Q1 Neuro Flashcards
If you have neuro symptoms, what 2 things could it be?
dysfunction of nerve itself or ischemia to the nerve
What is homonymous hemianopsia? Where would the lesion be?
Where each eye has a loos of 1/2 vision on the same side.
Optic tract or lateral geniculate Nucleus
What is a common symptom of papilledema?
Vision greys out transiently when getting up quickly.
What is the etiology behind papilledema?
Increased ICP or swelling of the optic nerve (hydrocephalus, brain tumor, brain bleed or cerebral edema).
HA is common symptom, n/v
If a patient has Cheyenne-Stoke respirations, where is the brain damage?
In the supratentorial. (Above the midbrain)
If a patient has central neurogenic hyperventilation, where is the brain injury? What is the result of this type of abnormal respirations?
Lower midbrain and upper pons.
Increased pH and PO2
If the brain is injured at the mid-pontine level, what type of respirations will you see?
Apneusis - prolonged pause at full inspiration and long expiration.
If you have a brain injury in the lower pons, what type of abnormal respirations will you have?
Cluster breathing.
What is ataxic breathing and where is the lesion that would cause it?
Completely irregular breathing - no pattern to it.
Lesion at RAS of medulla.
What can cause 1 dilated, sluggish and fixed pupil
Dysfunction of 3rd cranial nerve
What can cause small reactive pupils?
Diencephalic dysfunction
What can cause midposition fixed pupils?
Midbrain dysfunction
What do pupils look like in setting of the roof of the midbrain dysfunction? What medication can cause this?
Large and fixed.
Scopolamine patches and atropine.
What can cause pinpoint fixed pupils?
Meds?
Pontine dysfunction
Opiates.
What is a normal response to the oculovestibular reflex test?
Normal Doll’s eyes?
Eyes turn towards the ear that is being injected with water
Eyes keep looking forward as the head is turned side to side.
Decorticate posturing is indicative of a lesion __________.
Decerebrate posturing is indicative of a lesion _________.
ABOVE the midbrain
IN the midbrain
What is agnosia? What is a frequent cause of this?
Deficit in pattern recognition. Unable to identify a safety pin by touching but may still be able to identify by looking at it.
CVAs
Is broca’s aphasia motor or sensory? What about Wernicke’s?
Motor. - can’t speak words
Sensory. - can’t understand.
What is prosopagnosia? What part of the brain is affected?
Inability to recognize faces.
Temporal/occipital lobe
How is Neuronal ageing involved with Delirium?
Draw this out!!
Causes increased astrocyte and microglial activity which results in brain inflammation and Neuro degenerative activity.
Pro inflammatory cytokines and ROS produce chronic inflammation. Leukocytes increase permeability of BBB and can cause cerebral edema and Apoptosis
ROS damage myelin sheath and injure tissue.
Physiological stress can result in neuroendocrine dysfunction through high glucocorticoid levels.
Circadian dysregulation from sleep deprivation increases pro inflammatory cytokines and cortisol levels.
What are some patient associated risk factors for developing delirium?
Depression
Dementia
Advanced age
Chronic disease
Poor nutrition
What are some precipitating associated risk factors for developing delirium?
Surgical stress
Electrolyte imbalance
AKI
CHF
Stroke
Dehydration
What are some hospital associated risk factors for developing delirium?
Pain
Sensory overload/deprivation
Long length of stay
Sleep deprivation
Ventilation > 96hrs
What type of delirium has the highest rate of mortality if undiagnosed and untreated?
Hypoactive.
How is dementia classified?
Based on etiologic factors such as genetics, trauma, tumors, vascular disorders, infections
what is the most common type of dementia?
Alzheimers
T/F: Alertness is impaired in dementia.
FALSE. Alertness is not impaired.
Alzheimer’s is more common in ______ and 5-10% of early onset cases have ________ mutations on chromosome _______
Women (2/3)
Autosomal dominant
21
Dx of Alzheimer’s unusually occurs in the _______ stage
Hospitalization in the ______ stage and comfort care in the ______ stage
Middle
Late
End
What are the tau tangles and amyloid plaques in Alzheimer’s disease?
Tau - protein microtubules that are hyperphosphorylated and detach to form an insoluble intracellular filament. Blocks the transport of nutrients into the cell causing cell death.
Plaques: misfiled proteins in the spaces between cells.
ICP is defines as pressure above___. Normal ICP is _______
20-25mmHg
5-15mmHg
what happens to the pupils during stage 3 and 4 of increased ICP
Stage 3 is the beginning of decompensation. Pupils start to become bilaterally smaller however are still reactive.
Early stage 4 (herniation) one pupil becomes “blown” and late stage 4, both pupils become fixed and dilated.
What happens to the pulse pressure as ICP increases? HR?
It widens. Decreases
how does the body try to compensate for increased ICP?
Widens pulse pressure.
Vasoconstriction
Hyperventilation.
How does vasogenic cerebral edema resolve? What is the main cause?
By slow diffusion back into the blood stream.
Trauma causing increased capillary permeability.
What is the most common cause of cytotoxic cerebral edema?
Hypoxia/ischemia. Pumps fail and cells swell and burst as Na enters the cell.
what is the main cause of interstitial cerebral edema?
Non-communicating hydrocephalus.
What is normal pressure hydrocephalus and what causes it and what population is usually affected most?
Increase of fluid/dilation of ventricles without increased ICP. Subarachnoid hemorrhage or head injury
Elderly
T/F: noncommunicating hydrocephalus is most common in children.
True
Spastic paralysis is present in _________ syndrome. Results from the _________.
UMN.
GTO - golgi tendon organ which is activated during passive stretch of arm.
Positive babinski’s sign is seen in ________
UMN in jury.
F/T: Babinski’s sign is positive in LMN injury.
False. Flaccid paralysis is present.
T/F: Bells’ Palsy is a form of UMN injury.
False. It is a LMN syndrome (flaccid paralysis) the facial muscles (even though high up in the body) are still alpha motor second order neurons.
What is the difference between intentional tremor and essential tremor? Seen in _________ EPS
Intentional tremor (with movements)
Essential tremor (while holding still)
Cerebellar.
Difference between basal ganglia EPS and cerebellar EPS
Basal ganglia: scarce voluntary and excess involuntary movements. Stress and tension makes worse. Improves with relaxation
Cerebellar: equilibrium and posture, issues with gait. Essential tremor is common.
Tardive Dyskinesia is an example of
extra pyramidal symptoms (EPS)
What medications can cause TD?
Dopamine agonists or atypical antipsychotics ex. Haldol, Thorazine and reglan.
Dyskinesia is too _________ (NT) while Parkinson’s is too __________
Much Dopamine.
Little. Dopamine
Where is dopamine produced?
In the substantia Niagara in the midbrain.
T/F: ALS has upper and lower motor neuron loss.
True
The current theory behind ALS is the “dying _______ theory”. This means:
Forward.
Cortical motor neurons affected first, and then scarring and degeneration follows the neuromuscular neurons/junctions through glutamate excitotoxicity.
What nerves/fxns are NOT affected with ALS?
CN 3, 4+6 - EOMs!
ALS has _______ tendencies similar to _______ injury
Spastic
UMN
ALS has 2 kinds of onset :
Spinal (starts in the limbs and progresses cranio-centrally
Bulbar (starts in neck and descends)
What disease is characterized by chromosomal defects causing abnormal folding of proteins. Excitotoxic glutamate pathways induce dysregulated dopamine function. And has a fatal disease progression with no known treatment.
Huntingtons.
What’s the difference between chorea and EPS?
Chorea is non-repetitive muscular contractions, irregular, random, extremities and face.
What is one main difference between the patho Phys of ALS and MS?
MS is autoimmune can have flairs and pauses while ALS is has an unknown cause - fatal w/in 2-5yrs
What is a key sign in MS relapse attack?
Visual changes
Difference between MS and MG
MS - damage and degeneration of myelin and scarring/loss of axons
MG - damage to acetylcholine receptors at post synaptic membrane.
main differences btwn spinal shock and neurogenic shock
Spinal- temporary, reversible usually in 2-3 days, disruption of SNS
Neurogenic - above T6. Loss of SNS with unopposed PSNS = dilation of BV, hypotension, bradycardia and poikilothermia.
SCI at ____ can shrug shoulders, bend elbows and turn palms face up.
SCI at _____ can STRAIGHTEN elbows
SCI at ____ has limited or natural hand fxn.
SCI at _____ has more abdominal control
SCI at ___ has hip and knee mobility
C5
C7
T1
T7-12
L1-5
In autonomic dysreflexia in SCI above T6, _______ is intact below the level of injury and _____ is intact above.
SNS
PSNS
When hypertensive crisis is detected through baroreceptors, unable to inhibit.
LOSS OF SNS WITH UNOPPOSED PSNS
Clinical Presentation of Brown-Sequard Syndrome (BSS).
_____ recovery rate with PT/OT
Penetrating injury to one side of spinal cord. Rare
Ipsilateral hemiplegia or paralysis below level of injury
Ipsilateral loss of touch , pressure, vibration (dorsal columns) and proprioception (Spinocerebellar tracts)
Contralateral loss of pain and temp sensation. (ASTT)
90%
What SCI syndrome is characterized by more weakness/paralysis in UEs than LEs?
Central Cord Syndrome.
What is the clinical presentation of anterior cord syndrome?
BILATERAL loss of pain/temp sensation
Preserved vibration/proprioception
Paraplegia below level of injury.
A seizure if classified according to its ______ not its most ____ manifestation
FIRST
Prominent
3 types of seizure classification?
Focal onset (Aware/impaired aware; motor, non motor, progression?)
Generalized onset (motor (tonic-clinic or other motor) no motor, absence)
Unknown onset (motor or non motor)
Window of opportunity to protect the penumbra is _____.
3 hours.
Clinical presentation of ACA stroke
Contralateral leg, a kinetic mutism and incontinence if bilateral vessel involvement
MCA stroke clinical presentation
Contralateral arm weakness, Ipsilateral hemianopsia and aphasia if in dominant hemisphere.
PCA stroke clinical manifestations
Contralateral weakness, dizziness, hemianopsia and ataxia.
