Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical medicine > Neuro > Flashcards

Neuro Flashcards

1
Q

Viral Meningitis

A 
WBC <250 
Lymphocyte predominance
PMN early predominance
Protein <150mg/dl 
Glucose <0.5 serum glucose (pretty normal , 0.6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bacterial Meningitis

A 
>1000 WBC 
PMN predominance (neutrophils for infection/imflammation)
Glucose <18 mg/dl Strong predictor
Protein <250 mg/dl
Glucose <45mg/dl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

EEG

Electrocephalography

A

measures electrical activity in the brain

ID abnormal electric activity =seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

EMG

electromyography

A

muscle diseases - fan on how well the repond to stimuli
neuromuscular junction
peripheral nerve disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NCV

Nerve Conduction Studies

A

Amplitude and velocity of signal coming down axon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Visual evoked potential studies

A

MS, Cerebellopontine, brainstem lesion (all demyelination disorders)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MRI

Magnetic Resonance Imaging

A 
Hi Res -1-2 mm slice
Contrast=Gadolinium (safe for CKD)
Slow 30-45 minute
uncomfortable
expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ct

Computed Tomography

A

5mm slice
iodine Contrast (allergies shellfish)
prednisone and bendryl
CKD= cause contrast induced neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

MR and CT Angiography

A

non invasive visulization

head and neck vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Non invasive ultrasound

A

Carotid and vertebral disease
look for the plaque that causes stroke
Transcranial Doppler: looks for spasm of inter cranial vessels that can cause stoke following SAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SPECT

Single photon Emission

A

Looks at blood flow (inter cranial)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PET

Positive emission topography

A

functional imaging
id’s metabolic disorders (Oncology)
light up metasticies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

blood in Subarachnoid Space

meningeal irritation

A
  1. Traumatic Bleed- leaking of the vessels due to trauma
  2. Aneurysm
    Blood out of vessels is toxic, causes inflammatory response.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hemispheric mass lesion

A 
Either expands across midline laterally 
or vertically
- Structural hemispheric lesion 
       Pushes contents to one side
-lateral herniation 
Transtentorial herniation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Structural Hemispheric Lesion

A

Pushes contents over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lateral Herniation

A

add something to one side it will shift the contents over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Transtentorial herniation

A

Pushes down-something big on top pushes down into cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Tonsilar Herniation

A

Cerebellar tonsil gets pushed into foramen magnum(complete herniation)

  • once it happens vasculature gets clamped and no flow into the head
  • no blood flow=infaction =brain dead
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Herniation

A

displacement of object into another compartment in which it wasn’t designed to go

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Dolls Eye Reflex

A

Normally eyes can maintain focus on object
Lose=Pressure on the brainstem
Lack of dolls eye
- Turn head to the side quickly - eyes will go with turn and slowly drift back to focal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Oculocephalic Reflex

A

Cold Caloric Test

  • ice water into syringe
  • person faking catatonia or lack of consciousness
  • squirt water into eye drum
  • effects balance - nystagmus
  • NO MOVEMENT OF EYES=lack of dolls eye
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Thiamine Deficiency

Deficiency State

A

Found in Alcoholics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Glucose Deficiency

Deficiency State

A

Hypoglycemic=may be delirious and confused

- < 20 Glucose (around this lower point=goofy, confused, delirious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Na Deficiency

Electrolyte Deficiency

A

Lack of Na
Causes mental changes
Hyponatremia-can cause mental status changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Exogenous Substances (toxins)

A

Medications can cause delirium, confusion, and coma (ex: heroin OD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Endogenous Substances (toxins)

A

Stuff we make inside our body

  • ex Lactic Acid
    • anaerobic metabolism =hypoxia (low O2) byproduct is Lactate
    • Lactate causes severe confusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Uremia

A

High Levels of Waste
- Profound encephalopathy
- People who stop dialysis, die peaceful death, get high build up of uremia, loose consciousness, and K rises and heart block
=Endogenouse Substance
(#1 cause of delirium and confussion in geriatric population is UTI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

(what to think?)

Headache First

A

Headache
Meningitis (inflammation of brain &spinal cord)
encephalitis (inflammation of brain)
intracranial hemorrhage (bleed inside skull)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q 
(what to think?)
First they were:
Intoxication
confused
delirium
A

infection causes: ex-Meningitis

exogenous toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

(what to think?)

Apoplectic (big) event causing coma

A
  • ischemia

- hemorrhagic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q 
(what to think?)
Lateralizing symptoms of
Hemiparesis
Aphasia 
before coma
A

Hemiparesis=m. weakness or partial paralysis on 1 side
Aphasia= language difficulties
Think about
Mass Brain Tumor (lesion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Early Diencephalic

Based on lesion

A

Stage of eye reflex occur diencephalon above Thalmus
Pupillary -normal pupils
-constrict with light
eye Reflex: Dolls eyes are intact
Motor Response: movement of extremity toward pain, nudge away from pain, contralateral extremity paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Late Diencephalic

based on lesion

A

Thalamus and above
Pupillary: Eyes Round, equal, and reactive to light
eye Reflex: Dolls eye is positive
Motor: Lose of consciousness with arm/ leg flexion (called Decorticate posture)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Midbrain

based on lesion

A

Pupils: unresponsive, mid and fixed, no light response-first unilateral then bilateral
-things are getting non reversable
eye reflex: no dolls eye
- occulocephalic reflex intact (cold water in ear eyes will bounce toward eye with water
Moter: Extension arms and legs (decerebrate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Pons of Upper Medualla

(based on lesion

A 
Pupils: equal, not responsive to light, dilated
Eye reflex: Dolls eyes are negative
      - getting close to brain death
Motor: Lost extensor of Midbrain
     -Flaccid paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Glasgow Coma Scale

A 
EVM    456
Eye opening Response 1-4 
4- SPONTANEOUS (looking around) 
3- TO SPEECH
2- TO PAIN
1- NO RESPONSE
verbal Respons 5
5- ORIENTED TO TIME, PLACE, AND PERSON
4- CONFUSED or disoriented (ask for mom) 
3- INAPPROPRIATE WORDS (incoherent) 
2- INCOMPREHENSIBLE SOUNDS 
1- NO REPSONE
Best Motor Response 6
6- OBEYS COMMANDS (2 part command to check) 
5- MOVES TO LOCALIZED PAIN  push away (very purpose)
4- ABNORMAL WITHDRAWAL (purposful move
3- ABNORMAL FLEXION (DECORTICATE)
2- ABNORMAL EXTENTION (DECEREBRATE)
1- NO RESPONSE
TotAL 
COMATOSE 8 OR LESS
TORALLY UNRESPONSIVE DEAD 3 
is no zero
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Differentiate between Structural and Metabolic Causes of coma?

A

3 Features of Physical Exam

  1. motor response to painful stimuli
  2. Pupillary function
  3. Reflex Eye Movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Structural Lesions

A

Present in stepwise fashion.
-pupils will be reactive to Midbrain
-doll’s eye will be intact till midbrain medulla
-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Non structural lesion in brain like inflammation or infection

A

Stages will all be jumbled up won’t be stepwise down the brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Metabolic lesions

A

do not progress stepwise-pupils intact until resp and cardiac support.

  • quickly go from delirium to requiring respiratory and cardiovascular support
  • happens quickly
  • inflammation affecting respiratory drive center in the brain stem.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Seizure

Occurrences

A

Number of reasons they occur

1) hereditary seizure
- epilepsy: not associated with metabolic dis, not brain hemorrahge, not imflammation
2) ACUTE: encephalitis, hypo-hyperglycemia, hyponeutremia, HTN
3) Chronic: Dementia, metal retardation (RARE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Seizure in coma

Clinical Sign

A

Seen in a Prolonged postictal state,
-reactive pupils and inducible eye movements.
+/- Babinski sign (toes go up) NORMALLY supposed to go down
-focal paresis- paralysis for short period of time (todd’s paralysis)
-in coma see during prolonged post ichtal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pre Ictal or Seizure Phase

A

“Aura”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Seizure

A

Ictus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Post Ictal Phase

A

no movement, no vasiculations, no contractions, no mild tonic/clonic movement of the body.
-confusion, disorientation, usually lose of bladder control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Todd’s Paralysis

A

focal paresis

  • paralysis for a short period of time
  • facial m. or extremity
  • no area of selection
  • prolonged post-ictal phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Non Convulsive Status epilepticus

A

prolonged postictal stage

  • impaired consciousness
  • episodic blank staring, aphasia, or automatism ( blinking of eye, protruding of tongue rhythmically)
  • diagnosis between coma and prolonged seizure made by EEG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Automotism’s in seizure

A

Blinking of eye, protruding tongue rhythmically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Locked in Syndrome

A
  • lesion that transects the brainstem BELOW reticular activating system ABOVE the ventilatory nuclei(triggers breathing, monitor CO2.) we breath primarily based on CO2
  • Awake, Eyes open (Vertical, little horizontal, sleep wake cycle intact
  • Can’t move or speak
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Psychogenic Unresponsiveness

A 
Faking it
2 things cause
1. Emotional upset or anxiety
2. Malingering (exaggeration, fabrication)
avoidance from incarceration 
USE COLD CALORIC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Vegetative States

Unresponsive Wakeful Syndrome

A 
TERMED PERMANENT/Terminal AFTER
-3 MONTHS DUE TO MEDICAL CAUSE
-12 MONTHS DUE TO TRAUMA
- Eyes open, sleep/wake cycle
-responsive eye movement, pupil response intact
-loud noises will look toward
-look at person speaking
-can yawn, chew, swallow
-spontaneous roving eye movement
-motor response are primitive, 
-Painful stimuli=decorticate or decerebrate posture
-no awareness to environment
Most famous case=Terry shivo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Aspiration

A

something (Saliva) goes into Airway

Typically- Right middle Lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Emergency Management of COMA Pt.

A
  1. All start w/ Airway-must get open and clear -aspiration (right middle lobe) saliva
  2. Support Ventilation and circulation
    - breath for them w. bag, valve
    -no BP and no pulse= or High Quality CPR
  3. Obtain blood looking metabolic Abnormal
    -check electrolytes (BMP), Blood Sugar, -
    -Endogenous toxins (BUN) urea, lactic acid, NH4 (nitrogenous waste)
    -Coagulation factor=pt (extrinsic)ptt (intrinsic)
    could be stroke, clotting to much not enough
    -Hemorrhagic stroke=didn’t clot after bleed
    - Ishemic Stroke=clotted to much and reduced blood flow
    THYMINE=ALCOHOLICS
    HYPOGLYCEMIC COMA=dextrose 25 g
    Exogenous (drugs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hypoglycemic Coma PT

A

Admininster 25 g of Dextrose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Opiate Overdose

exogenous toxin

A

Naloxone 0.4-2 mg every 2-3 minutes (Narcan)- no side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Benzodiazepine

(adavan, valum, xanex

A

Flumazenil ( 0.2 mg IV)

never used causes acute onset seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Brain Death

A

Irreversible cessation of brain function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Brain Death Assessment Exam

A

Has to be done twice separated by 6 hours

  1. Check oculocephalic (dolls eyes) absent, or oculovestibular (cold caloric) absent
  2. Corneal reflex absent-wisp of cotton and open an rake eyelid and touch cornea.
  3. Pt. doesn’t rouse, groan, grimace or withdraw limbs. Spinal reflex may be maintained (see lower extremity movement cord generated reflex- not nigher cortical
  4. No ventilatory effort in setting of max C02 stem. (Keep CO2 at 40, if don’t breath for a minute your CO2 rise 3mm a min. Give O2 flow with no pressure. Need to go to 60)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Positive Brain Death

A
  1. no respiratory effort (nothing)
  2. 1 min. 3mm increase CO2, 7 minutes rise 60( we are driven due to respiratory acidosis to blow off CO2)
    Happens 2 times in 6 hours and if nothing person is declared brain dead along with other test)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Confirmatory testing Brain Death

A 
1. EEG - time consuming difficult to get
Nuclear imaging
2. SPECT: shows O2 flow consumption
3. PET: metabolic Activity
4. Transcranial Doppler
5. CT Angiography
Brain herniated = no flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Excessive Daytime Sleepiness

A

Sleep Disorder caused

  • medications (antihistamines, allergy meds, xanex, anti depressants, pain meds)
  • systemic illness (sick want more sleep)
  • circadian rhythm disorders
  • sleep deprivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Polysomnography

A

Sleep Study

  • monitor you at home or in/out pt study
  • sleep w/electrodes monitoring brain activity
  • monitor=O2 levels, # respirations, # of times slow respiration down, # you quit breathing=tongue falling back)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Sleep Latency Test

A

How long it takes you to get to sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Stages of Sleep Exam

A

How long you spend in and out of REM sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Obstructive Sleep Apnea

A 
Most Common Disorder breathing
- 2-4% of population
- most common men, increases w/ age
HIGH PREDICTORS
- BMI > 35*
-NECK CIRCUMFERENCE > 43*
Confirmed Sleep Study 
Reduces O2 flow up to 90%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Pathophysiology of Obstuctive Sleep Apnea

A
  • Recurrent upper airway closure and collapse resulting in oxygen desaturation leading to arousal(wake you up- leads to depression, headaches, daytime sleepines)
  • Occurs at the nasopharynx and oropharynx
  • Results in fragmented sleep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Clinical Manifestation of Obtructive Sleep Apnea

A
  • Snoring, apneic pauses, choking witnessed by bed partner
  • Morning headache, depression (big one), impaired cognition, sexual dysfunction
  • BMI and neck circumference predict OSA
  • O2 rate goes down natural and you are now becoming hypoxic- if you have something like ischemic heart disease making it more hypoxic will only make worse.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

CPAP or BPAP importance

A

Important to get airway open for there longevity to prevent Hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Hypopnea or Apnea

A

Sleep Disorder related
Apnea (>90 redcution airflow)
Hypoxia Slowed Breathing (30-90 reduction in airflow)
-lasting more 10 seconds use index to judge obstruction degree

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Treatments for Sleep Apnea

A
  1. Weight Lose (last thing usually done)
  2. Don’t sleep supine (falls backwards)
  3. Zyppah- mouthpiece prevents fall back
    Primary Treatment is CPAP
    air flowing through keeping throat airway open. Compliance is low.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Complications of Obstructive Sleep Apnea

A

HTN, CAD, DM, CVA (Stroke), Depression, Cognitive Impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Narcolepsy

A

-Affects 2 in 1000
- onset mid 20’s (bimodal peak 15-35)
Symptoms
-excessive sleepiness
-Cataplexy = brief loss of muscle tone triggered by emotional state (laughter most common) result head nod, or slurred speech
- Sleep Paralysis: inability to move while aware, usually on wakening
-Hypnagogic Halluciantions: vivid and dreamlike occur at sleep onset
RESULT of Disordered REM sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Narcolepsy Treatment

A 
Stimulant: something to wake you up
-amphetamine, 
methylphenidate, 
modafinil
armodafinil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Idiopathic Hypersomnia

(Sleep Disorder_

A

Life long excessive daytime sleepiness with non REM naps (wakes unrefreshed with prolonged fogginess
-Treatment=Stimulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Periodic Limb Movement Disorder

Sleep Disorder

A

-Repetitive movement of the legs during sleep(also called restless legs)
-Caused by decreased dopamine transmission
-Accompanied by EDS, insomnia, symptoms of RLS (urge to move legs)
-Diagnosed by PSG Sleep study
Treatment= Parkinson’s medications in lower doses, ie pramipexole or ropinirole (increasing dopamine)

76
Q

Insomnia

A

-Difficulty initiating or maintaining sleep
-Most common sleep complaint, found in 1/3 pop
-Major health consequences = Depression, anxiety, drug and alcohol dependence, increased mortality rate
Causes=
Pain, medications, psychiatric conditions(depression)
-Almost never a symptom of neurologic disease usually psychiatric (like bipolar, schizophrenia

77
Q

Insomnia Diagnosis and Types

A

-Diagnosis requires daytime symptoms
-Fatigue, EDS, poor concentration, altered
mood, headache
Types
-Adjustment insomnia – reaction to stress
-Psychophysiologic – most common, poor sleep habits a little stressed
-Paradoxical insomnia – its all in their head, switches turned around.

78
Q

Insomnia Treatment

A

-Non-Drug sleep hygiene recommendations
No caffeine, laptop, tablet, TV, lights, exercise

-Pharmacologic
Lowest effective dose, intermittent, short term

Antihistamine, Melatonin, Trazadone(anti depressant), Seroquel(anti psychotic), Zolpidem(ambien), Amitriptyline(antidepressant)

79
Q

Parasomnias

Sleep disorder

A

Sleeptalking, Sleep walking(usual children or elderly-sundowner syndrome), night terrors, nocturnal wandering and confusion arousals.

80
Q

Rapid Eye movement Behavior Disorder

sleep disorder

A

Disordered regulation of REM
Dissociation of REM features with muscle atonia(no muscle tone)
Patients act out their dreams
Seen with Parkinson’s, Multiple system atrophy, dementia and Lewy Body disease

81
Q

Central Sulcus

A

Separates
Primary Motor Cortex
Primary Somatosensory cortex
(Don’t touch, if both are involved talking a big lesion)

82
Q

Sylvian Fissure

A

Separates

Frontal, Temporal, and Parietal

83
Q

Broca’s Area Location

A

Frontal

84
Q

Visual Cortex Lobe

A

Occipital

85
Q

Wernikes’ location

A

Posterior Parietal

86
Q

Visualspatial

A

Typical on Right or non dominant in hemispheric lateralization

87
Q

Aphasia

A

Loss or impairment of language function

88
Q

Dysarthria

A

Disturbance in articulation of speech w/ language function intake
-Speech Impediment

89
Q

Broca’s Aphasia

A
  • Sever Disruption of fluency of speech (can say just not fluent)
  • Profound impairment in speech and writing (can’t write fluent
  • contralateral face and arm weakness on right side)
90
Q

Warnicke’s Apahasia

A
  • *-Inability to comprehend spoken or written language

- Pt speaks fluently but content is meaningless

91
Q

Conduction Aphasia

A

Normal comprehension and fluent speech with inability to reapeat

92
Q

Global Aphasia

A

Frontal Lobe Lesion

-no speech, no fluency, no comprehension

93
Q

Agnosia

A

Inability to identify a specific sensory stimulus despite intact sensory function

  • Visual, Auditory, Color, Prospagnosia (faces)
  • Lesion usually in occipitotemporal region
94
Q

Apraxia

A

Inability to perform learned motor tasks

  • Ask patient to pantomime a task, ie blowing out a candle or brushing hair
  • Dominant inferior parietal lobe
95
Q

Hemispatial Neglect

A
  • Patient does not attend to stimuli in the contralateral (usually left) visual field or contralateral side of the body
  • Non dominant parietal lobe
96
Q

Delirium

A
  • An acutely disturbed state of mind that occurs in fever, intoxication, and other disorders (alcohol intox)
  • characterized by restlessness, illusions, and incoherence of thought and speech
  • not a illness it’s a symptom
97
Q

Delirium Acute Causes

A

Sepsis (most common)
Overdose
Glucose abnormalities
Electrolyte abnormalities

98
Q

Hyperglycemia

A
  • Cause imbalance of Na…means glucose not transporting into the cell
  • due to resistance/ lack of insulin
  • cell cannot get sugar-breaks down fat
  • breakdown of fat=lactic acid (LACTATE can cause severe confusion/delerium) i.e.
99
Q

Dementia

A
  • Dementia is a progressive loss of intellectual function with loss of meaningful function in daily life
  • Memory loss is central feature
  • recall distant past but can’t recall short or middle memories
100
Q

Dementia Abnormalities

A
  • abnormalities of cognition in language, -
  • spatial processing= can’t put things in order, -praxis (learned behavioral function) apraxis
  • executive function (inability to plan and sequence events)
101
Q

Common cause of Dementia

A 
Neurodegeneration at axon level is the most common underlying cause
Include
Alzheimer’s, 
Frontotemporal dementia and 
diffuse Lewy body disease
102
Q

Diagnosis of exclusions

A

Go straight to something and exclude all the others…but might miss something big. Make sure the others don’t exist and assume to go with most likely
-make sure it’s not something else correctable and more serious

103
Q

Dementia Differentail Diagnosis

A

-Structural process=is it something structurally
-Infectious
(delirious and dementia lots of crossover)
incoherence, lost ability to communicate
Delirium is accurate and rapid
Dementia is long standing and slow progress
-Metabolic & nutritional disease
(must have substrate to make brain work,
Main electrolyte that makes brain work=Na
Hyper/Hypo nutremia

104
Q

Dementia basic work up

A
  • Electrolytes, Vit B12, LFT’s, Renal and Thyroid function(makes everything work, sets metabolic rate)
    -If risk factors exist, serologic studies for syphilis, Lyme disease
    Tertiary Syphillis(had a long time) =neurosyphillis
    -Rule out chronic infections and normal pressure hydrocephalus
    -Advanced brain imaging
    • CT=is fastest but not going to see what we need to see(help rule out hydrocephalus, increased inter cranial pressure)
    • MRI: tell us
      functional MRI usually done after ID’d mass
105
Q

Neuropsychological testing

A

Characterizes the pattern of cognitive and memory impairments that substantiates our suspicion
2 test
1)Mini Mental Status Exam (MMSE)
2) Montreal Cognitive Assessment (MoCA)-more specific and more broad test

106
Q

Specific Neuropyschological test

A

**Montreal Cognitive Assessment (MoCA)
-Broad Assessment of wide array of domain
-Test areas for dementia. elements to consider:
-Visual, Spatial, Executive function, naming, attention, fluency, abstract, Short term memory encoding and retreival, orientation
Choose the MoCA its a better test
Praxis is covered

107
Q

Praxis Test

A

show how you would come your hair

108
Q

Neglect Test

A

testing of double simultaneous extinction to visual, tactile and auditory, stimuli
-person dismisses half body(hemi neglect)

109
Q

Alzheimers

A

-Accounts for 70% of dementia
-5.3 million persons in the US
-Annual expenses estimated at $150 billion goes to care not medication (cannot be cured only few meds make diff in ADL
Rate of occurrence
-32-47% in age 80 and greater
-Incidence at 65 is 1 in 200
-Incidence at 80 is 1 in 10

110
Q

Alzheimers Disease Pathogenesis

A

-loss of cortical neurons
-displaced by amyloid plaques and neurofibrillary tangles
(Beta Amyloid is major component of plaques
Aggregates of proteins that become folded into a shape that allows many copies of that protein to stick together forming fibrils
Hyperphosphorylated tau protein primary component of neurofibrillary tangles
Paired helical filaments in neurons undergoing degeneration)

111
Q

Beta Amyloid

A

Major component of plaque in Alzheimers

  • Protein that didn’t fold right and messes everything up
  • Aggregates of proteins that become folded into a shape that allows many copies of that protein to stick together forming fibrils
112
Q

Hyperphosphorylated TAU

A

Protein that is primary component of neurofibrillary tangles

-Paired helical filaments in neurons undergoing degeneration

113
Q

Alzheimers Disease Process

A

1) Starts in hippocampus (elongated ridges on the floor of each lateral ventricle of the brain, thought to be the center of emotion, memory, and the autonomic nervous system)
2) Spreads diffusely throughout the cortex
3) Creates relative loss of acetylcholine
- Thus the rationale of treating with acetylcholinesterase inhibitors

114
Q

Hippocampus

A

Memory and emotion

115
Q

Acetylcholinesterase inhibitors

A

Amyloid and Tau creat deficit of AcH

-use this to block break down of AcH at receptor site in order to preserve the effect.

116
Q

Alzheimers Progression

A

-Gradual effect on memory, orientation, language, visuospatial processing, praxis, judgement and insight
-Depression is common early (1st symptom)
-Psychosis with agitation, behavioral disinhibition occurs late(taking cloths off, act inappropriately)
-Progressively dependent on others for all ADL’s
Timeline
5-15 years from onset to advanced disease with great variability

117
Q

Alzheimers Primary Medication

A 
Acetylcholinesterase Inhibitors
1) Donepezil (Aricept), Main one
2) Memantine (Namenda) 
has shown to prolong daily fun with moderate to advanced disease
Gingko Does nothing
118
Q

Alzheimers Medication for behavioral disturbances

A

Antipsychotics, antidepressants, anxiolytics (Behavios modifiers)
-used to treat complications —where money goes)

119
Q

Lewey Body Disease

A 
Pathologic inclusion bodies in substantial nigra (as in parkinsonism) 
-isolated to the brain stem, limbic system and cortex
-Second most common cause of dementia
Symptoms include 
-Slowed movement
-Rigidity
-Balance problems
-Early and prominent dementia
-Visual hallucinations
-Cognitive fluctuations
-very aggressive disease
-untreatable
Levadopa and Donepezil
120
Q

Vascular Dementia

A

-A dementia syndrome that begins with a STOKE and a stepwise progression of the illness
-10-20% older patients with dementia will exhibit radiographic evidence of a focal stroke on CT or MRI
-Non focal small vessel cerebral ischemia is called Multi-Infarct Dementia( tiny ischemic dots) (lack of emotion, executive fan)
Typical Presentation
-Early incontinence
-Gait disturbance
-Flattened affect

121
Q

Frontal Temporal Dementia

A 
Lesser known, lesser found
A familial disorder
-Several Variants
     -Behavioral
        Socially disinhibited
        Lethargy, without motivation or 
        spontaneity
     -Progressive Non Fluent Aphasia
        Loss of speech fluency and articulation 
        with retained comprehension
     -Semantic
        Normal phonation with progressive 
        difficulty with naming and word 
        comprehension
122
Q

Parkinsons Dementia

A

50% of patients with PD become demented by age 85
-Affects executive function out of proportion to language and visuospatial activity
-Thought process slows (as with movement)
- Parkinsonion march
-Medications used to treat Parkinson’s can cause psychosis(levodopa)
-Medications that increase dopamine and dopaminergic transmission
Treatment
-Acetylcholinesterase Inhibitors have shown to help helping dementia (Donezpil) -Aricept
Memantin (Namenda)

123
Q

Cardinal Rule 1 of Visual Eye Exam

A

Do a eye exam (don’t want to get credited for causing disease)
-don’t touch until you have established eye.

124
Q

Snellen Chart

A

20’ large chart

14” pocket chart

125
Q

Ishihara Chart

A

Test for Color Vision

126
Q

Lesion anterior (before) optic Chiasm on optic never

A

Partial or complete vision loss in 1 eye only -implies damage to the retina or optic nerve

127
Q

Lesion posterior (after) the chasm

A

Visual field loss involving BOTH eyes implies defect posterior (after) the chiasm

128
Q

Scotomas

A

Areas of partial or complete vision loss

  • peripheral or central
  • like a blind spot
129
Q

Hemianopia

A

“Scotoma: affecting 1/2 the visual Field

130
Q

Homonymous

A

a field cut that is the same in both eyes

131
Q

Homonymous hemianopia

A

implies a post chasmal lesion

-posterior to chasm

132
Q

Congruous

A

Field cut is is identical in each hemifield

133
Q

Incongruous

A

Field cut is not identical in each hemifield

134
Q

Bitemporal Hemianopia

A

Lesion on Optic Chiasm pushing down where temporal field crosses causing Scotoma on 1/2 of both eyes Temporal region where crosses at Chiasm

135
Q

Central Scartoma

A

Caused by inflammation of the left optic disk (optic neuritis) or optic nerve (Retrobulbar neuritis)
-anterior to chiasm

136
Q

CN III

A

Keeps eyelid open, parasympathetics going to eye for constrictions

137
Q

CN VII

A

Close Eye

138
Q

Anisocoria

A

imbalance between Parasympathetics and Sympathetics -unequal pupils (20% population)

139
Q

Light Constriction of eye

Normal and abnormal

A

Normal Both eyes constrict at same time with light stimuli

Optic Nerve Abnormality when light is moved from 1 side to other the other eye dilates

140
Q

Argyll Robertson Pupil

A

Small irregular pupils that constrict to near vision (accommodation), but NOT in response to light
—Neurosyphilis and Diabetes

141
Q

3rd Nerve Palsy

A

Large, unreactive pupil with ptosis

  • interrupted parasympathetic supply
  • down and out eye due to paralysis of the medial, inferior rectus and inferior oblique
  • Diplopia (double vision-palsy of any occular m. )
142
Q

Cranial Nerves fxn of eye

A

LR6 SO4 everything else is CN3
CNIII Superior Rectus- Inferior Rectus- Medial Rectus- Inferior Oblique
CN IV= Superior Oblique Down
CN VI = Lateral Rectus out

143
Q

Ptosis

A

drooping of eyelid

Palsy of 3rd nerve

144
Q

3rd Nerve Palsy Causes

A

Compression by aneurysm of the poster communicating artery

  • Transtentorial herniation
  • Ischemia
145
Q

Horners Syndrome

A
  • Small poorly reactive pupil with ptosis
  • Damage to the sympathetic fibers to the pupil along course from hypothalamus, brainstem, and ascending sympathetic chain
  • Associated unilateral anhidrosis(sweating 1/2 face other half none)
  • Possible first sign of lung cancer in the apex, “Pancoast Tumor”*
146
Q

Pancoast Tumor

A

In apex of lung possible first sign of Horners syndrome

Lung Cancer Associated with this

147
Q

Tonic (Addie) Pupil

A
  • Constricts slowly and incompletely to light

- usually incidental finding

148
Q

Diplopia that is not consistent and varies throughout the day

A

Mysathenia Gravis

149
Q

Monocular Diplopia

A

Disease of the Retina or lens

-rest of the time Binocular

150
Q

4 eye movements

A

Pursuit
Saacadic
Vestibulo-occular
Convergence

151
Q

Pursuit Eye movements

A

smooth fixation on a moving object

-no bouncing of the eye

152
Q

Saacadic Eye Movement

A

Rapid Switching of gaze from one object to another

153
Q

Vestibulo-Ocular

A

enables fixation on an object even if the head is coming

154
Q

Convergence

A

ability to track an object as It is brought closer to limit of accommodation

155
Q

Deviated Eye

how to test for

A

light shined into eye in dark room
normal reflection off center 1mm to nose
abnormal-= one eye the light reflected will displace laterally

156
Q

Cerebral hemisphere lesion eyes look?

A

eyes will look away from the side with the problem

157
Q

Brainstem mass the eyes look

A

toward the problems (ipsilateral)

158
Q

Monocular vision loss

A

Optic Neuritis, lesions of cornea, lens, vitreous, retina, optic never

159
Q

Optic Neuritis

A

Inflammation of the optic nerve accompanied by non-homonymous visual defects
-Associated with MS (COMMON)
-Difficulty with vision in the affected eye
-Can bensidious, only notice when the normal eye is blocked
+/- periorbital pain with eye movement

160
Q

Papillitis

optic Neuritis

A

Can see defects and inflammation with ophthalmoscopically

-observable changes in the optic nerve

161
Q

Retrobulbar neuritis

optic neuritis

A

“the PA sees nothing on exam and the patient sees nothing”

162
Q

Optic Neuritis Pt presentation

A

Natural Course
Evolution is variable
Progresses over less than 1 day to several weeks
Maximum visual deficit reached at 3-7 on average
Bilateral disease is uncommon

163
Q

Optic Neurtitis

Complaints and exam findings

A

Blurred or dimmed vision
Colors may appear less bright
At onset, V/A can range from 20/20 to near blindness
Field defect will be within the central 25 degrees
APD (afferent pupil defect) is usually present
Treatment with high dose iV corticosteroids

164
Q

Conductive Hearing loss

A

Lesions involving the external and middle ear
Can hear speech in a noisy or quiet background
The ear feels full as if it is blocked
Weber lateralizes to the deaf ear

165
Q

Sensorineural Hearlng loss

A

Lesions of the cochlea. Or the auditory division of the Vestibulocochlear nerve (CN 8)
Cannot hear speech mixed with loud background noise; sensitive to loud speech
Can hear low tones better than high frequency

166
Q

Optic Neuritis monoculear Vision presents

A

Difficulty with vision in the affected eye
-can be insidious, only notice when normal eye blocked
+/- periorbital pain with eye movement

167
Q

Treatment for Optic Neuritis

A

IV Corticosteroids

168
Q

Tinnitus

A

Noise or ringing in the ears only audible to the patient

169
Q

Suggest Aneurysm

with Auditory cause

A

Tinnitus that is pulsatory and synchronous with the heartbeat

170
Q

Salicylates can cause what in Ears

A

Tinnitys

171
Q

Menieres disease associated with tinnitus is >?

A

LOW Pitched and continuous

-increases intensity just before a vertigo attack

172
Q

Rinne Test

A

Compares air conduction to bone conduction on the mastoid
Normal test = hear twice as long via air conduction than bone conduction
ABNORMAL if bone is longer than air, a CONDUCTIVE hearing loss is suspected

173
Q

Weber

A

Compares bone conduction hearing in both ears
Normal test = will hear on the central forehead
Unilateral CONDUCTIVE loss will hear the tone of the affected side
Unilateral sensorineural loss will hear the tone on the opposite side of the loss

174
Q

Presbycusis

A

Multiple effects of aging on the auditory system

Conductive or central

175
Q

Otosclerosis

A

Disease of the bony labyrinth, immobilizing the stapes (conductive loss)
Onset ages 11 – 30, familial in 50%
Stapedectomy and replacement with a prosthesis is curative

176
Q

Vestibular Schwannoma

A

Unilateral hearing loss that progresses slowly & tinnitus
Compression of the cochlear nerve in the tight confines of the canal

177
Q

Meniere’s Disease

A

Characterized by fluctuating hearing loss, tinnitus, episodic vertigo and a feeling of ear fullness
Presentation
Feeling of fullness in one ear, rapidly followed by vertigo with a max intensity within minutes
Patient have dizziness and unsteadiness for days

178
Q

Menieres Treatment

A

symptomatic +/- diuretics, sodium restriction, meclizine, Valum

179
Q

Medication that cause Bilateral hearing loss

A

Aminoglycosides(#1), cisplatin, furosemide, salicylates

180
Q

Vertigo

A

A false sense of movement typically spinning

181
Q

Pathology of Vertigo

A

Can arise from many different systems

Must differentiate between a benign peripheral cause and a focal brain lesion

182
Q

Characteristic Sign of vestibular imbalance

A

nystagmus in the plane of affected semicircular canal

183
Q

Vertigo and Dizziness workup

A 
Clinical Presentation
Complain of acute, constant dizziness with recurrent spontaneous attacks
General PE is unrevealing
Thorough ocular and hearing exam
Differential diagnosis
Broad categorization
Peripheral
Central
Medical Condition
184
Q

Vestibular neurits

A

Abrupt onset of severe nausea, imbalance without other neurologic findings
Usually a viral cause (similar to Bell’s Palsy)
Head thrust test is positive in the direction of the affected ear (direction opposite of the fast phase of nystagmus)

185
Q

Menier’s disease

A

Recurrent episodes of vertigo, nausea, imbalance lasting hours with prominent auditory features (hearing loss, roaring tinnitus and fullness)

186
Q

BPPV (Benign paroxysmal positional vertigo)

A

Brief episodes, < 1 min in duration, triggered by head movement (tilting head up to look back, getting in or out of bed, rolling over in bed)
Caused by otoliths entering posterior canal
Diagnosed by the Dix-Hallpike test (upbeat-torsional vertigo on positive test)

Clinical medicine (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions