine)

158
Q

Define Huntingtons

A

Genetic autosomal transmission

Onset 25-45

Genetic mutations causes premature cell death, resulting in atrophy in cerebral cortex and caudate

Concentrations of GABA and ACh in the basal ganglia are reduces which INCREASE dopamine

159
Q

What is the treatment approach to huntingtons Dz

A

Treat the S.s

Haloperidol -block movements
Reserpine- can delplete dopamine
SSRI- moodiness and aggression
Benzos- help with sleep and anxiety

160
Q

What is the largest S/s finding of cerebral palsy

A

Spasticity

161
Q

Define Wilson Dz

A

An autosomal recessive disorder

Increased copper levels in the blood

Build up in the CNS, Cornea, and kidney

S/s: Tremor, ataxia, Dysarthria, Dyskenisia, Parkisoninsim
KAYSER FLEISHER RINGS

162
Q

What are the three most predictive exam finding for acute stroke (ischemic)

A

Asymmetric facial paresis

Arm drift/weakness

Abnormal speech (dysarthria)

163
Q

What are the major RSk factors for stroke

A

Primary Arterial Hypertension

A. Fib

Smoking

Medical HX

Previous TIA

1/3 will have a full stroke in 5 years

Age

164
Q

What is the most common vascular pathology that causes Ischmic strokes

A

Atherosclerosis

165
Q

Define anoxic brain injury

A

Decreased blood flow to the brain from Low systemic perfusion pressure

Most common cause is from:
-Cardiac pump failure due to
MI
-Arrhythmia
-Systemic hypoperfusion
-Blood loss
-Hypovolemia

The lack of perfusion is more generalized and affects the brain diffusely and bilaterally

166
Q

Describe lacunae infarcts

A

Small Vessel Disease
(AKA Lacunar Infarcts)

Small (0.5-1.5 mm) arteries from…
-Distal vertebral artery
-Basilar artery
Middle cerebral artery stem

Causes
-Lipohyalinosis 
-Atheroma formation  
(fatty deposits)
-arteriolosclerosis
167
Q

What is the most important DX test in Stroke pts

A

Noncontrast CT!

Ischemic stroke – looks dark - may be normal in first 24 hours

Hemorrhagic stroke – looks bright/white - should show up earlier

168
Q

How do hemorragic strokes appear on CT

A

Noncontrast CT: acute hemorrhage appears bright on CT scan, whether in the brain itself, or outside the brain parenchyma (subarachnoid, subdural hemorrhage).

Sensitivity: 89%; specificity: 100%

169
Q

What are the C/I to thombolysis in stroke Pts

A

Sustained BP >185/110 mmHg despite treatment

Bleeding disorder/diathesis
(plt <100,000, HCT <25%)

Recent head injury/stroke/intracerebral hemorrhage
(in the prior 3 months)

Major surgery in the past 14 days

GI bleeding in the previous 21 days

Recent Myocardial Infarction
(in the prior 3 months)

170
Q

How does ischemic stroke present on CT

A

DARK AREAS!

White areas mean its hemmorhagic

171
Q

What is the timeframe for TPA administration

A

Within 3 hours!

172
Q

If a pt is not a candidate for tPa what should be done for their stroke?

A

If not candidate for Tissue Plasminogen Activator (tPA), should be given ASA, after exclusion of hemorrhage on CT.

Manage BP, vitals and complications of stroke
i.e. swelling

173
Q

What is permissive hypertension in Ischemic Stroke

A

Permissive hypertension:
Don’t let the SBP >220,
or DBP over 120

  • B1-adrenergic Beta-blocker such as esmolol
  • works by relaxing blood vessels and slowing heart rate to improve blood flow and decrease blood pressure.
174
Q

What are the vascular screening methods for Strokes

A

Carotid Doppler:
-Used in the evaluation of suspected stenosis of the intracranial internal carotid artery, middle cerebral artery, or basilar artery.

MRA

Conventional xray angiography is “gold standard” for AVM or SAH but has a 1% risk of stroke during procedure.

175
Q

What are the three steps to stroke tx

A

Identify the stroke

Plan of action: lytics and Anticoagulant

Long term prevention

176
Q

A pt presents with sudden severe HA followed by LOC,

Think DDX

A

Aneurysm (berry)

177
Q

What is the most common medically cause of SAH

A

Ruptured cerebral aneurysm

178
Q

What are the two common morphologies of SAH

A

-Saccular- (most common)
Aka Berry/ Congenital that occurs at the bifurcation of the large cerebral arteries at either the circle of Willis or at the MCA/Sylvian fissure
Or
-Fusiforme

179
Q

What are the 4 hallmark S.s of SAH

A

headache
Syncope
Nausea
Vomiting

180
Q

Subhyaloid retinal hemorrhages are a sign of…

A

Intracranial Hemm,..

most likely SAH

181
Q

A pt presents with Severe HA, with retro orbital pain, and a stif neck

Think

A

SAH

182
Q

A pt presents with 3rd cranial nerve palsy, with diminished light reflex and pupillary dilation

Think what bleed in the brain

A

PCA! In the circle of Willis

183
Q

What are the imaging of choice for SAH

A

NOn Con CT

If pos then send for cerebral angiogram
If neg, evaluate lumbar puncture
Positve RBCs?

184
Q

What is the gold standard imaging for SAH

A

Cerebral angiography

185
Q

What is the tx approach to SAH

A

Absolute bed rest

EHOB 15-20 degrees

Mild Sedation

Stool softeners

Maintain platelet function

Treat Hyponatremia

CCB to reduce vasospasms
(Nimodipine)

Cerebral artery angioplasty

Anticonvulsants to reduce SZR

186
Q

What are the 4 major complications of SAH

A

Cerebral ischemia: from vasospasm
Acute hydrocephalus: from clot
Bleeding: from the rupture
Increased risk of future normal chronic hydrocephalus

187
Q

What two groups have increased risk of Intracerebral Hemorrhage

A

Asians and African Americans

188
Q

What is the classic location of intracerebral hemm.

A

Basal ganglia due to HTN

Common in African Americans

189
Q

What is the approach to BP control in HEMORRHAGIC stroke

A

Intracerebral hemorrhage:
Presents w/ acute ICH SBP
150 – 220 then lower to 140mmHg

> 220mmHg then lower
140 -160mmHg

Subarachnoid hemorrhage
-Keep SBP lower than 160 mmHg

Monitor for signs of cerebral hypoperfusion

Stop all antiplatelet/anticoag drugs or reverse

190
Q

What is an AVM

A

Arteriole-Venous Malformations
Congenital Art. Venous connections w/o a capillary bed in-between
High flow of blood
Not completely normal blood vessels

191
Q

What is the most common brain vascular malformation

A

DVM!

These are composed of anomalous veins

These are morphologically different from brain parenchyma

These have one or more central draining vein that are Conspicuous

May be dilated into a varix or varices

192
Q

What is a Cavernous Angiomas

A

These are a relatively compact mass of sinusoidal vessels

They are packed close together

They have no intervening brain parenchyma

They are well encapsulated

Form within deep hemisphere white matter and brainstem without normal intervening neural structures

193
Q

What is telangiectasia’s

A

True capillary malformations that often form extensive vascular networks through an otherwise normal brain.

Pons and deep cerebral white matter are typical locations.

If bleeding does occur, it rarely produces a mass effect or significant symptoms.

No treatment options exist.

194
Q

What is the treatment for vascular malformations

A

All are tx with

  • Medical therapy to reduce seizures
  • Surgery to prevent rebleeding
  • Interventional obliteration
  • Radiotherapy

Tx depends on presentation

195
Q

What is the most common MOI in younger individuals

A

TBI from MVA

196
Q

What is the most common MOI in older adults

A

Falls

197
Q

Define TBI

A

alteration in brain function caused by an external force and characterized by the following:

  • Any loss or decreased consciousness
  • Any loss of memory for events immediately before (retrograde) or after (posttraumatic) the injury
  • Neuro deficits and/or alternation in mental state at time of injury
198
Q

How do you grade severity of TBI

A

GCS

199
Q

What are the eye ratings in GCS

A

Eyes open spont (4)
Open to verbal command (3)
Eyes open to pain (2)
No eye opening (1)

200
Q

What is the Verbal rating for GCS

A

Oriented (5)

Confused conversation/ can answer questions (4)

Inappropriate responses (3)

incomprensible sounds or speech (2)

No verbal response (1)

201
Q

Motor response for GCS

A

Obeys command for movement (6)

Purposeful movement (5)

Withrdrawls from pain ( 4)

Spastic decorticate posture (3)

Decerebrate posture (2)

No motor response (1)

202
Q

A GCS of 13-15 is…

A

Minor brain injury

203
Q

What is a GCS of 9-12…

A

Moderate brain injury

204
Q

What is a GCS of 3-8 ..

A

Severe Brian injury

205
Q

A pt presents with a brief LOC, and within minutes is fully alert with nausea, difficulty concentration, mild blurred vision

GCS of 13-15

What is this ?

A

Concussion

206
Q

What is the CT criteria for a mTBI

A

Persistent severe HA

Repeated vomiting (two or episodes)

Severe MOI (speed over mph)

Underlying coagulopathy

Age > 65 years

> 30min of retrograde or persistent anterograde amnesia

Intoxicated

207
Q

What is Post Concussion Syndrome

A

Post-concussion syndrome is the sequelae of a mTBI/concussion that is defined by the continuation of symptoms of headache, dizziness, and cognitive impairment.

A mild traumatic brain injury is a mild injury to the brain caused by a blunt force or shaking of the brain inside of the skull.

208
Q

What is the diff between Post Concussion Syndrome Vs Post Concussion Disease

A

PCS: symptoms that continue seven to 10 days after the initial injury

PCD: > 3 months

209
Q

A pt presents with a GCS 9-12

What is the Tx approach

A

Admit for Mod/Int TBI

Head CT
may find contusion or hematoma

210
Q

A pt has a concussion with S./s that persist beyond 6 days is termed

A

Post Concussion Syndrome

211
Q

Describe Epidural Hematoma

A

Typically present as

  • Trauma
  • Progressive coma
  • lucid intervals

Most common cause is a trauma to the middle meningeal artery

Suspect in a patient with temporal skull fracture

Classic CT finding: Convex hyper-density o/s brain tissue in the pariotemporal region

Mortality is 100% if left untreated

Get urgent CT scan

212
Q

Describe Subdural hematoma

A

Accumulation of blood in the subdural space

Bleeding is from the cerebral vasculature

Blow from front or back or when skull hits fixed object (windshield)

Bridging veins between the dura and the arachnoid are torn when the two separate

Chronic in the elderly

213
Q

Define Coma

A

deep sleeplike state with eyes closed from which the patient cannot be aroused

214
Q

Define Stupor

A

higher degree of arousability in which the patient can be transiently awakened by vigorous stimuli, accompanied by motor behavior that leads to avoidance or withdrawal from uncomfortable or aggravating stimuli.

215
Q

Define Drowsiness

A

simulates light sleep and is characterized by easy arousal and the persistence of alertness for brief periods.

216
Q

What are the most important brainstem reflexes

A

Pupillary signs

Ocular movements

RR patterns

217
Q

What are the three cardinal features of brain death

A

Coma/unresponsiveness
-No response to painful stimuli

Absence of brainstem reflexes
-Pupils, oculocephalic, gag, grimacing

Apnea
-No respiratory attempts even with PCO2 > 60mmHg

218
Q

Define meningitis

A

Inflammation of the leptomeninges.
Caused by infection: viral, bacterial, fungal, or other.

Headache is a prominent feature: pain due to inflammation of intracranial pain sensitive structures.

219
Q

What is the classic triad in meningitis

A

Fever
HA
Nuchal Rigidity

220
Q

What are the classic CSF abnormalities

A

(1) polymorphonuclear (PMN) leukocytosis (>100 cells/μL in 90%),
(2) decreased glucose concentration (<2.2 mmol/L [<40 mg/dL] and/or CSF/serum glucose ratio of <0.4 in ~60%),
(3) increased protein concentration (>0.45 g/L [>45 mg/dL] in 90%),
(4) increased opening pressure (>180 mmH2O in 90%).

221
Q

What is the Tx approach to Menigitis

A

Age 1-3 months: ampicillin + Ceftriaxone

Age 3 mon to 55 y/o Ceftriaxone PLUS Vanc

Alcoholism/? Ampicillin +Ceftriaxone +Vanc

Impaired cellular immunity
- ampicillin plus Ceftazadime plus Vanc

222
Q

What is the characteristic rash for N. Minigitidis

A

Purpuric rash

223
Q

What time frame should you give ABX for meningitidis

A

Within 60 min of admin

224
Q

What is the MC cause of viral meningitis

A

Enterovirus

225
Q

A pt CSF has increased cell count
With normal protein concentration
With normal gl and normal opening pressure

With S.s of menigitis

Think

A

Viral

226
Q

What are the common cause of encephalitis

A

Herpesviruses: human to human transmission
Herpes simplex 2, Varicella-zoster, Epstein-Barr virus

Enterovirus: fecal-oral transmission

Arboviruses: mosquitoes, ticks (ie West Nile)

227
Q

What are the important labs for Encepahlitis

A

Head Ct before LP to R/o

  • Elevated intracerebral pressure (ICP)
  • Obstructive hydrocephalus
  • Mass effect

MRI and EEG and eval the CSF

228
Q

What is the general approach to Encephalitits

A

Appropriate management of the airway

Fluid and electrolyte balance

Nutrition

Avoid and treat secondary infection

Treat hyperpyrexia (fever)
Manage ICP
-Head elevation
-Diuresis
-Mannitol
-Seizure precautions
229
Q

What is the pathogenesis of Migraine

A

Trigeminovascular system

Serotonin

Dopamine

Inherited

230
Q

Define Migraine without aura

A

A lead 5 attacks that:
Last 4-72 hours with at least 2 of the following

Unilateral location
Pulsating quality
Moderate or severe intensity
Aggravation by or causing avoidance of routine physical activity (e.g., walking, climbing stairs)

During the headache they have at least Nausea, vomiting, or both
Photophobia and phonophobia

231
Q

Define Migraine with aura

A

A least 2 attacks with one or more of:

reversible aura symptoms:
Visual, sensory, speech and/or language, motor, brainstem, retinal

With at least 2:

One aura symptom spreads gradually over ≥5 min, and/or two or more symptoms occur in succession
Each aura symptom lasts 5-60 min
At least one aura symptom is unilateral
The aura is accompanied, or followed within 60 min, by headache

232
Q

What does POUNDING stand for

A 
Pulsatile
Onset/duration: 4-72 hours
Unilateral in location
Nausea and vomiting
Disabling in intensity: headache is moderate to severe
233
Q

What defines chronic headache

A

8 or more days per month
AND
At least 15 total days of HA per month

234
Q

What are the DOC for acute mild migraine attacks

A

Simple Analgesics
Acetaminophen, aspirin, caffeine (Excedrin Migraine) Two tablets or caplets q6h (max 8 per day)

NSAIDs
Naproxen (Aleve) 220–550 mg PO bid
Ibuprofen (Advil, Motrin) 400 mg PO q3–4h
Tolfenamic acid (Clotam Rapid) 200 mg PO; may repeat ×1 after 1–2 h
Diclofenac K (Cambia) 50 mg PO with water

235
Q

What is Ergotamine used for

A

Non selective Stimulating Seretonin receptor

Start at first sign of migraine

236
Q

When do you give triptans in Migraines

A

AFTER THE AUREA

237
Q

Triptans can be combined with what other medication to reduce HA recurrence

A

Combine with naproxen

238
Q

What are the two most efficacious Triptans

A

Rizatriptan and Eletriptan are most efficacious

239
Q

What is the role of using dopamine receptor antagonist in Migraines

A

Adjunctive therapy
Improves gastric motility –

improved absorption of other meds

Relieves nausea

240
Q

When would you start using metoclopramide or prochloperazine

A

Pts w/
-increasing frequency

-Attacks unresponsive or poorly responsive to abortive treatments

-4 or more attacks per months
Takes 2 to 12 weeks before an effect is seen

241
Q

What is the only proven drug for Tension headache prophylaxis

A

Amitryptyline

IPAP JUNIOR SEM. (43 decks)

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