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Neuroscience > Case Study Notes > Flashcards

Case Study Notes Flashcards

1
Q

where are cell bodies located in upper VS lower motor neurons?

A

UMN: cell body in motor cortex and processes connect with motor nuclei in brain stem or anterior horn of spinal cord
LMN: cell body in brainstem or spinal cord and axon innervates skeletal muscle fibers

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2
Q

what are some upper motor neuron deficit signs?

A 
limbs
-spastic paralysis
-hyperreflexia and hypertonia
-Babinski sign
CN7: contralateral lower face droop
CN12: tongue deviates to side opposite lesion
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3
Q

what are some lower motor neuron deficit signs?

A 
limbs
-flaccid paralysis
-hyporeflexia and hypotonia
muscle atrophy
muscle fasciculations
CN7: entire half face paralysis
CN12: tongue deviates to side of lesion
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4
Q

how does cortical control of upper VS lower facial nucleus differ?

A
  • upper: supplies upper part of face is bilateral
  • -UMN lesion leads to only lower quadrant deficits of contralateral side
  • lower: supplies lower part of face is contralateral
  • -LMN lesion leads to ipsilateral facial weakness over entire half of face (Bell’s palsy)
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5
Q

what does herniation do to the uncus? what other symptoms does it cause?

A

uncus displacement over tentorial notch and elevated ICP, putting pressure on brainstem (especially CN III)
-ipsilateral pupil dilation and eye deviation

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6
Q

why are glioblastoma multiforme so dangerous?

A

tumor of astrocytic origin

  • can grow rapidly and reach large sizes before clinical presentation
  • cases present over less than 3 mo. in 50% of patients, mostly with motor weakness and headaches
  • large tumors with necrosis and hemorrhaging due to increased vascularity
  • increased ICP may cause seizures
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7
Q

symptoms of lesions in somatomotor cortex are?

A

contralateral weakness/paresis

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8
Q

symptoms of lesions in somatosensory cortex are?

A

controlateral loss of sensation

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9
Q

symptoms of lesions in visual cortex are?

A

contralateral loss of vision w/ macular sparing

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10
Q

symptoms of lesions in auditory cortex are? (unilateral VS bilateral)

A

uni: no apparent deficits
bi: loss of ability to recognize sounds

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11
Q

symptoms of lesions in Wernicke’s area (in left hemisphere) are?

A

Wernicke’s aphasia: loss of ability to produce/understand spoken/written language; makes paraphrasic errors

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12
Q

symptoms of lesions in Broca’s area (in left hemisphere) are?

A

Broca’s aphasia: loss of ability to produce spoken/written language, but comprehension remains intact; speech is unintelligible

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13
Q

symptoms of lesions in supramarginal gyrus (in right hemisphere) are?

A

contralateral hemi-neglect syndrome

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14
Q

symptoms of lesions in inferior/medial temporal lobes (bilateral) are?

A

memory deficits

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15
Q

where is Broca’s area? what does it do?

A

posterior inferior frontal gyrus

-controls output of spoken language

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16
Q

where is Wernicke’s area? what does it do?

A

posterior superior temporal gyrus (AKA inferior parietal lobule)
-receives info from auditory cortex, assigns word meanings

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17
Q

characteristics of Broca’s aphasia

A

halting speech
repetitive (perseveration)
disordered syntax, grammar, and structure of words

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18
Q

characteristics of Wernicke’s aphasia

A

fluent speech
little repetition
adequate syntax and grammar
contrived/inappropriate words

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19
Q

what are symptoms of “top of the basilar” occlusion?

A
  • acute onset of typical symptoms (ischemic stroke)
  • bilateral visual field deficits (frequently causes blindness)
  • memory loss
  • bilateral somatosensory loss
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20
Q

what are symptoms of blocking both posterior cerebral arteries?

A

affects medial surface of temporal and occipital lobes: memory and visual problems, respectively
-usually don’t survive

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21
Q

what are symptoms of blocking deep penetrating branches of posterior cerebral arteries?

A

blocks blood to thalamus causing sensory deficits

-usually don’t survive

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22
Q

how can basilar artery thrombosis come about?

A

slow/progressive: due to atherosclerosis and atherembolis

  • collateral circulation often will develop
    sudden: due to thromboembolism
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23
Q

what is the risk, mortality rate, and age ranges that get basilar artery thrombosis?

A

27% of posterior circulation ischemic strokes
>70% mortality rate, halved with recanalization
-progressive: in 50s-60s, sudden in 30s

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24
Q

symptoms of basilar artery thrombosis

A
  • vertigo/nausa/vomiting
  • motor deficits
  • dysarthria/speech impairment
  • headache
  • change in consciousness
  • visual disturbances
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25
Q

what 2 things can basillar artery thrombosis manifest as?

A
  1. locked in syndrome: lesion at base of pons
    - quadriplegia with preserved consciousness and vertical eye movements
  2. top of basilar syndrome
    - changes in consciousness and visual changes
    - motor symptoms often include abnormal movements/posturing
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26
Q

what symptoms can an anterior cerebral artery stroke cause?

A
  • contralateral paralysis of leg/foot
  • contralateral sensory loss of leg/foot
  • apraxia
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27
Q

what symptoms can a posterior cerebral artery stroke cause?

A
  • contralateral visual field blindness
  • if on left: alexia
  • if bilateral (top of the basilar): blindness, memory loss, somatosensory loss
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28
Q

what symptoms can a middle cerebral artery stroke cause?

A
  • contralateral paralysis
  • contralateral sensory loss
  • apraxia
  • visual field deficits
  • if on left: aphasia
  • if on right: hemineglect
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29
Q

what are the external and extreme capsule?

A

association fibers

30
Q

what is the claustrum?

A

gray matter that has connections with insula and other parts of cortex

31
Q

where would the lesion be if…

  • motor signs are in the upper motor neuron
  • no uncrossed symptoms?
A

forebrain (uncrossed symptoms would suggest direct involvement of CNs)

32
Q

what would localize lesions to the internal capsule, posterior limb, of the right side?

A

motor and sensory problems over the left side, with blindness in the left side of both eyes and no language problems

33
Q

what are the 3 main types of ischemic stroke? what are they caused by?

A
  1. large artery infarct - thromboemboli from atherosclerotic vessels
  2. small vessel/lacunar infarcts - primarily from HTN (13-20% of ischemic strokes)
  3. cardioembolic - from atrial fibrilation (20% acute strokes)
34
Q

what is the core and penumbra of strokes?

A

core - dies within minutes and is not recovered

penumbra - surrounding tissue that is ischemic, but regains function after a while if treated w/in hours

35
Q

what are intra-cerebral hemorrhagic strokes? what are they associated with?

A

10-15% of all strokes w/ higher mortality than other stroke types
-associated with HTN, amyloidosis, neoplasms, iatrogenic anticoagulation, cocaine use, etc.

36
Q

what do lenticularstriate arteries supply?

A

all of internal capsule (anterior, genu, and posterior)

37
Q

what does the anterior choroidal artery supply?

A

posterior limb of internal capsule

38
Q

what do Huntington’s disease patients present with?

A

progressive choreiform (dancelike) movement disorder, psychiatric disorders, and dementia

  • anticipation: expansion of mutated repeats from one generation to the next (increasing affliction w/ younger onset)
  • causes atrophy of caudate and putamen
39
Q

what are neurologic symptoms of Huntington disease?

A
  • chorea (dance-like movements)
  • dystonia
  • eye movement slowing
  • hyperreflexia
  • gait abnormality
  • myoclonus (rare)
  • Parkinsonism (late)
40
Q

what are psychiatric symptoms of Huntington disease

A
  • apathy
  • irritability
  • depression
  • delusions
  • aggression
  • anxiety
  • disinhibition
  • paranoia
41
Q

what are cognitive symptoms of Huntington disease?

A
  • poor judgement
  • inflexibility of thought
  • loss of insight
  • decreased concentration
  • memory loss
  • subcortical dementia
42
Q

what is the classic triad of normal pressure hydrocephalus?

A

wet, wobbly and wacky (urinary incontinence, gait disturbance, and dementia

43
Q

what is normal pressure hydrocephalus?

A

pathologically enlarged ventricular size w/ normal opening pressures on lumbar puncture and only intermittently elevated CSF pressure
-potentially reversible cause of dementia, so must recognize and accurately diagnose

44
Q

what is the pathophysiology of normal pressure hydrocephalus?

A

impaired absorption secondary to subarachnoid hemorrhage, chronic meningitis, Paget’s disease of skull, infection, tumor, etc.

  • eventually leads to inflammation and fibrosis of arachnoid granulations
  • decreased CSF resorption causes gradual accumulation of CSF w/in ventricular system
  • while increased ICP is not measured on LP, pressure effect occurs on periventricular white tracts
45
Q

what is the initial and most prominent symptom of normal pressure hydrocephalus

A

gait; expansion of lateral ventricles lead to traction on corticospinal tract fibers going into spinal cord
-creates weakness, leg tiredness, magnetic gait, shuffling steps

46
Q

why is there dementia with normal pressure hydrocephalus?

A

traction on frontal and limbic fibers that run in periventricular region
-frontal lobe (forgetfulness) and subcortical (slowed processing speeds) in nature

47
Q

why is there urinary incontinence with normal pressure hydrocephalus?

A

spastic hyperreflexic, increased urgency due to decreased inhibition of bladder contractions and detrussor instability/over-activity
-associated with lack of concern for micturition b/c frontal lobe cognitive impairment

48
Q

what is treatment for NPH?

A

ventriculoperitoneal shunt

49
Q

what is hemineglect usually caused by? what side is it usually on?

A

left sided neglect due to right inferior parietal lobule lesion

50
Q

what comprises the inferior parietal lobule? what do the left and right lobules do?

A

supramarginal gyrus + angular gyrus

  • left = language (lesion causes aphasia)
  • right = visual-spatial (lesion causes left-sided neglect)
51
Q

what are visual radiations?

A

deep white matter in parietal cortex area

52
Q

why would an arm be weak and hyperreflexic?

A

descending corticospinal neurons from motor cortex cause inhibitory effect on motorneurons they synapse on
-loss of descending neuron’s input causes increased excitability of spinal reflex circuits

53
Q

what would decreased ADH cause?

A

causes excessive thirst and secretion of diluted urine

54
Q

what hormones are secreted by posterior pituitary?

A

oxytocin and ADH

55
Q

what hormones are secreted by anterior pituitary?

A

TSH, ACTH, FSH/LH, GH, prolactin, endorphins

56
Q

what is alexia?

A

inability to read

57
Q

what is agraphia?

A

inability to write/copy

58
Q

what does the angular gyrus do? what could damage to it cause?

A

brings visual information from visual cortex to Wernicke’s area
-damage causes many aphasic deficits

59
Q

does alexia w/o agraphia suggest angular gyrus damage?

A

no, it suggests that it remained intact

60
Q

what is alexia caused by?

A

damage to left visual cortex + damage to splenium of corpus callosum (carries axons from right visual cortex to angular gyrus)

61
Q

what is writing mediated by? what are these areas supplied by?

A

Broca’s area and Wernicke’s area, both supplied by MCA

62
Q

what is the Romberg’s sign? how can they compensate, and what does that mean?

A

patient stands with feet together and closes his/her eyes

  • if unsteady or falls, is positive sign
  • if compensate by opening eyes, it’s a posterior column disorder
  • if cannot compensate by opening eyes, it’s a cerebellar disorder
63
Q

what causes “word deafness”?

A

absence of auditory cortex or its input via auditory radiations

64
Q

what is “word deafness”?

A

inability to recognize words as language

65
Q

what is spinal shock? what do patients present with?

A

immediately follows spinal cord injury, and lasts hours to weeks

  • loss of all spinal cord function caudal to level of lesion
  • may present with flaccid paralysis, anesthesia, areflexia, loss of bladder/bowel
66
Q

do people recover from spinal shock? why does this happen?

A

complete recovery is rare, and often patients develop spastic paresis

  • younger patients more likely to have full recovery
  • mechanism of loss might be due to changes in [K+] associated with cell injury
67
Q

what is Brown-Sequard syndrome?

A

spinal cord hemisection with unknown incidence (trauma, herniated disc, etc.)
-can affect symmetrical sides or any other “half” divisions

68
Q

what can damage to the hypothalamic-reticulo-spinal tract cause?

A

ipsilateral Horner’s syndrome (loss of sympathetic input to eye)

  • sympathetic neurons that pass UNCROSSED along lateral funiculus of spinal cord
  • these synapse in intermediolateral cell column before exiting around T1 to the sympathetic chain ganglia
69
Q

what is syringomyelia? what is it caused by?

A

development of fluid-filled cavity (syrinx) w/in spinal cord

-50% of cases due to obstruction of CSF circulation (Arnold-Chiari malformation)

70
Q

what is Arnold-Chiari malformation I?

A

cerebellar tonsils that are abnormally shaped and downwardly displaced below level of foramen magnum

Neuroscience (39 decks)

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