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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

10% of patients have this

progressively worse sxs from the start

stady increase in disability without attack

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

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

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

1. polysomnography (sleep study)

2. thyroid study

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

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

3 mo and older: ceftriaxone + vancomycin

immunocomprimized/hospital acquired: amipcilin + ceftazidime + vancomycin

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

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

1.  LP

-lymphocytes

other stuff normal

tx:

1. supportive unless HSV origin, then give acyclovir

2. tx sxs

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

mycobacterium tumberulosis

fungi ( crytococcus, coccidioides, histoplasma)

spirochetes (treponema pallidium, borellia)

highest occurrance in immunocomprimised patients

weeks to months to develop

DX:

CULTURE

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

ichemia and infart from thromus/emboli (85%)

hemmorage/blled (15%)

myocardial infarction

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

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**

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)

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

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

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

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

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

1. HTN most powerful RF, esp systolic

2. smoking 2-4x 

3. athlerosclerosis

4. diabetes 3x

5. atrial fib-cardiac emboli

80-90%  have no warning sxs

most abrupt onset with nonconvulsive focal defect in vascular territory

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

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

1. HOSPITALIZE

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

3. supportive

4. consider tPA

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

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

1. CT showing hemmorage

if neg

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

1. recent bleeding

2. prior stroke

3. BP over 185/110

4. recent major sugery

**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

between skull and dura

MC-skull fracture

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

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

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!!!

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 

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

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

1. cautious reduction of BP

2. conservative/supportive

3. surgical evacation of hematoma

4.surigal decompress (limited usefullness)

1. Bedrest!

2. supportive with cautious reduction in BP

3.angiography once patient stable

4. surgery or coil placement once stable to prevent rebleeding

provoking

stress

fatigue

CNS stimulants

voluntary activity

palliating

ETOH

BB

rest

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!!!!!!!!!!!!!!!!!

1. primidone-anticonvulsant

no in asthma

SE:

a. dizziness

b. nausea

c. mood changes

2. BB propanolol

no in cardiac, bradycardia, conductions defects

1. action tremor

2. neurological exam normal

3. slow onset

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

1. coffee

2. smoking

3. NSAIDS

4. estrogen replacement

loss of melanin containing, dopaminergic neurons in the substantia nigra

lewy bodies

-pathological hallmark of PD

when in basal ganglia

1. no response to levodopa

2. symmetrical and bilateral presentation

3. rapid progression and early falls

4. early cognitive deficits

5. abnormal eye movements

FH 5-10% increase in risk

male

pesticide exposure

head trauma

rural living

well water

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

1. festinating gate "slow start"

2. short fast steps

3. turn on bloc, stop before changing direction

1. Mask like face

2. decreased blinking

3. dementia 6x normal rate

4. micrographia

5. hypophonia

6. depression

7. akinesia

1. PILL ROLLING

2. GAIT DISTURBANCES

3. START HESITATION

4. SLOW ONSET

5. TREAT WHEN FUNCTIONABILITY DISABILITY BEGINS

6. DOPAMINE

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

deep brain stimulation

surgical implanted neurostimulation in subthalmic nucleus

**blocks the abnormal signals that cause PD**

autosomal dominant neurodegenerative disorder

1. decreased GABA

2. decreased acetylcholine 

3. increased dopamine

age of onset:

30-50 fatal in 15-20 years

1. motor

2. cognitive

3. psychiatric

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

**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

1. depression

2.mania

3. OCD

4. apathy

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

NO CURE

1. neuroleptics

-haloperidol

-risperodone

-fluphenazine

2. benzodiazepines

-cloneazepam

-diazepam

3. dopamine depleting agents

-reserpine

-tetrabenzine

4. REFER TO SPECIALTY

autosomonal dominant disease

50% chance of child getting it

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

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

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

2. strength training

3. botulinum toxin

1. epilepsy

2. developmental delay

3. behavior issues/learning disabilities

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

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

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

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***

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

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

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

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

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

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

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****

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

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

over 20 subtypes

-muscle weakness patterns

-cardiac involvement

-contractures

-AFFECTS THE SHOULDER GIRDLE AND HIP GIRDLE

TX:

1. STRETCHING TO PREVENT CONTRACTURES

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

1. steroids

2. Ca/vit D

3. ACE1

4. BB

5. face/defibulator

6. pulmonology support

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 !***

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

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"

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

obsessive compulsive behaviors 25%

attention deficit 50-80%

rage/poor impulse control 30%

anxiety 25%

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

1. TX GOAL: FUNCTION PRESERVATION

2. MANY WILL HAVE OTHER PSYCHIATRIC ISSUES

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