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)
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
3
Q
EEG
Electrocephalography
A
measures electrical activity in the brain
ID abnormal electric activity =seizures
4
Q
EMG
electromyography
A
muscle diseases - fan on how well the repond to stimuli
neuromuscular junction
peripheral nerve disease
5
Q
NCV
Nerve Conduction Studies
A
Amplitude and velocity of signal coming down axon
6
Q
Visual evoked potential studies
A
MS, Cerebellopontine, brainstem lesion (all demyelination disorders)
7
Q
MRI
Magnetic Resonance Imaging
A
Hi Res -1-2 mm slice Contrast=Gadolinium (safe for CKD) Slow 30-45 minute uncomfortable expensive
8
Q
Ct
Computed Tomography
A
5mm slice
iodine Contrast (allergies shellfish)
prednisone and bendryl
CKD= cause contrast induced neuropathy
9
Q
MR and CT Angiography
A
non invasive visulization
head and neck vasculature
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
11
Q
SPECT
Single photon Emission
A
Looks at blood flow (inter cranial)
12
Q
PET
Positive emission topography
A
functional imaging
id’s metabolic disorders (Oncology)
light up metasticies
13
Q
blood in Subarachnoid Space
meningeal irritation
A
- Traumatic Bleed- leaking of the vessels due to trauma
- Aneurysm
Blood out of vessels is toxic, causes inflammatory response.
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
15
Q
Structural Hemispheric Lesion
A
Pushes contents over
16
Q
Lateral Herniation
A
add something to one side it will shift the contents over
17
Q
Transtentorial herniation
A
Pushes down-something big on top pushes down into cerebellum
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
19
Q
Herniation
A
displacement of object into another compartment in which it wasn’t designed to go
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
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
22
Q
Thiamine Deficiency
Deficiency State
A
Found in Alcoholics
23
Q
Glucose Deficiency
Deficiency State
A
Hypoglycemic=may be delirious and confused
- < 20 Glucose (around this lower point=goofy, confused, delirious
24
Q
Na Deficiency
Electrolyte Deficiency
A
Lack of Na
Causes mental changes
Hyponatremia-can cause mental status changes
25
Exogenous Substances (toxins)
Medications can cause delirium, confusion, and coma (ex: heroin OD)
26
Endogenous Substances (toxins)
Stuff we make inside our body
- ex Lactic Acid
- anaerobic metabolism =hypoxia (low O2) byproduct is Lactate
- Lactate causes severe confusion
27
Uremia
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)
28
(what to think?)
| Headache First
Headache
Meningitis (inflammation of brain &spinal cord)
encephalitis (inflammation of brain)
intracranial hemorrhage (bleed inside skull)
29
```
(what to think?)
First they were:
Intoxication
confused
delirium
```
infection causes: ex-Meningitis
| exogenous toxins
30
(what to think?)
| Apoplectic (big) event causing coma
- ischemia
| - hemorrhagic stroke
31
```
(what to think?)
Lateralizing symptoms of
Hemiparesis
Aphasia
before coma
```
Hemiparesis=m. weakness or partial paralysis on 1 side
Aphasia= language difficulties
Think about
Mass Brain Tumor (lesion)
32
Early Diencephalic
| Based on lesion
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
33
Late Diencephalic
| based on lesion
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)
34
Midbrain
| based on lesion
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)
35
Pons of Upper Medualla
| (based on lesion
```
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
```
36
Glasgow Coma Scale
```
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
```
37
Differentiate between Structural and Metabolic Causes of coma?
3 Features of Physical Exam
1. motor response to painful stimuli
2. Pupillary function
3. Reflex Eye Movement
38
Structural Lesions
Present in stepwise fashion.
-pupils will be reactive to Midbrain
-doll's eye will be intact till midbrain medulla
-
39
Non structural lesion in brain like inflammation or infection
Stages will all be jumbled up won't be stepwise down the brainstem
40
Metabolic lesions
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.
41
Seizure
| Occurrences
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)
42
Seizure in coma
| Clinical Sign
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
43
Pre Ictal or Seizure Phase
"Aura"
44
Seizure
Ictus
45
Post Ictal Phase
no movement, no vasiculations, no contractions, no mild tonic/clonic movement of the body.
-confusion, disorientation, usually lose of bladder control
46
Todd's Paralysis
focal paresis
- paralysis for a short period of time
- facial m. or extremity
- no area of selection
- prolonged post-ictal phase
47
Non Convulsive Status epilepticus
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
48
Automotism's in seizure
Blinking of eye, protruding tongue rhythmically
49
Locked in Syndrome
- 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
50
Psychogenic Unresponsiveness
```
Faking it
2 things cause
1. Emotional upset or anxiety
2. Malingering (exaggeration, fabrication)
avoidance from incarceration
USE COLD CALORIC
```
51
Vegetative States
| Unresponsive Wakeful Syndrome
```
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
```
52
Aspiration
something (Saliva) goes into Airway
| Typically- Right middle Lobe
53
Emergency Management of COMA Pt.
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)
54
Hypoglycemic Coma PT
Admininster 25 g of Dextrose
55
Opiate Overdose
| exogenous toxin
Naloxone 0.4-2 mg every 2-3 minutes (Narcan)- no side effects
56
Benzodiazepine
| (adavan, valum, xanex
Flumazenil ( 0.2 mg IV)
| never used causes acute onset seizures
57
Brain Death
Irreversible cessation of brain function
58
Brain Death Assessment Exam
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)
59
Positive Brain Death
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)
60
Confirmatory testing Brain Death
```
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
```
61
Excessive Daytime Sleepiness
Sleep Disorder caused
- medications (antihistamines, allergy meds, xanex, anti depressants, pain meds)
- systemic illness (sick want more sleep)
- circadian rhythm disorders
- sleep deprivation
62
Polysomnography
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)
63
Sleep Latency Test
How long it takes you to get to sleep
64
Stages of Sleep Exam
How long you spend in and out of REM sleep
65
Obstructive Sleep Apnea
```
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%
```
66
Pathophysiology of Obstuctive Sleep Apnea
- 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
67
Clinical Manifestation of Obtructive Sleep Apnea
- 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.
68
CPAP or BPAP importance
Important to get airway open for there longevity to prevent Hypoxia
69
Hypopnea or Apnea
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
70
Treatments for Sleep Apnea
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.
71
Complications of Obstructive Sleep Apnea
HTN, CAD, DM, CVA (Stroke), Depression, Cognitive Impairment
72
Narcolepsy
-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
73
Narcolepsy Treatment
```
Stimulant: something to wake you up
-amphetamine,
methylphenidate,
modafinil
armodafinil
```
74
Idiopathic Hypersomnia
| (Sleep Disorder_
Life long excessive daytime sleepiness with non REM naps (wakes unrefreshed with prolonged fogginess
-Treatment=Stimulants
75
Periodic Limb Movement Disorder
| Sleep Disorder
-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
Insomnia
-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
Insomnia Diagnosis and Types
-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
Insomnia Treatment
-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
Parasomnias
| Sleep disorder
Sleeptalking, Sleep walking(usual children or elderly-sundowner syndrome), night terrors, nocturnal wandering and confusion arousals.
80
Rapid Eye movement Behavior Disorder
| sleep disorder
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
Central Sulcus
Separates
Primary Motor Cortex
Primary Somatosensory cortex
(Don't touch, if both are involved talking a big lesion)
82
Sylvian Fissure
Separates
| Frontal, Temporal, and Parietal
83
Broca's Area Location
Frontal
84
Visual Cortex Lobe
Occipital
85
Wernikes' location
Posterior Parietal
86
Visualspatial
Typical on Right or non dominant in hemispheric lateralization
87
Aphasia
Loss or impairment of language function
88
Dysarthria
Disturbance in articulation of speech w/ language function intake
-Speech Impediment
89
Broca's Aphasia
- 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
Warnicke's Apahasia
* *-Inability to comprehend spoken or written language
| - Pt speaks fluently but content is meaningless
91
Conduction Aphasia
Normal comprehension and fluent speech with inability to reapeat
92
Global Aphasia
Frontal Lobe Lesion
| -no speech, no fluency, no comprehension
93
Agnosia
Inability to identify a specific sensory stimulus despite intact sensory function
- Visual, Auditory, Color, Prospagnosia (faces)
- Lesion usually in occipitotemporal region
94
Apraxia
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
Hemispatial Neglect
- Patient does not attend to stimuli in the contralateral (usually left) visual field or contralateral side of the body
- Non dominant parietal lobe
96
Delirium
- 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
Delirium Acute Causes
Sepsis (most common)
Overdose
Glucose abnormalities
Electrolyte abnormalities
98
Hyperglycemia
- 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
Dementia
- 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
Dementia Abnormalities
- 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
Common cause of Dementia
```
Neurodegeneration at axon level is the most common underlying cause
Include
Alzheimer’s,
Frontotemporal dementia and
diffuse Lewy body disease
```
102
Diagnosis of exclusions
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
Dementia Differentail Diagnosis
-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
Dementia basic work up
- 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
Neuropsychological testing
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
Specific Neuropyschological test
****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
Praxis Test
show how you would come your hair
108
Neglect Test
testing of double simultaneous extinction to visual, tactile and auditory, stimuli
-person dismisses half body(hemi neglect)
109
Alzheimers
-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
Alzheimers Disease Pathogenesis
-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
Beta Amyloid
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
Hyperphosphorylated TAU
Protein that is primary component of neurofibrillary tangles
| -Paired helical filaments in neurons undergoing degeneration
113
Alzheimers Disease Process
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
Hippocampus
Memory and emotion
115
Acetylcholinesterase inhibitors
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
Alzheimers Progression
-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
Alzheimers Primary Medication
```
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
Alzheimers Medication for behavioral disturbances
Antipsychotics, antidepressants, anxiolytics (Behavios modifiers)
-used to treat complications ---where money goes)
119
Lewey Body Disease
```
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
Vascular Dementia
-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
Frontal Temporal Dementia
```
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
Parkinsons Dementia
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
Cardinal Rule 1 of Visual Eye Exam
Do a eye exam (don't want to get credited for causing disease)
-don't touch until you have established eye.
124
Snellen Chart
20' large chart
| 14" pocket chart
125
Ishihara Chart
Test for Color Vision
126
Lesion anterior (before) optic Chiasm on optic never
Partial or complete vision loss in 1 eye only -implies damage to the retina or optic nerve
127
Lesion posterior (after) the chasm
Visual field loss involving BOTH eyes implies defect posterior (after) the chiasm
128
Scotomas
Areas of partial or complete vision loss
- peripheral or central
- like a blind spot
129
Hemianopia
"Scotoma: affecting 1/2 the visual Field
130
Homonymous
a field cut that is the same in both eyes
131
Homonymous hemianopia
implies a post chasmal lesion
| -posterior to chasm
132
Congruous
Field cut is is identical in each hemifield
133
Incongruous
Field cut is not identical in each hemifield
134
Bitemporal Hemianopia
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
Central Scartoma
Caused by inflammation of the left optic disk (optic neuritis) or optic nerve (Retrobulbar neuritis)
-anterior to chiasm
136
CN III
Keeps eyelid open, parasympathetics going to eye for constrictions
137
CN VII
Close Eye
138
Anisocoria
imbalance between Parasympathetics and Sympathetics -unequal pupils (20% population)
139
Light Constriction of eye
| Normal and abnormal
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
Argyll Robertson Pupil
Small irregular pupils that constrict to near vision (accommodation), but NOT in response to light
---Neurosyphilis and Diabetes
141
3rd Nerve Palsy
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
Cranial Nerves fxn of eye
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
Ptosis
drooping of eyelid
| Palsy of 3rd nerve
144
3rd Nerve Palsy Causes
Compression by aneurysm of the poster communicating artery
- Transtentorial herniation
- Ischemia
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Horners Syndrome
- 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”***
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Pancoast Tumor
In apex of lung possible first sign of Horners syndrome
| Lung Cancer Associated with this
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Tonic (Addie) Pupil
- Constricts slowly and incompletely to light
| - usually incidental finding
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Diplopia that is not consistent and varies throughout the day
Mysathenia Gravis
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Monocular Diplopia
Disease of the Retina or lens
| -rest of the time Binocular
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4 eye movements
Pursuit
Saacadic
Vestibulo-occular
Convergence
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Pursuit Eye movements
smooth fixation on a moving object
| -no bouncing of the eye
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Saacadic Eye Movement
Rapid Switching of gaze from one object to another
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Vestibulo-Ocular
enables fixation on an object even if the head is coming
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Convergence
ability to track an object as It is brought closer to limit of accommodation
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Deviated Eye
| how to test for
light shined into eye in dark room
normal reflection off center 1mm to nose
abnormal-= one eye the light reflected will displace laterally
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Cerebral hemisphere lesion eyes look?
eyes will look away from the side with the problem
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Brainstem mass the eyes look
toward the problems (ipsilateral)
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Monocular vision loss
Optic Neuritis, lesions of cornea, lens, vitreous, retina, optic never
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Optic Neuritis
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
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Papillitis
| optic Neuritis
Can see defects and inflammation with ophthalmoscopically
| -observable changes in the optic nerve
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Retrobulbar neuritis
| optic neuritis
“the PA sees nothing on exam and the patient sees nothing”
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Optic Neuritis Pt presentation
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
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Optic Neurtitis
| Complaints and exam findings
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
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Conductive Hearing loss
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
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Sensorineural Hearlng loss
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
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Optic Neuritis monoculear Vision presents
Difficulty with vision in the affected eye
-can be insidious, only notice when normal eye blocked
+/- periorbital pain with eye movement
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Treatment for Optic Neuritis
IV Corticosteroids
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Tinnitus
Noise or ringing in the ears only audible to the patient
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Suggest Aneurysm
| with Auditory cause
Tinnitus that is pulsatory and synchronous with the heartbeat
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Salicylates can cause what in Ears
Tinnitys
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Menieres disease associated with tinnitus is >?
LOW Pitched and continuous
| -increases intensity just before a vertigo attack
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Rinne Test
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
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Weber
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
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Presbycusis
Multiple effects of aging on the auditory system
| Conductive or central
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Otosclerosis
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
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Vestibular Schwannoma
Unilateral hearing loss that progresses slowly & tinnitus
Compression of the cochlear nerve in the tight confines of the canal
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Meniere's Disease
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
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Menieres Treatment
symptomatic +/- diuretics, sodium restriction, meclizine, Valum
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Medication that cause Bilateral hearing loss
Aminoglycosides(#1), cisplatin, furosemide, salicylates
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Vertigo
A false sense of movement typically spinning
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Pathology of Vertigo
Can arise from many different systems
| Must differentiate between a benign peripheral cause and a focal brain lesion
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Characteristic Sign of vestibular imbalance
nystagmus in the plane of affected semicircular canal
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Vertigo and Dizziness workup
```
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
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Vestibular neurits
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)
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Menier's disease
Recurrent episodes of vertigo, nausea, imbalance lasting hours with prominent auditory features (hearing loss, roaring tinnitus and fullness)
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BPPV (Benign paroxysmal positional vertigo)
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)
