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Rotation 2: IM Outpatient > Neuro > Flashcards

Flashcards in Neuro Deck (149):
1

dementia

what are 5 key features you may find?

1, memory loss

2. speech and language difficulties

3. problem solving difficulties

4. impaired judgement

5. may have mood issues

2

dementia

mood issues include? 5

depression

agitation

delusions

insomnia

disinhibition

3

what are 3 neurological features that might help explain the neuro changes seen in dementia?

1. changes in cerebral circuits

2. nerve loss

3. changes in neurotrasmitters

4

what is the most common form of dementia?!

alzheimers

5

what are the 8 causes of the different types of dementia?

1. alzheimers

2. vascular dementia

3. multi-infarct dementia

4. frontotemporal dementias (huntingtons)

parkinsons dementia

6. dementia with lewy bodies

7. ETOH/drugs

8. viral (creutzfeld-jakob)

 

6

what are the two most common forms of dementia?

#1- parkinsons dementia-50%

#2-vascular dementias-10-20%

7

alzheimers dementia

 

 

what to keep in mind about htis?

what causes this? 2

do they know they have it?

most common dementia

 

memmory loss can start as very subtle

progressive over years

 

NEURITIC PLAQUES (senile plaques) and amyloid deposition in arterial walls of neurons making neurofibillary tangles "neurons get all tangled up so they don't work as well"

 

 

don't recognize that they have it

behavior changes, may get lost

8

who is there a higher incidence of alzheimers dementia in?

down syndrome pts

9

alzheimers dementia

 

8 presentations

1. word finding issues/speech difficulties

2. wandering/getting lost

3. poor judgement

4. delusions

5. agression

6. sleep disturbance

7. incontinence

8. bedriddent status

10

alzheimers disease

 

why is it difficult to dx?

you can only confirm on autopsy with brain bx

11

what are the 3 most important risk factors for alzheimers dementia?

1. OLD AGE-----most important RF

2. family hx

3. female gender

12

how do you confirm alzheimer on autopsy?

apolipoprotein 4 on autopsy

13

vascular dementias

 

what to remember about this?

who do you find this in?

what are the type?

 

Q image thumb

SECOND MOST COMMON DEMENTIA

 

multi-infarct dementia in classically HTN pts

 

 

small or large infarcts known as lucunar and multiple cortical infarctions

 

**more sudden onset**

14

frontotemporal dementia

 

 

what is this caused by?

4 early sxs? what comes later?

what are 3 diseases that cause this?

caused by degeneration of the frontal (behavior) and temporal lobe

 

early features include:

1. attention issues

2. judgement impairment

3. awareness

4. behavior issues

***memory loss seen in later disease***

 

1. huntingtons chorea

2. picks disease

3. progressive supranuclear palsy

15

huntington's chorea

 

inheritance pattern?

where is defecT?

autosomal dominant-50% chance for kids

 

chromosome 4

16

frontotemporal dementia:

picks disease

 

what does this result in?

what do you see on testing?

tx?

anterior frontal and temporal cerebral cortex with MARKED personality changes

 

 

***intracellular inclusion (pick bodies) stain with silver stain

 

 

Tx:

NONE

tx behavior

17

what are the lewy bodies that are seen in dementia?

Q image thumb

intaneuronal cytoplasmic includsions that stain with PAS staining

18

demenia:

progressive supranuclear palsy

 

what are 4 things this is qualifed by?

how long does the person have to live?

tx?

 

 

 

1. falls

2. gaze paralysis cant look down

3.rigidity

4. dementia

 

death within 5-10 years, no tx

 

19

dementia:

normal pressure hydrocephalus

what are 3 sxs?

2 dx methods?

1 tx?

1. gate ataxia

2. dementia

3. urinary incontinence

**think falling adult who is incontinent**

 

DX:

1. LARGE VENTIRICLES ON IMAGING/CT

2. sume use MRI or CSF tap

 

 

tx: shunting

20

dementia:

korsakoff syndrome

 

what is this?

can't recall recent memory despite immediate memory retention

 

easily confusable

21

what is a vitamin deficiency that can cause dementia?

B12...macrocytic anemia...causes spinal cord issues "myelepathy"

 

REPLACE IT

22

dementia

 

5 workup you want to do

1. history

2. mini mental exam

3. full neuropsychiatric testing

4. B12, thyroid function

5. consider CT/MRI to turn our tumor/infarction

23

dementia

 

3 tx options for the actual dementia itself

1. anti-acetylcholinesterase

**increase ach by inhibiting cholinesterase**

effects last about a year

 

1. donepexil (aricept)

2. galantamine

3. riovastgmine

 

2. NMDA receptor antagonists

**blocks this over-excitatory neurotransmitter**

used for mod to severe disease WITH ANTI-CHOLINESTERASE DRUGS

1. Memantine (namenda)

 

3. COMBO MEMANTINE PLUS DONEPEZIL for alzheimer dementia "Namzaric"

 

 

***all can be used in AD or parkinson's dementia***

24

what are the goals of txing dementia with medication?

1. delay progression of the disease

2. improve caregiver disease

3. decrease agitation 

 

**can be used in AD and parkinsons...outcomes not as good in other dementia forms**

25

dementia

 

tx options for behavior

VERY DIFFICULT

antipsychotics:

1. haloperidol

2. resperidone

26

delirium

 

what is this?

how long can it last?

what are 3 things it can be attributed to?

acute confusional state with decreased attention

 

hours to days, even months-years

 

 

1. usually due to cerebral dysfunction

2. can be abnormal acetylcholine levels

3. high dopamine

**can minic dementia**

27

what are 4 things that can cause delirium?

1. older age

2. baseline dysfunction

failing health, dementia, nursing home pts

3. poor sleep

4. hospitalizations

catheters, restraints, sleep deprevation, multiple meds, pain

28

delerium:

ICU psychosis

 

what is this? 

4 causes?

r/o?

illness

(sepsis, fever, dehydration, drug abuse)

 

must rule out stroke

29

delerium:

sundowning

 

what is this?

2 tx options?

old people get worse at night

 

tx:

1. maintain day-awake, night sleep

2. reassurance/reorientation

30

delerium:

alcohol withdrawal/delirium tremens

 

 

what are these and when are they the worst?

4 sxs?

5 tx options?

delirium temors stem from acute alcohol withdrawal and peak 2-3 days after cessation

 

SXS:

1. agitation/axiety

2. tremor

3. hallucinations

4. ANS instability (increased BP, pulse, resp)

 

TX:

1. B vitamins

2. hydration

3. benzodiazepines

a. diazepam

b. chlordiazepoxide

IV or PO

c. high dose benzos for bad DTs

4. phenobarbitol

5. antipsychotics

a.haloperidol

31

delerium:

 

5 presentations and whicho ne is most important?

 

1. decreased attention

2. change in sleep/wake cycles

3. hallucinations

4. delusions

5. hypo/hyperactive status

32

delerium

 

what are 3 dx options?

what are 5 tx options?

dx:

1. clinical at bedside

2. compare baseline function (ask family)

3. check for meidcations causes (anticholinergics, sedatives, narcotics, benzos)

 

 

Tx:

1. supportive/reorientation

2. day-night normalcy

3. bed alarms, sitters

4. antipsychotics- haloperidol

5. benzodiazepine-diazepam

VERY DIFFICULT

33

seizure

 

what are the two maine categories of this?

what causes each?

1

3

partial:

a. deranged area of the cerebral cortex often due to STRUCTURAL ABRNOMALITY CONCIOUSNESS IS PRESERVED

**keep in mind in the subcategory of this complex partial conciousnesses is IMPARIED=PARADOX..it just doesn't make sense**

 

 

generalized:

a. diffuse region of the brain firing

b. often widespread problem:

-cellular disorder aka mental retardation

-biochemical disruption: low Na

-structual: brain tumor

 

34

PARTIAL:

SIMPLE PARTIAL SEIZURE

9 sxs of this

2 dx

sxs:

1. no loss of conciousness

2. isolated tonic/clonic with repetitive flexion and extension 

3. hand tremor on opposit side of issue

4. jacksonian march

motor activity begins distally like fingers and spread through entire extremity, can lead to entire side of body

5. todds paralysis

local parethesia lasting minutes to hours

 

6.changes in somatic sensations (parersthesias)

7. changes in vision (flashing lights, hallucinations)

8. changes in equilibrium (falling, vertigo)

9. autonomic changes (flushing/sweating)

 

 

DX:

EEG spike waves in FOCAL area of the brain or during jacksonian march

35

PARTIAL:

COMPLEX PARTIAL SEIZURE

 

what are 3 sxs with this? 3 examples

SXS:

1. impaired conciousness, loss of contact with environment "ictal stage"

a. STARING-kinda asleep and staring off into space, can't wake them

b. AMNESIA-forgetting/impaired memory

c. involuntary picking/chewing

2. preceeding aura

3. post ictal confusion

 

Lasts seconds to hurs, EEG notmal between spells

36

PARTIAL:

partial with secondary generalization

 

when does this occur?

what type of seizure does this produce?

electrical discharge spread and both hemispheres become involved

 

TONIC CLONIC SEIZURE

 

common when partial seizures occur in the frontal lobe

37

GENERALIZED:

absence seizures-petit mal

 

who does this occur in?

when do they stop?

3 sxs with 5 subtle findings?

1 DX with 3 findings?

childhood 4-8 years, 15-20% of childhood seizures, MOST RESOLVE IN CHILDHOOD

 

NO CONVULSIONS

 

1. LOSS OF CONCIOUSNESS

2. few seconds

3. subtle findings

eye blinking

FACIAL TWITCHING

chewing

clonic movement of hands

all day long daydreaming appearance

 

 

DX:

1. EEG

-general symmetrical discharge

-spike and wave

-WORSEN WITH HYPERVENTILATION MANEUVER

 

38

GENERALIZED:

atypical absence seizures

 

what differentiates these from absence seixures?

who might they occur in? 2

same as absence but LAST LONGER with more motor features

 

 

may have brain abnormlaity like mental retardation or developmental delay

 

 

HARDER TO TX

39

GENERALIZED: generalized tonic/clonic seziures "Grand mal" 

What is this most commone cause of this?

How fast do they occur?

6 sxs seen?

10% will have epilepsy

caused by metabolic derrangement

SUDDEN ONSET

 

SXS:

1. convulsive

2. increased muscle tone stiff

3. moan or cry

4. change in respiration (secretions, cyanosis, jaw clench)

5. clonic activity: muscle relax and contract

6. post ictal state: 

unresponsive,

flaccid,

salivation/airway obstruction, bowel/bladder incontinence

40

GENERALIZED:

tonic-clonic Grand mal seizures

 

what do you find on the EEG between the two phases?

dX EEG:

tonic phase:

increased low voltage fast activity

high amplitude polyspike discharge

clonic phase:

spike and wave activity develops

 

41

GENERALIZED:

tonic-clonic Grand mal seizures variation

myoclonic seizure

 

what is this?

who do you see this in?

brief contraction or jerk like when you fall asleep and twitch

 

*seen in brain injuries*

42

Generalized:

juvenille myoclonic seizure

 

who is this in? does it go away?

1 sxs?

when is it worse? 2

adolescence, spontaneous remission

 

billateral jerk with maintained conciousness

 

worse with awakening and sleep deprevation

43

GENERALIZED:

lennox gastaut syndrome

 

who is this in?

what are 4 things it is associated with?

children!!

 

impaired cognitive function

 

associated with CNS:

developmental delay

trauma

infection

neural injuries

44

GENERALIZED:

mesial temporal lobe epilepsy

 

what is the dx for this?

MRI shows hippocampal sclerosis

45

explain the patho of seizures?

 

6 steps

 

1. burst of electrical activity

2. influx of calcium, aided by NMDA

3. influx of sodium, aided by GABA or K channels

4. spikes discharge

5. inhibitory neurons overloaded with calcium and k

6. propogation of action potentials

46

what can seizures come from?

 

1 theory?

5 causes?

harrisons: shift in balance of excitation and inhibition of the CNS

 

1. change in seizure threshold

2. genetic role

3. traumatic brain injury

4. strokes infection

5. stress, sleep deprevation, menses, medications

47

febrile seizures

 

 

who does this occur in?

3 associations?

how many?

3 months-5 years

 

infection related:

ottitis media

respiratory

gastro

 

can be complex (multiple) or simple (single)

48

what causes 50% of new seizures in adults?

cerebrovascular disease

49

how do you dx a seixure?

 

4 (+findings)

1. hx is key, from bystander or witness

2. EEG: starts or stops abruptly activity during tonic-clonic inter-ictal-spikes or sharp waves

3. sometimes MRI

4. blood test, elevated prolactin in the first 30 mins

50

seizure tx

 

3 tx options?

specific medicaitons? 6

1. MEDICATION MANAGEMENT

-CARBAMAZEPINE

-PHENYTOIN

-lamotrigine

-valproic acid

-gabapentin (partial)

-pregabalin (partial)

 

2. SURGICAL

-temporal lobectomy

-focal lesion removal

 

3. VAGAL NERVE STIMULATOR

-put electrode in vagus nerve, increases the seizure threshold

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51

status epilepticus

 

 

what is this and how long does it last?

is this serious? why? 3

5 causes of this?

continuous seiziure

15-30 mins

 

MEDICAL EMERGENCY

-cardiovascualr implicaitons

-hyperthermia

-CNS injury

 

causes:

metabolic problems

drugs

CNS infection

head injury

refractory epilepsy

 

52

status epilepticus

 

4 tx options?

dx: metabolic workup

 

Tx:

1. benzodiazepine ( lorazepam, diazepam, midazolam)

2. phenytoin

3. phenobarbital

4. anesthesia

53

multiple sclerosis

 

 

what is this caused by?

when does it start?

who is it more common in?

what are the 5 types?

autoimmune that causes inflammation and demyleination of the CMS which makes the neurons not able to function

 

 

onset usually 20s to 30s

more common in women, more severe in men

 

 

types:

1. CIS

2. RRMS

3. Primary progressive

4. secondary progressives (SPMS)

5. progressive relapsing

54

what are 5 RF for multiple sclerosis?

1. northern europe

2. southern canada

3. northern US

4. western europe in temporate zones

5. family hx

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55

multiple sclerosis:

relapsing remitting MS

 

ehsy is the pattern of this?

5 things it can lead to over time?

6 sxs?

an initial episode then months or years later sxs emerge or previous sxs return for more than 24 hours

 

cycle of incomplete reission and progressive disability

-weakness

-spasticity

-ataxia in limbs

-impaired vision

-urinary incontinence

 

 

despite remission steady decline still dominates the disease course

 

sxs:

optic atrophy

nystagmus

dysarthria

cerebellar deficits

uhthoffs pnehomenon-SXS GET WORSE IN HOT ENVIRONMENT!!!

internuclear opthalmaplegia-eye move independent

 

think sensory issues in teh limb followed by vision change

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56

multiple sclerosis:

secondary progressive (SPMS)

 

what is this?

most patients will progress to this

 

 

initial relapsing-remitting that sudddenly begins to have decliend without periods of remisssion (gets more  disabiltiy)

A image thumb
57

multiple sclerosis:

progressive relapsing

 

what is the pattern of this?

steady decline since onset with superimposed attacks

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58

multiple sclerosis:

 

10 sxs of this

1. numbess/weakness

2. numbness and tingling

3. unsteadiness in th limb

4.spastic paralysis

5.retro neuritis/ optic neuririrs

-sudden color loss

-impaired night vision

-pain with eye movemtn

-blurred or dimmed vition

6. vertigo

7.urinar incontinence from loss of spincter control

8. interneuclear opthalmaplegia (eyes move independently)

9. uhthoff pnenomenon-gets worse in the heat

10. l'hermettes syndrome: shock like feeling throughout body

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59

multiple sclerosis:

 

3 dx methods/criteria?

what do you find on each?

Q image thumb

1. mcdonald criteria:

2 or more different areas in central white matter in the brain that are affected at differnt times

***aka you get two lesions on imaging at different times**

 

2. MRI IS TOC FOR THIS!!:

SEE PLAQUE THAT IS REGION OF DEMYLEINATION WITH PRESEVED AXON

 

**FIND LESIONS IN: PERIVENTRICULAR, JUXTACORTICAL, INFRATENTORIAL, OR SPINAL CORD**

 

3. LUMBAR PUNCTURE

a. oligoclonal bands highly suggestive of MS

b. lymphocytosis

c. albumin (disruption of BBB)

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60

multiple sclerosis:

 

what is the goal of txing?

for acute attacks?

what are the three choices?

Q image thumb

goal: improve quality of life and limiting disabiltiy!! NOT ACTUALY TREATMENT FOR CURE

 

acute attacks: glucocorticoids aka methylprednisone

 

initials DOC options for RRMS:

1. injection with interferon or glatiramer "SAFTEY OPTION"

2. oral therapy with dimethyl fumarate or teriflunomide "CONVIENCE OPTION"

3. infusion therapy with natalizumab "EFFICACY OPTION"

 

****keep in mind there is no right way to do this!!!....its a crap shooot because there aren't guidelines!!***

 

 

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61

potenital for a Multiple sclerosis cure

 

what is the option?

what is included in this? 2

what is the benefit of htis?

Q image thumb

stem cell treatment (HALT-MS)

 

high dose immmunosuppresive tx WITH stem cell transplant

 

by rebooting the immune system it doesn't seem to attack itself anymore

-86% without relapses

-91% without progression

62

multiple sclerosis:

primary progressive MS

 

what percent or patients have this?

what is the pattern like?

10% of patients have this

progressively worse sxs from the start

 

stady increase in disability without attack

63

insomnia

 

3 characterizations

2 big causes?

4

3

 

characterized by:

difficulty falling asleep or staying awake

intermittent wakefullness during night

early morning awakenings

 

2 big causes:

1. depression

-fragmented sleep

-decreased total sleep time

-quicker onset REM

-REM shifts to earlier in the night

 

2. manic disorder

-total sleep time is decreased

-shortened REM latency

-increase REM activity

64

hypersomnia

 

what is this?

3 causes?

excessive daytime sleepiness

 

causes:

1. sleep apnea

Tx: weight loss, CPAP

 

2. narcolepsy

may have sxs preceeding sleep:

-sudden brief sleep attacks

-cataplexy

-sleep paralysis

-hallucinations

TX: stimulants: dextroamphetamine and modafinil

 

3. nocturnal myoclonus

clonzepam

65

parasomnias

 

4 presentations of this?

what part of sleep do each effect?

tx options for 2?

abnormal occurances during sleep

 

1. night terrors stage 3, 4 delta sleep

tx: benzodiazepine

2. nightmares REM sleep

3. sleepwalking stage 3 4 delta sleep

Tx: benzodiazepine

4. enuresis 3-4 hours of bedtime

66

what do you use to dx sleep disorders?

1. polysomnography (sleep study)

2. thyroid study

67

bacterial meningitis

 

what are the 3 most common bacteria?

5 sxs? including 2 signs?

2 dx? 5 findings?

strep pneumoniae

neisseria meningitidis Petechial rash

group B strep (esp in infants)

 

SXS:

1. FEVER CHILLS!!!

2. meningeal signs

-kernig-can't extend leg

-brudzinskis- head flexion causees knee raise

3. nuchal rigidity

4. nausea vomiting

5. altered mental status

 

 

DX:

1. CT PRIOR TO LP

2. LP!!!!

1. increase turbidity

2. increased pressure

3. INCREASED PMN, neutrophils

4. decreased glucose

5. increase proteins

 

 

68

tx for bacterial meningitis

 

2 groups

if CSF is cloudy....TX EMPIRICALLY and START ASAP

 

3 mo and older: ceftriaxone + vancomycin

 

immunocomprimized/hospital acquired: amipcilin + ceftazidime + vancomycin

 

 

69

wnat is absolutely crucial to do when txing a patient for bacterial meningitis?

repeat the lumbar puncture within 24 hours of starting tx because should see improvement in the quality of the CSF

70

viral meningitis

4 main causes of this?

4 sxs and 2 signs?

enteroviruses

coxsackievirus A or B

echoviruses

HSV

 

SXS:

1. meningeal signs

-kernig-can't extend leg

-brudzinskis- head flexion causees knee raise

2. nuchal rigidity

3. nausea vomiting

4. moderate altered mental status

 

71

viral meningitis

 

1 dx and finding

tx?

1.  LP

-lymphocytes

other stuff normal

 

tx:

1. supportive unless HSV origin, then give acyclovir

2. tx sxs

72

viral encephalopathy

WHAT IS EFFECTED?

2 causes?

4 sxs

tx?

infxn of brain parachyma

 

HSV MC

childhood exathems

 

SXS:

1. MARKED ALTER CONCIOUSNESS BECAUSE IT INVOLVES THE BRAIN ITSELF

2. SEIZURE

3. PERSONALITY CHANGE

4. NEURO SIGNS

 

tx: supportive unless HSV then give IV valcyclovir

73

granulomatous meningitis

 

what are 6 causes of this?

who does it occur in?

how long does it take to develop?

dx?

mycobacterium tumberulosis

fungi ( crytococcus, coccidioides, histoplasma)

spirochetes (treponema pallidium, borellia)

 

highest occurrance in immunocomprimised patients

 

weeks to months to develop

 

DX:

CULTURE

74

what is the definition of a stroke?

 

sudden or rapid onset of neurological deficit in the distribution of a vascular territory lasting over 24 hours

75

what are the two origins of stroke and the percentages of each?

ichemia and infart from thromus/emboli (85%)

 

hemmorage/blled (15%)

76

what is the most common cause of death in a patient with cerebrovascular disease is....

myocardial infarction

77

occlusive stroke:

3 main causes

4 others

1.  atherlosclerosis (thicking of vessel)

2. lunar infarct

3. cerebral/cardioemboli (originate outside brain)

 

 

others:

4. vasculitis

5. sickle cell disease

6. hyperviscous syndromes

7. drug abuse: cocaine, amphetamines

 

78

ischemic stroke:

origin:

athrosclerosis

 

what vessels are involved?

accounts for what percent of ischemic strokes?

4 MC origins?

outcome dependent on what 3 things?

 

Large vessels often involved

50% of ischemic strokes

 

thrombus in situ (stays in the artery that it is formed and happens frequent in carotids) vs artery to artery embolus (breaks off carotid and goes into brain)

 

most common locations:

aorta

carotid bifurcation

origina of internal carotid

external carotid

 

**outcome dependent on: adequacy of collateral circulation, circle of willis, and duration of ischemia**

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79

ischemic stroke:

Cerebral/cardioemboli

 

where do these come from?

make up what percent of ischemic strokes?

what two arteries does it commonly effect?

2 conditions that increase risk?

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embolism from carotid to brain or heart to brain and occludes distal artery in brain

 

20% of ischemic strokes originate form the heart

***often effect the MIDDLE CEREBRAL ARTERY (MCA) OR ANTERIOR CEREBRAL ARTERY (ACA)

 

afib or atrificail valve common causes (hence why they are heavily anticoagulated)

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80

ischemic stroke in middle cerebral artery (MCA)

 

what are the 4 ares you should think of when you think of being effected?

what are 5 sxs of blockage of proximal MCA?

what are the two sxs present wtih each subdivision blockage?

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damage depends on what part of the MCA is affected, can be proximal or one of the two divisions

 

effects of GENERAL MCA BLOCKAGES:

THINK HANDS/FACE/TRUNK/SPEECH CENTER

1. contralateral hemiplegia (loss of movement) and  contralateral (loss of feeling)

 

2. inital 1-2 days gase preference towards infarcted side of brain

 

3. hemianopia: visiual field defect

 

4. if stroke occurs in dominant hemisphere (aka they are right handed and occurs in left hemisphere) can lead to aphasia like above

 

5. if stroke occurs in nondominant hemisphere:  (aka they are right handed and occurs in right side of brain) anosognosia where speech and language are preserved but get neglect and denial of deficit or confused state (aka don't know something is wrong with their arm etc) can cause construction apraxia where they can't draw or construct 2 and 3D images

 

 

EFFECTS IF DIVISION OF MCA IS EFFECTED/BLOCKED

SUPERIOR DIVISION:

1. contralateral motor and sensory loss

2. BROCAs aphasia: non-fluent (expressive) aphasia, can understand language but can't speak fluently or create sentences

 

iNFERIOR DIVISION:

1. WERNICKES (fluent) aphasia: inability to comprehend spoken language the CAN speak but what they have a hard time getting what they want to say out, speech may lack meaning

2. homonymous hemianopsia: loss of half the field of view on the same side in both eyes

 

81

ichemic stroke in anterior cerebal artery (ACA)

 

what areas are the most common effected? 2

7 sxs of this including 2 reflexes?

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THINK FEET/LEGS

 

less common than MCA

***if occluded proximal to anterior communicating artery, very little sxs because the cicle of willis takes over if intact***

 

1. paralysis of contralateral leg

 

2. urinary incontinence

 

3. GRASP REFLEX: stroke skin between thumb and index finger, if positivie cuases the patient to grasph finger

 

4. SUCK REFLEX: stroke center of the lips/tongue, if positive causes sucking movement by patient

 

5. abulia: slowness to respond; lack of spontaneous movement

 

6. impariemnt of grait!!

 

7. behavior changes/memory distrubance

 

82

ischemic posterior circulating stroke

 

what arteries can this effect? 2

3 general sxs?

4 sxs of total occlusion?

7 sxs of a partial occlusion? 

 

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least common, often asymtomatic if cirlce of willis in intact

vertebral artery (branch of subclavian) or basilar artery

 

 

sxs

1.  homonymous hemianopsia

2. contralateral motor/sensory loss

3. ipsilateral bulbar/cerebellar signs

 

TOTAL OCCLUSION (very serious)

-pinpoint pupils

-flaccid quadriplegia

- sensory loss

-loss of cranial nerves

 

PARTIAL OCCLUSION 

-vertigo

-ataxia

-dysarthia (loss of control of tongue)

-diplopia

-visual loss

-weakness of sensory loss in the extrememites

-CN disturbances

 

83

ischemic stroke:

lacunar infarcts

 

what type of vessels does it occur in?

what percent of ischemic strokes? 

causes 2 things?

major RF?

size of dead space?

how is usually detected?

prognosis?

4 tx options

small vessel disease of deep penetrating arterioles

 

accounts 20% of ischemic strokes, causes small strokes or TIAs

 

HTN major RF!!!

less than 1.5 cm on CT/MRI

 

often dectect on CT as incidental findings

prognosis for recovery of function is usually good

 

 

 

Tx:

supportive

ASA or clopidigrel

aggressive BP and lipid control

84

what to do you do dx stroke?

Q image thumb

1. CT to r/o hemmorage

don't usually see the infarcts on CT, only 5% visible in first 24 hours which is why you have to go to the next stage!!

 

2. Angiography "gold standard" and most acurate

 

3. MRA-noninvasive

replaces need for angiogram in some patients

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85

what are 5 important risk factors for stroke?

1. HTN most powerful RF, esp systolic

2. smoking 2-4x 

3. athlerosclerosis

4. diabetes 3x

5. atrial fib-cardiac emboli

86

what percent of people with sroke don't have any WARNING sxs with stroke?

80-90%  have no warning sxs

 

most abrupt onset with nonconvulsive focal defect in vascular territory

87

how can you prevent a stroke?

4

1. carotid doppler US for screening

 

2. CHD preventrion

 

3. RF modification

-Bp control

-lipids

-diabetes

-smoking

-exercise

-diet

 

4. atrial fib and embolization

-full anticoagulation for most patients

 

 

88

what is the tx for an ischemic/infarct stroke?

2

1. CT r/o hemmorage if less than 4.5 hours use tPA given over 1 hour!!

increases potential for favorable outcomes by 50%

2. solitare device--revascularization for future

89

tx for all stroke patients both hemmorage and ischemic?

4

1. HOSPITALIZE

2. avoid rapid BP reduction-leave alone unless over 200/100

3. supportive

4. consider tPA

90

hemmorhagic stroke:

INTRACEBRAL HEMMORAGE

 

what are the vessels that are involved?

4 things it can quickly lead to?

mortality rate?

Q image thumb

RUPTURE OF SMALLE ARTERIES OR MICROANEURYSM OF THE PERFORATING VESSELS

 

RAPID PROGRESSION OF NEUROLOGIC DEFICIT

OFTEN PROGRESSING TO

HEMIPARESIS

HEMIPALEGIA

HEMISENSORY LOSS

LOSS OR IMPAITED CONCIOUSNESS 50%

 

50% MORTALITY

91

hemmoragic stroke:

subarachnoid space

 

what are the 2 causes? MC?

5 key sxs to look for?

Q image thumb

CAUSES:

MC BLEEDING FROM SACCULAR ANEURYSMS "BERRY ANEURYSM" 75% of cases

AVM

 

 

sxs:

1. MOST SEVER HEADACHE-THUNDERCLAP

2. followed with N/V

3. nuchal rigidity

3.positive kernigs-can't extend leg when lifted

4. positive brudzinskis sign-lift head causes knees to rise

***kernigs and brudzinskis are positive in meningitis but are also positive here!!**

5. fever up to 102

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92

what are the 2 dx for hemmorhagic stroke? finding?

1. CT showing hemmorage

if neg

2. spinal tap to r/o subarachnoid hemmorage via presence of blood or xanthochromia

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93

what are 4 ABSOLUTE contraindications for tPA use??

1. recent bleeding

2. prior stroke

3. BP over 185/110

4. recent major sugery

94

post stroke what are the indications for full anticoagulation? 3 medications to consider

**DECREASE RISK OF FUTURE STROKE**

 

1. embolus from the heart

2. atrial fib over 72 hours

 

heparin to warfarin bridge:

unfractioned heparin or LMWH

bridge to Warfarin

95

epidural hematoma (hemmorage)

 

 

where does it occur?

MC cause?

presentation on CT? 2

between skull and dura

 

MC-skull fracture

 

CT: convex lense shaped lesion usually in temporal area and doesn't cross suture line

 

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96

subdural hematoma (hemmorage)

 

what type of blood and from what vessel?

MC MOA?

image on CT? 2

venous bleed between dura and arachnoid MC from tearing of bridging veins

 

MC blunt trauma, contre coup and causes bleeding on opposit side of injury

 

CT: concave cresent shaped and can cross suture lines

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97

transient ischemic attack (TIA)

 

what is the defiition of this?

how long do most of these last?

what does it case increase risk for?

how does it occur?

how does pt present between episodes?

 

sudden or rapid onset of neurological deficit lasting LESS THAN 24 hours; most last less than 30 minutes

 

reversible ischemic damage done to brain cells that recover but increase risk of future stroke

 

embolic from carotid stenosis/plaque OR cardiac

 

 

EXAM BETWEEN EPISODES NORMAL!!!

 

98

how do you treat transient ischemic attack (TIA)? who qualifies for which?

3

1. carotid endarterectomy

BEST RESULTS:

1. IF SYMPTOMATIC AND OVER 70% STENOSIS

2. USE IN PTS WITH SXS AND 50-70% BLOCKAGE

 

2. carotid angioplasty/stenting

*only in non surgical candidate*

 

3. antiplatelet agents ASA or clopidigre 

99

ASA for stroke prevention

 

2 things it inhibits?

2 overal causes

inhibits:

1. cyclooxygenase

2. thromboxane A2

decreasing aggrevation and constriction

 

 

decreases frequency of TIAs and risk of subsequent stroke, or in those with previous strokes

100

clopidigrel for stroke prevention

inhibits:

1. platelet aggregration 

2. activations of glycoprotein IIb/IIa

 

slightly better effects in those who can't use ASA and those with TIA over ASA

101

tx for intracerebral hemmorage/hemmoragic stroke

 

4

1. cautious reduction of BP

2. conservative/supportive

3. surgical evacation of hematoma

4.surigal decompress (limited usefullness)

102

tx for subarachnoid hemmorage/hemmoragic bleed?

4

1. Bedrest!

2. supportive with cautious reduction in BP

3.angiography once patient stable

4. surgery or coil placement once stable to prevent rebleeding

103

benign essential tremor

 

4 provoking

3 palliating

 

provoking

stress

fatigue

CNS stimulants

voluntary activity

 

palliating

ETOH

BB

rest

104

benign essential tremor

 

key fact?

6 key things you need to know about this

most common movement disorder

 

KEY:

1. OLDER, ESP OVER 60

2. INSIDIOUS ONSET, SLOW PROGRESSION

3. UNILATERAL PROGRESSES TO BILLATERAL

4. 95% START ON THE ARM (UPPER EXTREMITY)

5. GETS WORSE WITH ACTION

 (not at rest w/o influence of gravity, only gonna see when moving)

6. NORMAL NEURO EXAM!!!!!!!!!!!!!!!!!

105

benign essential tremor

 

2 tx options

1. primidone-anticonvulsant

no in asthma

SE:

a. dizziness

b. nausea

c. mood changes

 

2. BB propanolol

no in cardiac, bradycardia, conductions defects

106

benign essential tremor

 

3 take home

1. action tremor

2. neurological exam normal

3. slow onset

107

parkinsons disease

 

what is the patho of this?

4 cardial signs?

3

3

4

3

neurodegenerative disorder resulting from diecrease dopaminergic transmission in basal ganglia parkinsons think dopamine

 

four cardinal sxs:

1. TREMOR

occurs in 85%

resting tremor, PILL ROLLING

one limb or one side for months to years

spares head

 

2. RIGIDITY

iincreased reistance to passive movement COGWHEELING rigidity

no weakness!!!!!!!!!!!!

no change in DTRS!!!!!!!!!!!!!!!!!

 

 

3. BRADYKINESIA

slowness to get moving "start hesitation"

effects voluntary movements and speech

 

4. POSTURAL IMPAIRMENT

difficulty with balance and gate

stooped over, leaning forward

occurs later in disease course

fenesterating gate, with stopping on turns

fast short steps

 

 

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108

what are 4 things that reduce your risk for parkinsons?

1. coffee

2. smoking

3. NSAIDS

4. estrogen replacement

109

what is the pathology of parkinsons?

pathological hallmark?

loss of melanin containing, dopaminergic neurons in the substantia nigra

 

lewy bodies

-pathological hallmark of PD

when in basal ganglia

110

what are five things that make it likely not parkinsons and oculd fool you?

1. no response to levodopa

2. symmetrical and bilateral presentation

3. rapid progression and early falls

4. early cognitive deficits

5. abnormal eye movements

111

what are 6 RF for parkinsons disease?

FH 5-10% increase in risk

male

pesticide exposure

head trauma

rural living

well water

112

myasthenia gravis crisis

 

 

what is this?

when does it occur?

5 things to consider as part of tx?

respiratory weakness that can lead to RESPIRATORY FAILURE

 

spontaneously or during active phase disease or trigger

 

TX:

admit to ICU

monitor FVC

stop ACH inhibitors

start IV IG or plasmaphoresis

high dose immunomodulating

113

what are the descriptions of the gait of parkinsons?

3

1. festinating gate "slow start"

2. short fast steps

3. turn on bloc, stop before changing direction

114

what are 7 other sxs you might find with on exam in parkinsons?

1. Mask like face

2. decreased blinking

3. dementia 6x normal rate

4. micrographia

5. hypophonia

6. depression

7. akinesia

115

what are 6 take homes of parkinsons disease?

1. PILL ROLLING

2. GAIT DISTURBANCES

3. START HESITATION

4. SLOW ONSET

5. TREAT WHEN FUNCTIONABILITY DISABILITY BEGINS

6. DOPAMINE

116

parkinson's disease

 

when do you treat?

5 medication options for this?

start when functional disability starts

Goal:  maintain function and ADLS

 

1. Levadopa Gold standard comboed with carbidopa or entacapone 

(increases the length that medications could work)

 caution though because these meds wear off in about 5 years and then nothing left, so not a good option! 

CONVERTED TO DOPAMINE IN THE BRAIN

asymptomatic once these drugps stop

 

2. dopamine agonist

stimulate receptor directly

used when levadope no longer working

-perdolide

-ropinirole

 

3. anticholinergic

primarily allevaites tremor

-benzotrophine

 

4. amantadine

5. MAO-B-inhibitor

decrease breakdown of dopamine

selegiline

117

parkinsons

what is a non-med option for parkinsons?

deep brain stimulation

surgical implanted neurostimulation in subthalmic nucleus

 

**blocks the abnormal signals that cause PD**

118

huntington disease

 

what type of disorder is this?

3 NT?

age of onset and fatality?

autosomal dominant neurodegenerative disorder

1. decreased GABA

2. decreased acetylcholine 

3. increased dopamine

 

age of onset:

30-50 fatal in 15-20 years

119

huntingtons disease

 

what is the triad associated with this?

1. motor

2. cognitive

3. psychiatric

120

hungtintons disease

motor

 

4 key catecorys of presentation

1. chorea

involuntary, irregular, rapid, uncontrolled, excessive movement

 

2. athetosis

proximal limb writhing

 

3. hemiballismus

violent, proximal limb flinging

 

4. impaired movement

abnormal eye movements

slow or uncoordinated fine motor control

dysarthria

dysphagia

gait disturbance

bradykinesia and rigidity late in course as chorea peaks and wanes

121

huntingtons disease

cognitive

 

4 sxs

**cognitively pt isn't bothered/notices it**

**movement disorder with significant cognitive affect**

 

1. dysfunction of executive functions like organization, regulation, and perception

2. problems with planning, judgement, emotion, regulation, attention, learning, cognitive speed, decision making

3. temper outbursts

4. usually result in placement outside of home before psychiatric or movement issues do

122

huntington disease

psychiatric

 

5 presentations

1. depression

2.mania

3. OCD

4. apathy

5. anxiety-rigid thinking develops and departure from routine very upsetting

123

hungtingtons disease

 

3 txs drug classes?

what else to do?

3

2

2

NO CURE

 

1. neuroleptics

-haloperidol

-risperodone

-fluphenazine

2. benzodiazepines

-cloneazepam

-diazepam

3. dopamine depleting agents

-reserpine

-tetrabenzine

4. REFER TO SPECIALTY

124

genetics of huntingtons

 

inheritance?

chance of child getting it?

where is the defect? what is it?

autosomonal dominant disease

50% chance of child getting it

 

4th autosomal chromosome with excess CAG sequence-40+ will cause this!!!

125

Cerebral Palsy

 

what is this?

3 options of presentation?

SXS

2

1

4

Q image thumb

involuntary sustained or intermittent muscle contractions cause twisting and repetitive movements, abnormal posture or both

 

presentaiton:

1. arm and leg on one side (hemiplegic)

FLOPPY OR SPASTIC HAND

WALKS ON TIP TOE OF EFFECTED SIDE

 

2. both legs only (diplegic)

CONTRACTURES OF THE ANKLES AND FEET

 

3. both arms and both legs (quadriplegic)

-ARMS HEAD AND MOUTH MAY TWIST STRANGELY

-SEVERE BRAIN DAMAGE THEY CAN'T WALK

-KNEES PRESS TOGETHER

-LEG AND FEET TURN INWARD

 

 

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126

cerebral palsy

 

3 tx options

1. sugery to cut extensors to prevent fracturs in fingers from being tense surgical release

2. strength training

3. botulinum toxin

127

cerebral palsy

 

4 associated conditions with this ?

1. epilepsy

2. developmental delay

3. behavior issues/learning disabilities

4. fractures-always suspect atraumatic because they contract so hard they can break bone

128

myasthenia gravis

 

what is important to remember about this?

what type of condition is it?

explain 3 patho of this?

what are the 2 types?

autoimmune

uncommon but MC disease of neuromuscular transmission

"fatiguability of muscles"

 

patho

1. antibody against nicotinic AchR at NMJ

2. Ab impairs that ability of the Ach to bind to AchR and some destroy the receptors

3. some Ab against MuSK **muscle specific typrosine kinase**

 

types:

1. ocular-eyes/lids only but within 2 years

2. generalized

129

myasthenia gravis

 

 

what do patients have a high correlation with?

when does this occur in men and women?

genetic relationship?

 

high correlation with thymic abnormalities

this is where T cells learn self from non self and where they mature

 

women: child bearing years

men: 6th-7th decade

 

 

HLADR3-genetic predisposition

 

130

myasthenia gravis

 

 

6 sxs of this?

pattern of sxs?

when is it worse? 2 things

1. facial-get worse over time

ptosis

diplopia

slack jaw-open mouth, can't hold shut

bulbar muscle weakess (chewing, swalling, speech)

expressionalism face

neck muscles (head drop)

can progress down to respiratory muscles and limb weakness

 

***can flucuate throughout the day***
****WORST AT NIGHT OR AFTER EXERCISE***

131

myasthenia gravis PE

 

two signs you can see while doing tests in the exam room? 2

1. simpson test-drooping eyelid with forced upward focus from fatigue

 

2. cogan lid twitch: follow finger and they get fatigue of the eyelid and it drops

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132

myasthenia gravis

 

what are the 5 tests you want to do?

which 2 would be the 2 tests you would want to make sure to do?

Q image thumb

1. Tensilon test

give short acting AchR inhibitor--allows for the ACH to stay around more and it fixes the fatigue (pick on the front)

 

2. Ice pack test

neuromuscular transmission improves at cold temps and the muscle fatigue disipates (pic on this side), 80% sensitive

 

3. antibody against NAchR (nicotinic ACH receptors) THIS IS THE FIRST THINK YOU WOULD REALISTICALLY DO!!

80-90% have this

 

4. CT/MRI of the thymus DO THIS FOR EACH PATIENT AS WELL

 

5. repetitive nerve stimualation studies

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133

myasthenia gravis

 

 

what are 4 tx options for this?

1. acetylcholinesterase inhibitor

inhibits the enzymes that break down ACH, leading to more avaliable ACH which leads to MORE muscle stimulation

pyridostigmine

 

2. immunomodulation

corticosteroids

azathioprine

cyclosporine

 

3. thymectomy only younger

4. plasmapharesis (plasma exchange)-$$$ but for myasthenia gravis crisis

 

134

muscular dystrophies

what is this? 

what does it cause?

wheere is the problem?

genetic link?

inherited disorder causing progressive muscles weakness and atrophy

 

this is a disorder of the muscle that prevents it from responding to signal

 

x-linked chromosomal

135

duchenne muscular dystrophy

what is this?

who does it occur in?

onset? progression? Life expectancy?

3 sxs? progression?

1 tx?

defective X chromosome so THEY DON'T PRODUCED DYSTROPHIN (leading to enzymatic breakdown of the muscle)

 

occurs in males, females asymptomatic carriers

 

ONSET: 2-3 years old

 may be wheelchair bound by 12

life expectancy into 20s

 

 

SXS: 

start on trunk and spread to extremities

-cardiomyopathy

-scoliosos

-fractures from falls

 

DX:

ELEVATED CK

 

TX: CORTICOSTEROIDS

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136

beck muscular dystrophy

 

wha tis this and how is it different than DMD?

genetic link?

survival age?

spread of sxs? 

1 tx?

similar to DMD, but

they make some dystrophin

-defective X chromosome

 

age of onset leter than DMD

likely elevation of CK

survival into 40s

 

 

sxs:

start on trunk and spread to legs

-can effect the heart

 

TX: corticosteroids

 

 

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137

emery-dreifuss muscular dystrophy

 

who do you find this is?

exaplin the sxs spreading pattern?

classic triad....what is this?

3 dx options?

unique to know about this?

many different inhertance patterns and in BOTH men and women

 

SXS:

MUSCLE WEAKNESS BEGINS IN ARMS AS TEEN AND PROGRESSES TO LEGS AND FACE

 

TRIAD:

1. CONTRACTION OF THE ELBOWS, PLANTOR FLEXORS, AND SPINE

2. HUMEROPERONEAL WEAKNESS

3. CARDIAC ABNORMALITIES (ARRYTHMIA, CARDIOMYOPATHIES)

 

DX:

1. CK slightly elevated

2. EMG

3. genetic testing

 

*****STILL AMBUATORY 20 YEARS AFTER SX****

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138

myotonic dystrophy

 

 what is this?

in who?

3 sxs? (where)

3 dx techniques?

most common form of MD

males and females

 

SXS:

1. muscle siffness

2. inability of muscles to relax after contraction **shaking somones hand and can't get go**

3.muscle loss and weakness

-facial

-arms/legs

-cardiac complications

-caracts

-abnormal intellectual functioning

 

DX:

1. slightly elevated CK

2. genetic testing

3. clinical findings

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139

facioscapulohueral muscular dystrophy

 

who is this in?

genetic pattern?

2 main findings?

1 main dx 2 others?

males and females

autosomal dominant

 

 

profound facial weakness "pouting appearance"

progresses to include shoulders/hips (WC bound by 9-10)

 

 

DX:

1. as patient try to push up and sip up

2. slightly elevated CK

3. genetic testing

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140

limb-girdle muscular dystrophy

 

what are the 4 characteristics of this?

1 tx option?

over 20 subtypes

 

-muscle weakness patterns

-cardiac involvement

-contractures

-AFFECTS THE SHOULDER GIRDLE AND HIP GIRDLE

 

TX:

1. STRETCHING TO PREVENT CONTRACTURES

141

what are the inheritance patterns for muscular dystrophies depending on:

 

1. one parent has gene

2. both parents have diease

3. both pareitns are carriers

4.only one parent is a carrier

1. 50% percent chance the child will get it the gene if one parent is effected

 

2. 75% chance if the parents BOTH have the gene and are effected

 

3. 25% chance if the parents are BOTH carriers of the gene that the child will get it

 

4. 50% change if one of the parents are carrier and one is NOT effected

142

what are some tx options you can give to help with the sxs of muscular dystrophies? 6

1. steroids

2. Ca/vit D

3. ACE1

4. BB

5. face/defibulator

6. pulmonology support

143

tourette disorder

 

what is this?

4 dx of criteria?

age of onset?

 

inherited neurobehavioral disorder characterized by sudden involuntary, repetitive muscle movements and vocalizations

 

DX CRITERIA:

1. multiple motor or one or more vocal tics at some time during the disorder 

2. tic episodes several times a day, almost every day or periodically during period over a year

3. change in type, severity, complexity, frequency, 

4. sxs before 18

 

 

sxs onset: 2-15 y/o

50% have sxs but age 7

***SXS BEFORE !***

 

144

tourettes

motor tics

 

initlal sxs

secondary sxs

1. initially

blinking

face twitch

head jerk

shrug

neck stretch

sniffing

 

2. over time

squatting

jumping

repetitive touching

deep knee bends

smelling things

spinning

echopraxia:  meaningless repetitiion or imitation of the movements of others

145

tourettes

vocal tics

 

simple tics

advance tics

1. simple tics

grunts

throat clearing

sigh

bark

hiss

snort

sniff

2. advanced tics

repeating words or phrases out of context

palilalia-repeating ones own words

echolalia-repeating heard words

coprolalia (common mainstream depictions) "dropping the F bomb"

146

course of tourette progression

4

waxing and waning course

usually combination of motor and verbal tics

few to many times a day often in clusters

lifelong but sxs decrease or resolve in adolescence or adulthood

147

what are the associated sxs of tourettes?

4

obsessive compulsive behaviors 25%

attention deficit 50-80%

rage/poor impulse control 30%

anxiety 25%

148

tourettes

4 tx options

 

do IF they present a problem

1. dopamine antagonists/antipsychotic

haloperidol

fluphenazine

risperidone

2. antianxiety

benzodiazepine

buspirone

3. antidepressants-ssri

4. alternatives

botox into involved muscles

habit reversal training

biofeedback relaxation training

149

what are the 3 take homes of tourettes?

1. TX GOAL: FUNCTION PRESERVATION

 

2. MANY WILL HAVE OTHER PSYCHIATRIC ISSUES

 

3. MEDS CAN BE USEFUL BUT DON’T FORGET BEHAVIOR MODIFICATION THERAPY