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DIT FACTS > NEURO > Flashcards

NEURO Flashcards

1
Q

5 regions of the brain included in the limbic system

A 
Septal nucleus
Mamillary bodies
Fornix
Hippocampus
Cingulate gyrus
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2
Q

Hypothalamic Nuclei that regulate the parasympathetic NS

A

Anterior

Preoptic

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3
Q

Hypothalamic Nuclei that regulate the sympathetic NS

A

Posterior

Lateral

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4
Q

Hypothalamic Nuclei that regulates the release of gonadotropic hormones such as LH and FSH?

A

Pre-optic

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5
Q

Patient presents with hypersexuality and hyperorality. Where is the lesion, and what virus is associated?

A

This is Kluver-Bucy syndrome due to bilateral amygdala lesion. It is associated with HSV-1.

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6
Q

Patient presents with make-up on only the right half of her face. When asked to draw a clock, she only draws 12 o clock to 6 o clock. She is not aware of these differences. Where is the lesion?

A

This is a non-dominant (often right) parietal lobe lesion, causing spatial neglect of the contralateral side of the world.

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7
Q

Patient presents without being able to write or calculate after a stroke. They also are not able to distinguish their fingers. Where was the stroke?

A

Dominant (left) parietal lobe. This is GERSTMANN syndrome.

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8
Q

Patient presents with ophthalmoplegia, ataxia, memory loss, and confabulation. What is the most likely cause of this lesion?

A

This is a bilateral mamillary body lesion due to Wernicke Korsakoff syndrome. It is associated with thiamine deficiency and excessive EtOH use although it can also be induced by giving glucose without thiamine to a thiamine-deficient patient.

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9
Q

Patient presents with intention tremor and loss of balance. They tend to fall towards their right side. Where is the lesion?

A

The right cerebellar hemisphere (fall to ipsilateral side of lesion).

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10
Q

Patient presents with right arm flailing. Where is the lesion?

A

LEFT subthalamic nucleus (contralateral hemiballismus)

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11
Q

What is the difference between a lesion to the PPRF and frontal eye fields?

A

In PPRF, eyes look AWAY from side of lesion.

In frontal eye fields, eyes look TOWARDS side of lesion.

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12
Q

Patient presents with paralysis of upward gaze. Where is the lesion?

A

This is Parinauds syndrome due to damage of the superior colliculi.

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13
Q

Patient presents following a stroke understanding what you are saying but with extremely broken spoken language. Where was the stroke?

A

This is Broca’s aphasia – inferior frontal gyrus of frontal lobe (left).

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14
Q

Patient presents following a stroke speaking fluently but mostly gibberish. She is not able to understand what you are saying to her. Where was the stroke?

A

This is Wernicke’s aphasia – superior temporal gyrus of the temporal lobe.

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15
Q

Patient suffers a stroke to the right inferior frontal gyrus. What is her most likely presenting symptom?

A

This is non-dominant Broca’s area. The patient has the inability to express emotion or inflection in speech.

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16
Q

Patient suffers a stroke to the right superior temporal gyrus. What is her most likely presenting symptom?

A

This is non-dominant Wernicke’s area. These patients are unable to understand emotion or inflection in others’ speech.

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17
Q

What information is communicated at the nucleus solitarius?

A

Sensory –taste, baroreceptors, gut distention.

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18
Q

What information is communicated at the nucleus ambiguus?

A

Motor –pharynx, larynx, upper extremity.

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19
Q

What information is communicated at the dorsal motor nucleus?

A

Autonomic –heart, lungs, upper GI tract.

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20
Q

What artery supplies the lateral INFERIOR pons? Name 8 structures located in this area.

A 
CN VII and nucleus (I/L)
Middle and inferior cerebral peduncle (I/L)
Vestibular nuclei 
Solitary nucleus (I/L)
Cochlear nucleus (I/L)
Spinal trigeminal nucleus, nerve (I/L pain and temp to face)
Spinothalamic tract (C/L pain and temp)
Descending sympathetic tract (I/L)

Supplied by AICA

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21
Q

What artery supplies the medial inferior pons? Name 4 structures located in this area.

A

Basilar a (paramedian branches)

Corticospinal tract (C/L)
Medial lemniscus (C/L loss of touch, vibration)
PPRF and abducens nucleus (I/L gaze)
CN VI (I/L lateral rectus)
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22
Q

What artery supplies the lateral medulla? Name 6 structures located in this area.

A

Inferior cerebellar peduncle (I/L ataxia)
Vestibular nuclei (vertigo, nystagmus, N/V)
Nucleus ambiguus (hoarseness, difficulty swallowing, gag reflex)
Trigeminothalamic tract (I/L pain and temp of face)
Spinothalamic tract (C/L pain and temp body)
Descending sympathetic tract (I/L Horners)

Supplied by PICA

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23
Q

What artery supplies the medial medulla? Name 3 structures in this area.

A

Anterior spinal a (paramedian branches)

Pyramid/corticospinal tract (C/L)
Medial lemniscus (C/L tactile, kinesthetic)
Hypoglossal nucleus/nerve

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24
Q

If the right vagus nerve or nuclei is damaged, to which side will uvula deviate?

A

Since the mm of the left soft palate ARE working to raise the palate and the muscles on the right are not, the uvula will deviate to the left.

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25
Q

If the portion of the right motor cortex or right corticobulbar tract that innervates the soft palate is damaged, to which side will the uvula deviate?

A

Since the soft palate fibers from the right motor cortex or right corticobulbar tract travel to the left nucleus ambiguus, the uvula will deviate to the right.

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26
Q

A patient comes to your office and before you notice any other sx, you see the patient’s uvula deviates to the left when she says “Ah.” What 4 areas might be damaged?

A 
Left deviation of uvula means that the muscles of the left palate are raising the palate and the muscles of the right palate are not.  
R. vagal nerve
R. nucleus ambiguus
L. corticobulbar tract
Soft palate portion of left motor cortex
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27
Q

If the right hypoglossal nerve or nuclei is damaged, to which side will the tongue deviate when sticking out?

A

Since the tongue is pushed out, the muscles on the functional (left) side will push the tongue to the non-functional side.

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28
Q

If the portion of the right motor cortex (or right corticobulbar tract) that innervates the tongue is damaged, to which side will the tongue deviate?

A

Since tongue fibers from the right motor cortex travel to the left hypoglossal nucleus, the tongue will deviate to teh left.

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29
Q

What should you immediately think about in a patient with bilateral Bells palsy?

A

Guillain barre or Lyme disease

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30
Q

A patient has leftward deviation of the tongue on protrusion and has a right sided spastic paralysis. Where is the lesion?

A

L. medulla

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31
Q

6 etiologies of Bell’s palsy

A 
My Lovely Belle Had An STD.
Lyme disease
Herpes zoster/simplex
AIDS
Sarcoidosis
Tumor
Diabetes
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32
Q

Map the pathway of the dorsal column beginning in the dorsal root ganglion.

A

Ascends ipsilaterally until it synapses in the ipsilateral nucleus cuneatus or gracilis in the medulla. It DECUSSATES in the medulla and ascends CONTRALATERALLY in the medial lemniscus where it synapses in the VPL of the thalamus. Transmits pressure, vibration, fine touch, and proprioception.

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33
Q

Map the pathway of the spinothalamic tract beginning in the A delta and C fibers of the dorsal root ganglion.

A

Ascends ipsilaterally in the gray matter until it DECUSSATES at the anterior white commissure. It now ascends CONTRALATERALLY where it synapses in the VPL of the thalamus. Transmits pain and temperature (lateral) or crude touch, pressure (anterior).

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34
Q

Map the pathway of the lateral corticospinal tract beginning in the primary motor cortex.

A

Descends IPSILATERALLY through internal capsule until DECUSSATING at caudal medulla where it now descends CONTRALATERALLY. It synapses in the cell bodies of the anterior horn and then leaves the spinal cord as an LMN and synapses again at the neuromuscular junction. This carries descending voluntary movement of the contralateral limbs.

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35
Q

How do sx of a lesion to the cortical motor region of the face differ from a lesion of the facial nerve or nucleus? Why?

A

Lesion in cortical motor face region –paralysis of CL side of lower face.
Lesion of face nerve or nucleus–paralysis of IL side of entire face.
The facial motor nucleus receives motor fibers for the lower face from the opposite motor cortex and motor fibers for the upper face from BOTH motor cortices. Therefore, if a lesion occurs in the facial region of the left motor cortex, there is still sufficient innervation for the right upper face from the right motor cortex. However, since the left motor cortex is the only cortex to innervate the right lower face, there will be paralysis in the right lower face.

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36
Q

What is the hallmark sign of a brainstem lesion?

A

Alternating syndromes – long tract sx on one side and cranial nerve sx on the other.

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37
Q

An infarct is noted in the midbrain. What does this patient present with? What artery is affected?

A

This is infarct of the paramedian branches of the PCA –WEBER syndrome.
Cerebral peduncle lesion causes C/L spastic paralysis.
Oculomotor nerve palsy causes I/L ptosis, pupillary dilation, and lateral strabismus (eye looks down and out).

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38
Q

An infarct is noted in the medial medulla. What does this patient present with? What artery is affected?

A

This is occlusion of a paramedian branch of the anterior spinal artery (rostral medulla).
C/L spastic hemiparesis (pyramid/corticospinal tract damage)
C/L tactile and kinesthetic defects (medial lemniscus damage)
Tongue deviates towards side of lesion (hypoglossal nucleus/nerve damage)
NOTE: pain and temperature are preserved.

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39
Q

An infarct is noted in the lateral medulla. What does this patient present with? What artery is affected?

A

Occlusion of PICA.
Loss of pain and temp over C/L body (spinothalamic tract)
Loss of pain and temp over I/L face (trigeminothalamic tract)
Hoarseness, difficulty swallowing, loss of gag reflex (nucleus ambiguus: glossopharyngeal and vagus damage)
I/L Horner’s syndrome (descending sympathetic tract)
Vertigo, nystagmus, nausea/vomiting (vestibular nuclei damage)
I/L cerebellar deficits like ataxia (inferior cerebellar peduncle damage)

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40
Q

An infarct is noted in the inferior medial pons. What does this patient present with? What artery is affected?

A

Occlusion of paramedian branch of basilar artery.
C/L spastic hemiparesis (corticospinal tract)
C/L loss of light touch/vibratory/kinesthetic sensation (medial lemniscus)
Paralysis of gaze to side of lesion (damage to pontine gaze center: PPRF and abducens nucleus)
I/L paralysis of lateral rectus muscle (damage to abducens nerve)
NOTE: pain and temperature are preserved.

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41
Q

An infarct is noted in the inferior lateral pons. What does the patient present with? What artery is affected?

A

Occlusion of AICA.
I/L facial nerve paralysis (facial n and nucleus)
I/L loss of taste from anterior 2/3 of tongue (solitary nucleus)
I/L deafness, tinnitus (cochlear nucleus, nerve fiber damage)
Nystagmus, vertigo, N/V (vestibular nucleus)
I/L limb and gait ataxia (middle and inferior cerebellar peduncles)
I/L loss of pain and temperature from face (spinal trigeminal nucleus and nerve)
C/L loss of pain and temperature (spinothalamic tract)
I/L Horner syndrome (damage to descending sympathetic tract)

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42
Q

An infarct is noted in the superior/rostral pons on the lateral side. What does the patient present with? What artery is affected?

A

AICA
I/L loss of tase from anterior 2/3 of tongue (solitary nucleus)
I/L limb and gait ataxia (middle and inferior cerebellar peduncles)
I/L loss of pain and temperature sensation from face (spinal trigeminal ucleus and nerve)
I/L loss of light touch and vibration sensation from face (main sensory trigeminal nucleus and nerve)
I/L jaw weakness and deviation of jaw toward side of lesion (trigeminal motor nucleus and nerve)
C/L loss of pain and temperature sensation from body (spinothalamic tract)
I/L Horner syndrome (descending sympathetic tract)

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43
Q

What artery supplies the LATERAL superior/rostral pons? Name 7 important structures located here.

A

AICA arteries

Solitary nucleus, nerve (I/L taste from anterior 2/3)
Middle, inferior cerebellar peduncles (I/L limb)
Spinal trigeminal nucleus, nerve (I/L pain and temp from face)
Main sensory trigeminal nucleus and nerve (I/L light touch, vibration from face)
Trigeminal motor nucleus and nerve (I/L jaw weakness and deviation of jaw toward side)
Spinothalamic tract (C/L pain and temperature
Descending sympathetic tract (I/L Horner syndrome)

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44
Q

Occlusion of what artery may cause locked in syndrome?

A

Basilar artery

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45
Q

Most common site of berry aneurysm and 3 diseases associated.

A

Anterior communicating artery

Associated with ADPKD, Ehlers-Danlos, Marfans syndrome

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46
Q

A 24 year old obese female presents with daily headaches accompanied by N/V. Papilledema is noted on PE. What is the most worrisome sequelae of this disease and what is the characteristic sign of this disease? Name 3 causes.

A

Most worrisome is vision loss.
CSF pressure will be elevated >200mmHg in non-obese patients, >250mmHg in obese patients.
This is pseudotumor cerebri often due to Vitamin A OD, tetracyclines, and corticosteroid withdrawal.

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47
Q

What do you suspect when a spinal tap appears yellow?

A

This is xanthochromic spinal tap. Heme degradation after a few days of hemorrhage causes the CSF to appear yellow. Generally subarachnoid hemorrhage.

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48
Q

A 80 year old patient presents with difficulty walking and memory problems. Why is your next step in management going to be a CT scan?

A

This patient sounds like they COULD be wet wacky and wobbly AKA Normal Pressure Hydrocephalus. This can be seen on CT, in which lateral ventricle enlargement in the absence of sulcal enlargement would be seen. Its important to identify this because its one of the only reversible kinds of dementia.

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49
Q

What are the differences between the 1a afferent motor pathway and the 1b afferent motor pathway?

A

1a: spindle, excitatory
1b: golgi tendon, inhibitory

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50
Q

Describe the general flow of info through the cerebellum.

A

Inputs (mossy and climbing fibers) –> cerebellar cortex – > Purkinje fiber – > deep nuclei of cerebellum –> output targetes.

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51
Q

What structure provides the major output pathway from the cerebellum?

A

Brachium conjunctivum (AKA superior cerebellar peduncle) – > contralateral VL of thalamus

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52
Q

Motor control on which side of the body would be affected with a lesion on one side of the cerebellar hemisphere?

A

IPSILATERAL because the cerebellum – > C/L thalamus – > cortex – > corticospinal tract – > body C/L to cortex.

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53
Q

What neurological abnormalities can be attributed to damage of the spinocerebellum (vermis and paravermis)?

A

Postural instability
Slurred/slowing of speech
Hypotonia
Pendular knee jerk reflexes

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54
Q

What sx are seen in anterior vermis syndrome? What is the most common cause?

A

The most anterior portion of the vermis belongs to the legs. Ataxia and dystaxia of the legs would be seen even if trunk is supported – > broad based, staggering gait. Its due to chronic alcohol abuse – > thiamine eficiency – > degeneration of cerebellar cortex starting at anterior lobe.

55
Q

What neurological deficits would be attributed to damage of the cerebrocerebellum (lateral hemisphere)?

A

Lack of coordination of voluntary movements with respect to both timing and rate of movement.
Delays in initiating and trouble stopping.
Dysmetria (impaired ability to control the distance, speed, an dpower of a movement)
Intention tremor

56
Q

What neurological deficits can be attributed to damage of the vestibulocerebellum (vermis and flocculonodular)?

A

Disequilibrium: difficulty in maintaining balance

Abnormal eye movements (such as cerebellar nystagmus that is more pronounced when patient looks to side of lesion.)

57
Q

What is most common cause of damage to flocculonodular lobe?

A

Medulloblastoma in childhood.

58
Q

Name 4 diseases that specifically damage the cell bodies of the anterior horn.

A

Polio
West Nile
ALS
Werdnig-Hoffmann disease

59
Q

What is the globus pallidus interna’s role in the basal ganglia?

A

Inhibitor of movement

60
Q

What is the subthalamic nucleus’ role in the basal ganglia?

A

It stimulates the globus pallidus interna, which is an inhibitor. Thus it is also an inhibitor of movement.

61
Q

What is the globus pallidus externa’s role in the basal ganglia?

A

Stimulator of movement

62
Q

What neurotransmitters are altered in Huntington’s disease?

A

Decreased ACh and GABA.

Increased dopamine

63
Q

What part of the basal ganglia does Wilson’s disease affect?

A

It affects the putamen. Instead of Lewy bodies gunking up the neurons (as in PD), copper is.

64
Q

What are Lewy bodies composed of?

A

Alpha-synuclein intracellular inclusions

65
Q

A patient from Pakistan presents to you complaining of lower extremity myalgias and pain with eye movement. He says he was feeling ill a few days ago with headache, fever, and nausea. On PE, you note a +1 reflex in the left patella and muscle strength 3/5 bilaterally in both plantar flexion and dorsiflexion. What CSF findings do you expect, and how did this patient acquire the infection?

A

This is poliovirus, an enterovirus (RNA) that is transmitted fecal-orally.
CSF findings would show increased WBCs, slightly increased protein, and normal glucose.

66
Q

A hysterical mother presents to you with her 4 month old baby. She says she has had trouble with feeding and her baby doesn’t seem to be able to sit on its own. The baby has a very weak cry and suffers from recurrent respiratory infections. What mutation do you suspect and how was this inherited?

A

This is Werdnig Hoffmann disease, which is an SMN1 mutation that causes degeneration of the anterior horns of the spinal cord. It is AR.

67
Q

Your patient is a 12 y.o. boy that complains of difficulty walking. He says his joints always hurt, and you note on PE he has kyphoscoliosis. What mutation do you suspect and what will be his most likely cause of death?

A

This is Friedrichs Ataxia, an AR trinucleotide repeat disorder (GAA) in the gene that encodes frataxin. It leads to impairment in mitochondrial functioning, particularly affecting the dorsal columns (causing the difficult in walking), and lateral corticospinal tracts (descending voluntary movement of contralateral limbs). These patients usually die from hypertrophic cardiomyopathy.

68
Q

Name 6 defects seen in a hemisection of the spinal cord.

A

This is Brown Sequard.

1) I/L UMN signs BELOW the level of the lesion (corticospinal tract)
2) I/L loss of tactile, vibration, proprioception BELOW level of lesion (dorsal columns)
3) C/L pain and temperature 2-3 SEGMENTS BELOW level of lesion (spinothalamic tract damage)
4) I/L loss of all sensation AT the level of the lesion
5) I/L LMN signs AT the level of the lesion
6) If lesion occurs above T1, patient may present with Horner’s syndrome.

69
Q

46 y.o. man presents to you complaining of frequent twitching in both of his arms and hands. You note +1 reflexes bilaterally at C7 as well as muscle strength 2/5 in both wrist extension and flexion. Upon further examination, you note signs of damaged spinothalamic tracts. How did this patient acquire this disease?

A

This is occlusion of the anterior spinal artery (stroke). While the UMN and LMN signs normally point towards ALS, this patient also has loss of pain and temperature sensation (spinothalamic tract lesion), which is characteristic for ASA occlusion.

70
Q

46 y.o. man presents to you complaining of frequent twitching in both of his arms and hands. You note +1 reflexes bilaterally at C7 as well as muscle strength 2/5 in both wrist extension and flexion. Upon further examination, you note pain and temperature sensation as well as eye movements remain intact. He is also oriented X3. How did this patient acquire this disease?

A

This is ALS. Combined UMN + LMN deficits with NO sensory, cognitive, or oculomotor deficits.

Caused by defect in superoxide dismutase 1.

71
Q

Snookie’s baby was delivered with complications, suffering trauma to the C5 and C6 nerve roots. How will the baby present?

A 
Limb hanging at side (abductors)
Medially rotated (lateral rotators)
Pronated forearm (biceps)
72
Q

A man fell out of a tree while hanging onto a limb. How will he present?

A

Atrophy of thenar and hypothenar eminences
Atrophy of interosseus mm
Sensory deficits on medial side of forearm and hand
Disappearance of radial pulse upon moving the head toward the ipsilateral side

73
Q

Injury to the distal ulnar nerve, such as at the hook of the hamate, will have what presentation?

A

Ulnar claw – loss of medial lumbrical function therefore inability to extend 4th and 5th digits when trying to straighten/open hand.

74
Q

A dislocated lunate will have what presentation?

A

Median claw. Distal median nerve lesion – > loss of lateral lumbrical function. 2nd and 3rd digits are clawed upon attempted finger extension.

75
Q

A proximal median nerve lesion will have what presentation?

A

Loss of lateral finger flexion and thumb opposition. When asked to make a fist, 2nd and 3rd digits remain extended and the thumb remains unopposed –> “hand of benediction”
There is also loss of opponens pollicis muscle, leading to an inability to abduct the thumb –> “ape hand”

76
Q

How can a patient get Klumpke’s total claw?

A

Lower trunk lesion –> loss of function of all lumbricals, forearm finger flexors (fed by part of median nerve with C5-C7) and finger extensors (fed by radial nerve) are unopposed –>clawing of all digits

77
Q

What is the role of the lumbrical muscles?

A

Flex at MCP

Extend at PIP and DIP

78
Q

Sensory receptor that communicates pricking pain

A

A delta fibers

79
Q

Sensory receptor that communicates burning or dull pain and itch

A

C polymodal

80
Q

Receptor for cold sensation

A

Cold thermoreceptors (A delta)

81
Q

Receptor for warm sensation

A

Warm thermoreceptors (C polymodal)

82
Q

Vibration and pressure receptors

A

Pacinian

83
Q

Dynamic/changing light, discriminatory touch receptors

A

Meissner corpuscle

84
Q

Receptor for static/unchanging light touch

A

Merkel receptor

85
Q

Proprioception information -muscle length monitoring (receptor)

A

Muscle spindle (intrafusal muscle fibers)

86
Q

This receptor is found particularly on the soles of the feet and is composed of robust spindle-shaped structures found particularly on the soles of teh feet

A

Rafiini

87
Q

This sensory receptor is found only in areas of skin without hair

A

Meissner corpuscle

88
Q

This is the simplest sensory receptor thought to be pain receptor or thermoreceptors

A

Free nerve ending

89
Q

This touch receptor is tough to distinguish from melanocytes

A

Merkel cell

90
Q

Landmark for pudendal nerve block

A

Ischial spine

91
Q

CSF changes in Guillain-Barre

A

Normal cell count with increase in protein (albuminocytologic disassociation)

92
Q

Weber Test results of a patient with conductive hearing loss

A

Lateralizes to side of affected ear

93
Q

Weber Test results of a patient with sensorineural hearing loss

A

Lateralizes to side opposite affected ear

94
Q

Patient presents with a positive Weber test in the right ear as well as AC>BC in the left ear and BC > AC in the right ear. What is your dx?

A

Right conductive hearing loss

95
Q

Patient presents with a positive Weber test in the left ear as well as AC > BC in both ears. What is your dx?

A

Right sensorineural hearing loss

96
Q

Patient presents with a normal Weber test and BC > AC in both ears. What is your dx?

A

Bilateral conductive hearing loss

97
Q

Patient presents with vertigo + tinnitus + hearing loss. What is the dx?

A

Meniere’s Disease (Endolymphatic Hydrops)

98
Q

Chronic otitis media can sometimes result in a cystic lesion that is lined by keratinizing squamous epithelium which can be metaplastic that is filled with amorphous debris. What is the name of this condition?

A

Cholesteatoma

99
Q

Outline the flow of aqueous humor.

A

Formed in a capillary bed in the ciliary body –> secreted into posterior chamber –> flows between angle formed by lens and iris diaphragm –> into anterior chamber –> reabsorbed by Canal of Schlemm.

100
Q

What is the pathogenesis of glaucoma?

A

Blocked canal of Schlemm–> aqueous humor not reabsorbed –> increased pressure –> atrophy of optic nerve

101
Q

What portion of the eye is opacified in a cataract?

A

Lens

102
Q

Outline the pupillary light reflex pathway.

A

Cells of retina – > optic tract – > optic tract/nerve –> pretectal nucleus –> bilateral Edinger-Westphal nuclei –> preganglionic parasympathetic fibers in oculomotor nerve –> ciliary ganglion –> post-ganglionic parasympathetic fibers –>pupillary sphincter of iris –> pupillary constriction (miosis)

103
Q

Describe what light reflexes will be seen in both eyes if the right optic nerve is damaged prior to the pretectal nucleus.

A

No constriction of either the left or right eye when light is shone in the right eye
Both pupils constrict if the light is shined in the left eye

104
Q

Describe what light reflexes will be seen in both eyes if the right oculomotor nerve is damaged.

A

Right eye will not respond to light shone in either right or left eye.
Left eye will constrict when a light is shined in either eye.

105
Q

What part of the visual tract is damaged causing bitemporal hemianopia?

A

Optic chiasm

106
Q

If a patient has a left homonymous hemianopia, what part of the visual pathway is damaged?

A

Right optic tract

107
Q

If a patient presents with left upper quadrantic anopia, where is the lesion?

A

Right temporal lesion (MCA)

108
Q

If a patient presents with a left lower quadrantic anopia, where is the lesion?

A

Right parietal lesion (MCA)

109
Q

If a patient presents with a left hemianopia with macular sparing, what do you suspect?

A

PCA infarct on the right since the macula has bilateral projection to the occiput

110
Q

If a patient presents with a central scotoma, what do you suspect?

A

Central scotoma (macular degeneration)

111
Q

If the oculomotor nerve is compressed by a PCA aneurysm or uncal herniation, what symptoms do you expect to find?

A

Diminished or absent pupillary light reflex (blown pupil) since the fibers on the periphery supply parasympathetic output

112
Q

If the oculomotor nerve’s vasculature is compromised, what kind of symptoms do you expect to find?

A

Ptosis and “down and out” gaze since motor output to the ocular muscles is found centrally and affected primarily by vascular disease due to decreased diffusion of oxygen and nutrients to the interior fibers from compromised vasculature that resides on the outside of the nerve.

113
Q

These are intranuclear inclusions found in neurons seen in herpes simplex encephalitis

A

Cowdry Type A inclusions

114
Q

These are cytoplasmic inclusion bodies found in neurons associated with aging

A

Lipofuscin granules

115
Q

These are eosinophilic, rod-like inclusions in hippocampus of Alzheimer patients

A

Hirano bodies

116
Q

These are filamentous inclusions that stain with silver and do not survive neuronal death

A

Pick bodies

117
Q

These are filamentous inclusions that stain with PAS and ubiquitin

A

Lewy bodies

118
Q

What are the 6 usual components of a “dementia workup”?

A
  1. Syphilis screen
  2. HIV
  3. TSH
  4. Vitamin B12
  5. Head CT, MRI
  6. MMS exam
119
Q

What allele is associated with Alzheimer disease?

A

APP gene on chromosome 21

ApoE4 allele

120
Q

Why is Alzheimer disease so common in patients with Down syndrome?

A

3 copies of APP on chromosome 21

121
Q

If a patient presents with headache and extraocular muscle palsies, what do you suspect?

A

Cavernous sinus thrombosis

122
Q

34 y.o. female patient presents with a throbbing headache and seizures that came on with acute onset. T2 weighted MRI shows a lobulated mass near the corpus callosum that crosses the midline, with central areas of necrosis and hemorrhage. What kind of cells would stain positive in this tumor?

A

Astrocytes would stain for GFAP in a Glioblastoma Multiforme. This is the most common primary brain tumor.

123
Q

34 y.o. female patient presents with new onset seizures. Biopsy of her brain shows spindle cells concentrically arranged in a whorled pattern. What is another histological characteristic of this tumor?

A

Psammoma bodies.

This is a meningioma.

124
Q

27 y.o. female patient presents with new onset bilateral hearing loss and tinnitus. Cells obtained from a biopsy are S-100 biopsy. What else can you most likely find in this patient’s history?

A

Neurofibromatosis type 2 – associated with bilateral acoustic schwannoma generally found at the cerebellopontine angle.

125
Q

46 y.o. female patient presents to you because her husband has recently been getting mad at her and complaining she is “not the woman he married 20 years ago.” He states that she has been more “sexually needy” and “open,” especially in public. Biopsy of a mass obtained with a CT of the head shows cells with round nuclei with clear cytoplasm with prominent delicate vasculature. What tumor do you suspect?

A

Oligodendroglioma –most often found in frontal lobes.

“Fried egg” appearance also found in seminoma and koilocytic change of HPV cancers.

126
Q

Biopsy from the brain of a 6 y.o. boy that presents with ataxia shows eosinophilic, corkscrew fibers that are GFAP positive. What tumor do you suspect?

A

Pilocytic astrocytoma

127
Q

Biopsy from the brain of a 6 y.o. boy that presented with hydrocephalus shows clusters of small blue cells surrounding fibrils. Describe the mutation most likely behind this disease and what this patient is at increased risk for if he survives.

A

This is Turcot syndrome – also known as Mismatch Repair cancer syndrome. It is a patient with medulloblastomas and familial polyposis of the colon.

The mutation involves DNA mismatch repair genes.

128
Q

6 y.o. boy presents with hydrocephalus. Biopsy of the brain mass shows clusters of cells surrounding blood vessels. What kind of tumor do you suspect?

A

Ependymoma

129
Q

3 most common primary brain tumors in adults

A
  1. GBM
  2. Meningioma
  3. Schwannoma
130
Q

3 most common primary brain tumors in children

A
  1. Astrocytoma
  2. Medulloblastoma
  3. Ependymoma
131
Q

3 structures compressed by uncal herniations

A

Ipsilateral PCA
Oculomotor nerve
Cerebral peduncle

132
Q

Which herniation can compress the anterior cerebral artery?

A

CIngulate/subfalcine herniation

133
Q

6 year old boy presents with ataxia. An eye examination reveals a yellow mound fed by a large arteriole and drained by an even larger vein in the retinal periphery. Biopsy of a mass in the brain shows foamy cells and high vascularity. What are some associated manifestations do you expect to see in this syndrome?

A

This is Von Hippel Lindau, an autosomal dominant gene mutation found on chromosome 3 that causes retinal angiomas, hemangioblastomas (most often found in the cerebellum), pheochromocytomas, renal cell CAs, and visceral cysts.*

134
Q

Triad associated with pineal germinoma

A

Found in young males usually.

Present with precocious puberty due to beta hCG production.
Aqueductal compression may lead to obstructive hydrocephalus.
Parinaud syndrome due to compression of tectal area of midbrain.

DIT FACTS (16 decks)

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