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Nervous System > Exam II Random Mix > Flashcards

Exam II Random Mix Flashcards

1
Q

Acoustic Reflex

A
  • VIII in and VII out

* stapedial contraction to decrease low frequency noises

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2
Q

Otoacoustic Emission

A
  • VIII in and VIII out
  • decrease in contractility of outer hair cells in the presence of high frequency noise
  • bilateral distribution, the inner hair cells can affect the outer hair cells of both ears
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3
Q

Vestibuloocular Reflex

A
  • 3 neuron Reflex arc
  • vestibular afferents project ipsilaterally to the vestibular nuclei which then project (mostly, not entirely) through the MLF to the oculomotor, trochlear and abducens nuclei
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4
Q

Meniere’s Disease

A
  • vertigo, hearing loss, tinnitus, fullness of affected ear
  • 20 min-4 hours
  • idiopathic endolymphatic hydrops
  • men and women affected the same
  • 20-50 yo
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5
Q

Benign paroxysmal positional vertigo

A
  • detachment of otoconia in the utricle, allowing them to enter the semicircular canal
  • posterior canal
  • vertigo and nystagmus
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6
Q

Vertigo

A
  • change in density of cupola and endolymph

* positionally dependent vertigo

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7
Q

Conductive hearing loss

A

•obstruction, processes that prevent sound from reaching the lymph

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8
Q

Sensoneuronal hearing loss

A
  • damage to hair cells, cochlear nerve fibers, cochlear nuclei
  • bone and air conduction loss
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9
Q

Ansomia

A 
•loss of sense of smell
•conductive or sensoneuronal
Others:
•hyposomia
•hypersomia 
•dysomia
•olfactory agnosia
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10
Q

Nystagmus

A
  • An involuntary eye movement which may cause the eye to rapidly move from side to side, up and down, or in a circle, and may slightly blur vision
  • refers to the fast movement
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11
Q

Presbycusis

A

• age related hearing loss that is progressive and bilateral due to loss of the stereociliated cells of the Organs of Corti most often at the base (loss of high frequency)

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12
Q

Meibomian glands

A

Sebaceous gland that prevent the desiccation of tears

Inflammation causes painful styes

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13
Q

Aniscoria

A

Aniscoria - unequal pupils

Difference in pupil sizes greater in darkness = sympathetic pathway problem

Difference in pupil size greater in bright light = parasympathetic pathway problem

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14
Q

Third Nerve Palsy

A

•pupil involving
- accompanied by some degree of motility dysfunction and/or ptosis
•pupil sparing
-diabetes or hypertension (microvascular injury to nerve fibers)
-physical compression of the nerve itself as it leaves the brainstem and heads to the orbit —>brainstem herniation and compression by tumors, intracranial aneurysm (junction of PCOM and ICA) angiography for diagnosis

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15
Q

Iris Damage

A
  • damage to iris musculature can cause both parasympathetic-mimicking and sympathetic-mimicking aniscoria - can be ruled out using slit lamp microscopic exam of the iris tissue
  • scarring of the pupil to the lens capsule typically freezes the pupil in a smaller state, miming a sympathetic lesion
  • injury, such as tearing, of the sphincter muscle mimics a parasympathetic lesion
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16
Q

Horner Syndrome

A

•interruption of the sympathetic pathway at any point
•miosis (sphincter muscles contracts against a weakened dilator muscle), ptosis (interruption of innervation to Müller’s muscle in the upper eyelid) and anhydrosis (decreased innervation to the sweat glands on the ipsilateral side of the face - disruption of 1st or 2nd order neuron)
•Is t 1st/2nd or 3rd Order neuron??? Pharmacologic testing with eye drops!
-4% cocaine, instilled into both eyes
cocaine blocks the reuptake of NE, causing a build up in the synapse and potentiates pupillary dilation IF NE is present

-hydroxyamphetamine instillation
releases NE from an intact neuron 
3rd Order - no dilation
1st/2nd Order - dilation
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17
Q

Pharmacologic Aniscoria

A

•most common is scopolamine patches, post auricular to treat postop nausea or neurology nausea

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18
Q

Light Near Dissociation

A
  • when the near response (pupil constriction to accommodation, or looking at a near target) exceeds the maximal light response (the largest amounts of contstriction with a very bright light)
  • unusual finding that can denote some very serious neurological conditions - syphilis (Argyll-Robinson pupil) or tumors/compression of the rectus of the midbrain
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19
Q

Neurofibromatosis

A
  • anterior eye nodules

* glioma

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20
Q

Tuberous sclerosis

A

•retinal hematomas, hyperpigmented lesions

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21
Q

Thyroid/Graves Disease

A

•Orbit - bulging due to fibrosis in muscles

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22
Q

Albinism

A

•Retina - lack of pigment

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23
Q

Osteogenesis Imperfecta

A

•blue sclera

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24
Q

Rubella

A

•retina - pigmentary retinopathy

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25
Q

Mucor/Invasive Fungal Disease

A

•orbit - scrape fungus out of eye

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26
Q

Diabetes

A

•retina - diabetic retinopathy, proliferative vs. No proliferative

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27
Q

Hypertension

A

•hypertensive retinopathy

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28
Q

Melanoma

A

•cancer

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29
Q

Central Retinal Artery Occlusion

A
  • lose vision suddenly and permanently
  • cherry red spot secondary to thinned retinal layers in the fovea that allow the color of the pigment epithelium show through
  • ”stroke in the eye”
  • localizing factors (severely high intracranial pressure), embolus, thrombus
  • if caused by emboli phenomenon, insults to the brain commonly follow
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30
Q

Tay Sachs Disease

A
  • deterioration of nerve cells due to accumulation of gangliosides
  • cherry red spot secondary to accumulation of sphingolipids within retinal ganglion cells and since the fovea does not contain retinal ganglion cells, the red spot shows through since the fovea receives its blood supply from the choriocapillaris while the surrounding retina is pale due to infarction
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31
Q

Niemann Pick Disease

A
  • accumulation of sphingomyelin
  • cherry red spot secondary to accumulation of sphingolipids within retinal ganglion cells and since the fovea does not contain retinal ganglion cells, the red spot shows through since the fovea receives its blood supply from the choriocapillaris while the surrounding retina is pale due to infarction
32
Q

Diabetic retinopathy

A
  • non-proliferative
  • proliferative
    • neovascularization
    • starts with mild findings: spots of blood in retina, cotton wool spots, edema within macula - diffuse loss of the capillary network within retinal tissue
    • as capillaries are lost, nutrition supplied to the area decreases and cellular function declines
    • VEGF initiates formation of new blood vessels in an attempt to restore blood flow
      • these blood vessels are thin, fragile and do not work well with ocular tissue - they bleed easily and cause damage to the retina and scarring —-> retinal detachment*
33
Q

Macular Degeneration

A

•age related
•metabolic by products (drusen) accumulate around the retinal pigment epithelium - non proliferative
•as more accumulation occurs, the boundary between the pigment epithelium and the choriocapillaris breaks down and new blood vessels grow between the layers
these blood vessels are fragile and bleed easily, causing damage to the retinal tissue
•mostly involves macula —> central visual deficits

34
Q

Amblyopia

A

•a condition where abnormal vision develops due to the inability of the visual system to receive, develop and process visual signals

35
Q

Accommodation reflex

A

•vergence movement, most reflexes involve brainstem or spinal cord, this one involves the cortex!

1) pupils constrict, which improves the optical performance of the eye and increases the depth of field
2) ciliary muscles contract, allowing the lenses to get fatter and so focus the eyes on the nearby object
3) the medial recti of both eyes contract, causing the eyes to converge. This causes the image of the nearby object to fall on both foveae.

36
Q

Abducens Palsy

A
  • damage to Abducens nerve fiber

* no or limited abduction seen of the involved eye

37
Q

Gaze Palsy

A
  • abducens nucleus damage

* no or limited abduction in involved eye, no or limited adduction in contralateral eye

38
Q

Internuclear opthalmoplegia

A
  • damage to MLF

* normal abduction in both eyes, limited or no adduction on the involved side (can be bilateral)

39
Q

Lower Motor Neuron Damage

A
  1. Weakness
  2. Hyporeflexia
  3. Fasiculations
  4. Atrophy
  5. Hypotonia

Also, fibrillation and giant motor units

40
Q

Spinal Muscle Atrophies

A
  • genetic diseases where there is a loss of LMN in the anterior horn
  • Werdnig-Hoffman: autosomal recessive that affects primarily proximal muscles in people of all ages and is progressive over time
  • many SMAs are due to a genetic mutation in the survival motor neuron protein - responsible for transcriptional regulation and cellular trafficking
41
Q

Myasthenia Gravis

A
  • antibodies attack and degrade nicotinic channels in the NMJ
  • eye muscle weakness (diplopia), droopy eyelid, difficult in swallowing, slurred speech, overall tiredness
  • edrophonium blocks breakdown of ACh
42
Q

Apraxia

A

• a neurological disorder characterized by the inability to perform learned (familiar) movements on command, even though the command is understood and there is a willingness to perform the movement.

43
Q

UMN Damage

A

•spinal cord injury, MS (demyelinating disease of the corticospinal and corticobulbar tracts thought to be due to CNS inflammation), amyotrophic lateral sclerosis (degenerationof UMN and/or LMN), cerebral palsy (abnormal development or damage/complications during pregnancy), most common cause? —->vascular events!

  1. Weakness
  2. Exaggerated reflexes
  3. Hypertonia
  4. Clonus
  5. Spasticity
44
Q

Damage to lateral hemisphere of cerebellum

A

•ipsilateral ataxia, especially pronounced in the limbs

45
Q

Damage to medial hemisphere of cerebellum

A

•intention tremors

46
Q

Damage to vermis

A
  • difficulty coordinating the movements of trunk muscles

* wide based, staggering gait, inability to walk heel to toe

47
Q

Damage to flocculonodular lobe

A
  • wide based, staggering gait accompanied by vertigo and nystagmus
  • deficits in tracking eye movements
48
Q

Friedrich’s Ataxia

A
  • autosomal recessive
  • begins in childhood and leads to impaired muscle coordination that worsens over time
  • spinal cord, peripheral nerves and cerebellum degenerate
  • awkward, instead movements, impaired memory, loss of tendon reflexes (especially in knees and ankles), scoliosis, dysarthria
  • defect in FXN
49
Q

Lesions of left hippocampus

A

•trouble with verbal memory

50
Q

Lesions of right hippocampus

A

•trouble with spatial orientation

51
Q

Bilateral damage to medial temporal lobes, including hippocampus and parahippocampal

A

•amnesia

52
Q

Retrograde amnesia

A

•prior to injury

53
Q

Antergrade

A

•after the injury

54
Q

Wernicke Korsakoff Syndrome

A

•lack of thiamine
•confusion, nystagmus, opthalmoplegia, aniscoria, ataxia, coma
•anterograde and retrograde amnesia, confabulation and hallucinations
•reduction in size and function of mammillary bodies
*alcoholics, gastric surgeries

55
Q

Damage to higher somatosensory association areas

A
  • unable to coordinate visual and motor functions

* Balint Syndrome

56
Q

Broca’s Area

A
  • opercular and triangular parts of the left inferior frontal gyrus
  • damage causes problems producing language
57
Q

Wernicke‘ s Area

A
  • posterior part of the left auditory association cortex

* damage causes problems with the comprehension of language

58
Q

Stroke in ACA

A
  • hemiplegia or hemiparesis of contralateral lower limbs and pelvic muscles; arms and face typically unaffected
  • contralateral sensory deficit on lower limbs and pelvic area; hands and face typically unaffected
  • no speech impairment
  • symptoms of disconnection caused by damage to the corpus callosum and cingulate gyrus
59
Q

Stroke in MCA

A
  • hemiplegia or hemiparesis of contralateral upper limbs; contralateral lower limbs can also be affected, but to a lesser degree; contralateral lower face,upper ace not affected due to bilateral cortical input
  • speech impairment: global aphasia or motor (Broca’s) or sensory (Wernicke) aphasia if stoke is on left side
  • spatial hemineglect (if right sided stroke)
  • anosognosia
  • apraxia and visuo-spatial disorientation (cannot button clothes)
60
Q

Stroke in PCA

A
  • visual deficits (cortical blindness or homonymous hemianopsia on contralateral side
  • prosopagnosia
  • visual agnosia (temporal damage to “what” pathway)
  • anomia (inabilityto name objects or colours sue to visual association areas)
  • amnesia (damage to hippocampus or parahippocampal gyrus)
  • spatial deficits (getting lost) due to damage to right hippocampus
  • alexia without agraphia (inability to read but able to write) due to damage to visual areas but motor areas in MCA territory are still functional
61
Q

Damage to fusiform gyrus (occipital-temporal gyrus)

A

•prosopagnosia

62
Q

Damage to Right Frontal Inferior Gyrus

A

•diminished ability to convey emotions through voice and gestures

63
Q

Damage to Right Superior Temporal Gyrus

A

•inability to comprehend emotion or emphasis in the voice or gestures of others

64
Q

Damage to Left Parietal Lobe

A
  • bilateral apraxia

* loss of purposeful movement

65
Q

Damage to Left Parietal Cortex

A

•math and reading problems - no math, alexia

66
Q

Damage to Right Parietal Cortex

A

•spatial awareness - hemineglect

67
Q

Damage to Dorsolateral Prefrontal Cortex

A

•management of cognitive processes - working memory, cognitive flexibility and planning

68
Q

Damage to Ventromedial Prefrontal Cortex

A

•moral judgement

69
Q

Lesions to ventromedial hypothalamus

A
  • overeating, obesity

* overproduction of leptin

70
Q

Lesions to lateral hypothalamus

A

•weight loss, decreased appetite, leading to cachexia and death

71
Q

Disconnection syndromes

A

•Loss of higher cortical functions

72
Q

Damage to left CNS

A

•language aphasias

73
Q

Meningioma

A

•A usually noncancerous tumor that arises from the membranes surrounding the brain and spinal cord.

74
Q

Ageusia

A

•loss of taste

75
Q

Pupil reflex

A
  • CN II in, III out

* consensual

76
Q

Gag reflex

A

•CN Ix in, CN X out

77
Q

Gastric Reflex

A

•CN I, VII, IX in, CN X out

Nervous System (11 decks)

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