Neuro Flashcards
(149 cards)
1
Q
dementia
what are 5 key features you may find?
A
1, memory loss
- speech and language difficulties
- problem solving difficulties
- impaired judgement
- may have mood issues
2
Q
dementia
mood issues include? 5
A
depression
agitation
delusions
insomnia
disinhibition
3
Q
what are 3 neurological features that might help explain the neuro changes seen in dementia?
A
- changes in cerebral circuits
- nerve loss
- changes in neurotrasmitters
4
Q
what is the most common form of dementia?!
A
alzheimers
5
Q
what are the 8 causes of the different types of dementia?
A
- alzheimers
- vascular dementia
- multi-infarct dementia
- frontotemporal dementias (huntingtons)
5 parkinsons dementia
- dementia with lewy bodies
- ETOH/drugs
- viral (creutzfeld-jakob)
6
Q
what are the two most common forms of dementia?
A
1- parkinsons dementia-50%
7
Q
alzheimers dementia
what to keep in mind about htis?
what causes this? 2
do they know they have it?
A
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
Q
who is there a higher incidence of alzheimers dementia in?
A
down syndrome pts
9
Q
alzheimers dementia
8 presentations
A
- word finding issues/speech difficulties
- wandering/getting lost
- poor judgement
- delusions
- agression
- sleep disturbance
- incontinence
- bedriddent status
10
Q
alzheimers disease
why is it difficult to dx?
A
you can only confirm on autopsy with brain bx
11
Q
what are the 3 most important risk factors for alzheimers dementia?
A
- OLD AGE—–most important RF
- family hx
- female gender
12
Q
how do you confirm alzheimer on autopsy?
A
apolipoprotein 4 on autopsy
13
Q
vascular dementias
what to remember about this?
who do you find this in?
what are the type?
A
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
Q
frontotemporal dementia
what is this caused by?
4 early sxs? what comes later?
what are 3 diseases that cause this?
A
caused by degeneration of the frontal (behavior) and temporal lobe
early features include:
- attention issues
- judgement impairment
- awareness
- behavior issues
***memory loss seen in later disease***
- huntingtons chorea
- picks disease
- progressive supranuclear palsy
15
Q
huntington’s chorea
inheritance pattern?
where is defecT?
A
autosomal dominant-50% chance for kids
chromosome 4
16
Q
frontotemporal dementia:
picks disease
what does this result in?
what do you see on testing?
tx?
A
anterior frontal and temporal cerebral cortex with MARKED personality changes
***intracellular inclusion (pick bodies) stain with silver stain
Tx:
NONE
tx behavior
17
Q
what are the lewy bodies that are seen in dementia?
A
intaneuronal cytoplasmic includsions that stain with PAS staining
18
Q
demenia:
progressive supranuclear palsy
what are 4 things this is qualifed by?
how long does the person have to live?
tx?
A
- falls
- gaze paralysis cant look down
- rigidity
- dementia
death within 5-10 years, no tx
19
Q
dementia:
normal pressure hydrocephalus
what are 3 sxs?
2 dx methods?
1 tx?
A
- gate ataxia
- dementia
- urinary incontinence
**think falling adult who is incontinent**
DX:
- LARGE VENTIRICLES ON IMAGING/CT
- sume use MRI or CSF tap
tx: shunting
20
Q
dementia:
korsakoff syndrome
what is this?
A
can’t recall recent memory despite immediate memory retention
easily confusable
21
Q
what is a vitamin deficiency that can cause dementia?
A
B12…macrocytic anemia…causes spinal cord issues “myelepathy”
REPLACE IT
22
Q
dementia
5 workup you want to do
A
- history
- mini mental exam
- full neuropsychiatric testing
- B12, thyroid function
- consider CT/MRI to turn our tumor/infarction
23
Q
dementia
3 tx options for the actual dementia itself
A
- anti-acetylcholinesterase
**increase ach by inhibiting cholinesterase**
effects last about a year
- donepexil (aricept)
- galantamine
- riovastgmine
- NMDA receptor antagonists
**blocks this over-excitatory neurotransmitter**
used for mod to severe disease WITH ANTI-CHOLINESTERASE DRUGS
- Memantine (namenda)
- COMBO MEMANTINE PLUS DONEPEZIL for alzheimer dementia “Namzaric”
***all can be used in AD or parkinson’s dementia***
24
Q
what are the goals of txing dementia with medication?
A
- delay progression of the disease
- improve caregiver disease
- decrease agitation
**can be used in AD and parkinsons…outcomes not as good in other dementia forms**
25
dementia
## Footnote
tx options for behavior
VERY DIFFICULT
antipsychotics:
1. haloperidol
2. resperidone
26
delirium
## Footnote
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
## Footnote
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
## Footnote
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:
## Footnote
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
## Footnote
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
## Footnote
what are the two maine categories of this?
what causes each?
1
3
_partial_:
## Footnote
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
## Footnote
\*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
## Footnote
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?
## Footnote
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?
## Footnote
1 theory?
5 causes?
harrisons: shift in balance of excitation and inhibition of the CNS
## Footnote
1. change in seizure threshold
2. genetic role
3. traumatic brain injury
4. strokes infection
5. stress, sleep deprevation, menses, medications
47
febrile seizures
## Footnote
who does this occur in?
3 associations?
how many?
3 months-5 years
## Footnote
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?
## Footnote
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
## Footnote
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
51
status epilepticus
## Footnote
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
## Footnote
4 tx options?
dx: metabolic workup
Tx:
1. **benzodiazepine ( lorazepam, diazepam, midazolam)**
**2. phenytoin**
**3. phenobarbital**
**4. anesthesia**
53
multiple sclerosis
## Footnote
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_**
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_**
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)
57
multiple sclerosis:
**_progressive relapsing_**
what is the pattern of this?
steady decline since onset with superimposed attacks
58
multiple sclerosis:
## Footnote
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**
59
multiple sclerosis:
## Footnote
3 dx methods/criteria?
what do you find on each?
1. **_mcdonald criteria_**:
## Footnote
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)_**
60
multiple sclerosis:
## Footnote
what is the goal of txing?
for acute attacks?
what are the three choices?
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!!\*\*\*
61
potenital for a Multiple sclerosis cure
## Footnote
what is the option?
what is included in this? 2
what is the benefit of htis?
stem cell treatment (HALT-MS)
## Footnote
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
## Footnote
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
## Footnote
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
## Footnote
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
## Footnote
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
## Footnote
2 groups
if CSF is cloudy....TX EMPIRICALLY and START ASAP
## Footnote
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
## Footnote
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_**
## Footnote
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
## Footnote
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:
## Footnote
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\*\*
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?
**_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)
80
ischemic stroke in middle cerebral artery (MCA)
## Footnote
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?
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)
## Footnote
what areas are the most common effected? 2
7 sxs of this including 2 reflexes?
THINK FEET/LEGS
## Footnote
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
## Footnote
what arteries can this effect? 2
3 general sxs?
4 sxs of total occlusion?
7 sxs of a partial occlusion?
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?
1. **_CT to r/o hemmorage_**
## Footnote
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
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:
## Footnote
**_INTRACEBRAL HEMMORAGE_**
what are the vessels that are involved?
4 things it can quickly lead to?
mortality rate?
**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?
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**
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_**
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)
## Footnote
where does it occur?
MC cause?
presentation on CT? 2
between skull and dura
## Footnote
MC-skull fracture
CT: convex lense shaped lesion usually in temporal area and **doesn't cross suture line**
96
subdural hematoma (hemmorage)
## Footnote
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
## Footnote
**_MC blunt trauma, contre coup and causes bleeding on opposit side of injury_**
CT: concave cresent shaped and can cross suture lines
97
transient ischemic attack (TIA)
## Footnote
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_**
## Footnote
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
## Footnote
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
## Footnote
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
## Footnote
4 provoking
3 palliating
provoking
## Footnote
stress
fatigue
CNS stimulants
voluntary activity
palliating
ETOH
BB
rest
104
benign essential tremor
## Footnote
key fact?
_6 key things you need to know about this_
most common movement disorder
## Footnote
**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
## Footnote
2 tx options
1. primidone-anticonvulsant
## Footnote
no in asthma
SE:
a. dizziness
b. nausea
c. mood changes
2. BB propanolol
no in cardiac, bradycardia, conductions defects
106
benign essential tremor
## Footnote
3 take home
1. action tremor
2. neurological exam normal
3. slow onset
107
parkinsons disease
## Footnote
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_**
i**_increased 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_**
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
## Footnote
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
## Footnote
when do you treat?
5 medication options for this?
**_start when functional disability starts_**
## Footnote
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
## Footnote
what type of disorder is this?
3 NT?
age of onset and fatality?
autosomal dominant neurodegenerative disorder
## Footnote
1. decreased GABA
2. decreased acetylcholine
3. increased dopamine
age of onset:
**_30-50 fatal in 15-20 years_**
119
huntingtons disease
## Footnote
what is the triad associated with this?
1. **_motor_**
2. **_cognitive_**
3. **_psychiatric_**
120
hungtintons disease
**_motor_**
4 key catecorys of presentation
1. **_chorea_**
## Footnote
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
## Footnote
3 txs drug classes?
what else to do?
3
2
2
NO CURE
## Footnote
1. neuroleptics
- haloperidol
- risperodone
- fluphenazine
2. benzodiazepines
- cloneazepam
- diazepam
3. dopamine depleting agents
- reserpine
- tetrabenzine
4. REFER TO SPECIALTY
124
genetics of huntingtons
## Footnote
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
## Footnote
what is this?
3 options of presentation?
SXS
2
1
4
**_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
126
cerebral palsy
## Footnote
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
## Footnote
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
## Footnote
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
## Footnote
what do patients have a high correlation with?
when does this occur in men and women?
genetic relationship?
high correlation with thymic abnormalities
## Footnote
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
## Footnote
6 sxs of this?
pattern of sxs?
when is it worse? 2 things
1. facial-get worse over time
## Footnote
**_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
## Footnote
two signs you can see while doing tests in the exam room? 2
1. _simpson test-_drooping eyelid with forced upward focus from fatigue
## Footnote
2. _cogan lid twitch_: follow finger and they get fatigue of the eyelid and it drops
132
myasthenia gravis
## Footnote
what are the 5 tests you want to do?
which 2 would be the 2 tests you would want to make sure to do?
**_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_**
133
myasthenia gravis
## Footnote
what are 4 tx options for this?
1. acetylcholinesterase inhibitor
## Footnote
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
136
beck muscular dystrophy
## Footnote
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
137
emery-dreifuss muscular dystrophy
## Footnote
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\*\*\*\*
138
myotonic dystrophy
## Footnote
what is this?
in who?
3 sxs? (where)
3 dx techniques?
most common form of MD
## Footnote
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
139
facioscapulohueral muscular dystrophy
## Footnote
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
140
limb-girdle muscular dystrophy
## Footnote
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
## Footnote
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
## Footnote
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
## Footnote
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
## Footnote
2. MANY WILL HAVE OTHER PSYCHIATRIC ISSUES
3. MEDS CAN BE USEFUL BUT DON’T FORGET BEHAVIOR MODIFICATION THERAPY
