Physiology

Question 1

What is apraxia?

Answer 1

Inability to execute learned purposeful movements (like walking etc) despite the desire and physical capacity to perform them.
Disorder of motor planning due to damage of the cerebrum.
It is NOT failure to comprehend simple commands (which you can test for in the neuro exam) The person I assume could repeat back to you what you said in the correct order, but then be unable to comply.

Question 2

Define vertigo

Answer 2

Defined as any abnormal sensation of motion between patient and surrounding

Example: Feel like the room is spinning, feel like you’re falling

Question 3

What is dizziness descriptive of? What may someone be trying to communicate by saying they’re dizzy?

Answer 3

Nonspecific term which can represent feelings of vertigo or disequilibrium (no head sensation). Ask for clarification and contex

Dizzy-Any sensation of discomfort of the HEAD ie. lightheaded

Question 4

Define disequilibrium

Answer 4

Dizzy with NO HEAD SENSATION
Suggestive of central lesion, but maybe peripheral
C/o difficulty walking

Question 5

What is hypoesthesia, paresthesia and dysesthesia?

Answer 5

Hypoesthesia-loss of sensation (neg symptom)
Paresthesia- abnormal sensations (pos symptom). May feel something without a stimulus
Dysesthesia-Can’t recognize a specific stimulus (sharp or dull, hot or cold.

Question 6

What are the three main causes of syncope ?

Answer 6

Neurogenic vasodepressor: withdrawal of centrally mediated sympathetic tone (vasodepressor effect) . Often accompanied with excessive vagal effect (bradycardia); vasovagal syncope

Failure of sympathetic innervation of blood vessels by autonomic compensatory responses (reflex tachycardia and vasoconstriction.) Leads to orthostatic hypotension

Diminished cardiac output due to disease of the heart, reduced blood volume

Question 7

What role does the nucleus tractus solitarius play in syncope?

Answer 7

It responds to increased baroreceptor activity (aortic arch and carotid sinus), by decreasing the HR via the peripheral nervous system and vagus nerve, and by inhibiting sympathetic activity to peripheral vasculature.

Question 8

Describe neurogenic vasodepressor syncope?

Answer 8

This is the classic vasovagal syncope, characterized by decreased sympathetic activity in the peripheral vasculature and increased vagal activity leading to bradycardia, in addition to nausea, perspiration, and increased gut motility.
This can be thought of as oscillation of the ANS. Activated sympathetics, then inactivated, then activated parasympathetics.

The integrating center is the brainstem/medulla primarily the nucleus tractus solitarius. NTS

Question 9

Name 4 types of neurogenic vasodepressor syncope

Answer 9

Vasodepressor syncope
Neurocardiogenic
CN IX neuraligia related syncope
Carotid sinus hypersensitivity

Question 10

Describe Vasodepressor syncope

Answer 10

The common faint
Triggered by pain or strong emotion
Vascular dilation, decreasing sympathetic output = blood in periphery and not brain
Bradycardia not essential

Question 11

Describe neurocardiogenic syncope

Answer 11

Type of neurogenic vasodepressor syncope
Rapid contractions of the left ventricle prevent proper filling of the heart leading to bradycardia and vasodilation.
Can be exercise induced

Question 12

Describe CN IX neuralgia related syncope

Answer 12

Type of neurogenic vasodepressor syncope
Pain in mouth: tounge, pharynx etc.
Pain–> bradycardia–> syncope
Bradycardia is the major player, not decreased sympathetic tone

Question 13

Describe carotid sinus hypersensitivity

Answer 13

Type of neurogenic vasodepressor syncope
Oversensitive high pressure mechanoreceptors in the carotid sinus trigger bradycardia, hypotension, or both when someone is wearing a tight collar.
More likely with atherosclerotic plaque in the carotid sinus (most common spot for it to accumulate), can detect bruits.

Question 14

What’s the equation for mean arterial pressure? In the case of orthostatic hypotension where is the failure of compensation?

Answer 14

MAP=CO x R
R=total periferal resistance

Failure to either increase CO or R

Question 15

Other than othostatic hypotension, what other pathologies can lead to impairment of peripheral vasoconstriction?

Answer 15

Diabetes can lead to peripheral neuropathy

Pure autonomic failure=slow degeneration of the ANS, similar pathology (LEWY body inclusions) in autonomic and enteric ganglia.

Question 16

What type of syncope is related to urination, coughing, and laughter?

Answer 16

micturition syncope- try to pee (parasympathetic), while decreasing sympathetic bladder constriction.

tussive (cough) and valsalva (exhale with closed mouth and nose) syncope. Increased intrathoracic pressure-obese

Question 17

Compare loss of consciousness in seizure vs syncope

Answer 17

Syncope doesn’t usually happen while lying down. Prodrome is pallor vs aura, incontinence is infrequent with syncope, recovery is faster and symptoms are not found following syncope.

Question 18

What did the Gastaut and Fischer Williams study learn about syncope?

Answer 18

3-7sec no EEG change
7-13 sec cardiac arrest: loss of consciousness, pallor, and muscle relaxation. Theta and delta waves in frontal lobes, some myoclonis
Beyond 14-15 sec EEG flat; sometimes tonic spasm and incontinence
20-30 seconds later EEG reverted to normal

Question 19

You have a patient that you observe feeling queasy and moments later they turn white. They begin sweating and start yawning and taking deep breaths. They then faint. How would you describe the other symptoms?

Answer 19

Prodrome

Question 20

After having a drink of beer one night your best friend starts feeling funny. His legs buckle and you catch him. Next to you a physician friend suggests you lay your friend on the ground; why?

Answer 20

Perhaps he’s concerned about convulsive syncope that results when you prevent someone who’s fainted from laying down.

Question 21

Balance is regulated by which systems?

Answer 21

Proprioceptive, vestibular, and visual systems. All three send afferent fibers to the vestibular nuclei which then distributes them to the flocculus of the cerebellum, the brainstem and spinal cord

Question 22

An skilled gymnast fell on the balance beam and hit the back of her head before landing on the floor. After a 5 minute break she got back on the beam but noticed she was unsteady. The neurons that control fine motor function were affected. What order neuron innervates the most likely point of the injury?
A) First
B) Second
C) Third
D) Fourth

Answer 22

B second order neuron coming from the vestibular nuclei to the flocculus of the cerebellum.

Question 23

The vestibule houses which structures? Which 3 nerves enter the internal auditory meatus?

Answer 23

Utricle and the saccule

3 nerves
Facial n
vestibular n
choclear n

Question 24

What’s the difference between menieres disease (endolymphatic hydrops) and benign paroxysmal positional vertigo?

Answer 24

The former is characterized by vertigo nausea hearing loss and fullness in the ears. hearing loss doesn’t accompany positional vertigo.

BPPV is when calcium crystals in the otolith membrane of the maculae become dislodged float into the semi-circular canal and then and bump into hair cells. This can make someone feel like they’re spinning.

Question 25

Where are the maculae and the statoconia located? What are the statoconia made of?

Answer 25

The maculae are located in both the utricle and saccule.
The statoconia/otoliths are on top of the otolith membrane/gell.

Statoconia/otoliths are made of calcium carbonate

Question 26

You spin clockwise in your chair. Will this move the stereocilia away from the kinocilium or toward it on the left side?

Answer 26

Clockwise is right so right side is excitatory, and left inhibitory during the spin. If the left is inhibitory then the stereocila will be moving away from the kinocilium.

Question 27

Describe the conversion of endolymph fluid into nerve impulse

Answer 27

The endolymph is rich in K+ and bathes the semicircular canals and vestibule. It’s at 0mV compared to the hair cell whose resting membrane potential is -40mV. When the stereovilli move toward the kinocilium due to endolymph flow this opens K+ channnels in the stereovilli and K+ ions move down the stereovilli and into the cell. The cell is depolarized and lets in Ca2+ which facilitates the release of neurotransmitters onto the dendrite next to.

Question 28

Why might you encourage a patient to reduce their salt intake if they have menieres disease?

Answer 28

They will retain water and exacerbate their condition which is typified by increased endolymph.

Question 29

How can you induce prostrotatory nystagmus?

Answer 29

spin them around and then stop suddenly and watch to see if their eyes move in the opposite direction to the rotation. Then have them attempt to walk and they will fall in the direction of original rotation, because they think they’re spinning opposite.

Question 30

You put cold water in your patients left ear. What direction will the stereocillia move?

Answer 30

Cold opposite-cold in left means they feel they’re spinning right, which means they’re experiencing inhibition below tonic levels?

Question 31

The sense receptor for measuring light touch is?

A ) pacinian corpuscle
B) meissner corpuscle
C) Golgi tendon organ
D) muscle spindle

Answer 31

B meissner corpuscle
A- the pacinian corpuscle measures vibration
C- Golgi measures muscle tension
D- muscle spindle measures fiber length

Question 32

What is brown sequard syndrome?

Answer 32

Incomplete lesion of the spinal chord characterized by ipsilateral upper motor neuron paralysis and loss of proprioception, with contralateral loss of pain and temperature sensation.

Presentation maybe mild to severe. Can be caused by herniated disk.

Question 33

What are merkels discs/cells designed to do? What about ruffinis corpuscles?

Answer 33

Merkels cells - touch and pressure

Ruffini’s corpuscles - stretch

Question 34

According to the rate model used to describe the basal ganglia how would increasing the direct pathway affect movement; indirect? What effect do these pathways have on the basal ganglia output? What disease states/movment disorders are associated with these changes in basal ganglia output?

Answer 34

Anything that increases the direct pathway will decrease BG output and thus increase movement. (Chorea, Dystonia, Hemiballism)

Increasing the indirect pathway will increase BG output and decrease movement (parkinsons)

Question 35

How does dopamine affect the direct and indirect pathway. What is the effect of dopamine on the globus pallidus (internal)?

Answer 35

It excites the direct path and inhibits the indirect path leading to inhibition of the globus pallidus (internal) in both cases.

Increased direct path with decrease BG output
Inhibition of the indirect will be similar to increasing the direct, with the same outcome of decreased BG output.

Question 36

According to the rate model what actions lead to chorea, , dystonia, and hemiballism?

Answer 36

Chorea weaker indirect path, decrease BG output
Dystonia is the result of an overactive direct pathway, decreases BG output
Hemiballism is the result of a weaker STN (subthalamic nuclei?) contribution to the indirect pathway which weakens it, decreases BG output

The effect is increased movement for all 3.

Question 37

A 62-year-old male with a history of hypertension and hyperlipidemia is admitted to the hospital for evaluation after demonstrating signs and symptoms of a stroke. Subsequent CT scans, perceptual tests, and a neurological examination provide evidence for impairment of the otolith pathways. This man will have problems associated with which of the following?

A. Detecting angular acceleration
B. Detecting the position of the head in space
C. Producing rotary nystagmus
D. Producing the stretch reflex
E. Producing the vestibular-ocular reflex

Answer 37

B is corrrect

Explanation: The otolith pathways—those associated with the utricle and saccule—are responsible for detecting the head in space (due to gravity’s effects) and for linear acceleration.

Question 38

A 24-year-old unconscious male presents with head trauma. His pupils are experiencing myosis. Both pupils are unresponsive. The most likely lesion would be in the patient’s

A. cerebral cortex.
B. cerebellum.
C. pons.
D. spinal cord.

Answer 38

OBJ: Relate the location of cortical and brainstem lesions to deficits in: pupillary function.
Explanation: The pupils are pinpoint and unresponsive. The lesion would be in the pons where the pupillary dilation pathway would be the disrupted pathway. For the pupillary function, remember that the constriction pathway (parasymapthetic) goes through the midbrain whereas the dilation pathway (sympathetic) goes through the midbrain, pons, medulla, and superior cervical ganglion.