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Case Study Notes Flashcards

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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
what 2 things can basillar artery thrombosis manifest as?
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
26
what symptoms can an anterior cerebral artery stroke cause?
- contralateral paralysis of leg/foot - contralateral sensory loss of leg/foot - apraxia
27
what symptoms can a posterior cerebral artery stroke cause?
- contralateral visual field blindness - if on left: alexia - if bilateral (top of the basilar): blindness, memory loss, somatosensory loss
28
what symptoms can a middle cerebral artery stroke cause?
- contralateral paralysis - contralateral sensory loss - apraxia - visual field deficits - if on left: aphasia - if on right: hemineglect
29
what are the external and extreme capsule?
association fibers
30
what is the claustrum?
gray matter that has connections with insula and other parts of cortex
31
where would the lesion be if... - motor signs are in the upper motor neuron - no uncrossed symptoms?
forebrain (uncrossed symptoms would suggest direct involvement of CNs)
32
what would localize lesions to the internal capsule, posterior limb, of the right side?
motor and sensory problems over the left side, with blindness in the left side of both eyes and no language problems
33
what are the 3 main types of ischemic stroke? what are they caused by?
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
what is the core and penumbra of strokes?
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
what are intra-cerebral hemorrhagic strokes? what are they associated with?
10-15% of all strokes w/ higher mortality than other stroke types -associated with HTN, amyloidosis, neoplasms, iatrogenic anticoagulation, cocaine use, etc.
36
what do lenticularstriate arteries supply?
all of internal capsule (anterior, genu, and posterior)
37
what does the anterior choroidal artery supply?
posterior limb of internal capsule
38
what do Huntington's disease patients present with?
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
what are neurologic symptoms of Huntington disease?
- chorea (dance-like movements) - dystonia - eye movement slowing - hyperreflexia - gait abnormality - myoclonus (rare) - Parkinsonism (late)
40
what are psychiatric symptoms of Huntington disease
- apathy - irritability - depression - delusions - aggression - anxiety - disinhibition - paranoia
41
what are cognitive symptoms of Huntington disease?
- poor judgement - inflexibility of thought - loss of insight - decreased concentration - memory loss - subcortical dementia
42
what is the classic triad of normal pressure hydrocephalus?
wet, wobbly and wacky (urinary incontinence, gait disturbance, and dementia
43
what is normal pressure hydrocephalus?
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
what is the pathophysiology of normal pressure hydrocephalus?
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
what is the initial and most prominent symptom of normal pressure hydrocephalus
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
why is there dementia with normal pressure hydrocephalus?
traction on frontal and limbic fibers that run in periventricular region -frontal lobe (forgetfulness) and subcortical (slowed processing speeds) in nature
47
why is there urinary incontinence with normal pressure hydrocephalus?
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
what is treatment for NPH?
ventriculoperitoneal shunt
49
what is hemineglect usually caused by? what side is it usually on?
left sided neglect due to right inferior parietal lobule lesion
50
what comprises the inferior parietal lobule? what do the left and right lobules do?
supramarginal gyrus + angular gyrus - left = language (lesion causes aphasia) - right = visual-spatial (lesion causes left-sided neglect)
51
what are visual radiations?
deep white matter in parietal cortex area
52
why would an arm be weak and hyperreflexic?
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
what would decreased ADH cause?
causes excessive thirst and secretion of diluted urine
54
what hormones are secreted by posterior pituitary?
oxytocin and ADH
55
what hormones are secreted by anterior pituitary?
TSH, ACTH, FSH/LH, GH, prolactin, endorphins
56
what is alexia?
inability to read
57
what is agraphia?
inability to write/copy
58
what does the angular gyrus do? what could damage to it cause?
brings visual information from visual cortex to Wernicke's area -damage causes many aphasic deficits
59
does alexia w/o agraphia suggest angular gyrus damage?
no, it suggests that it remained intact
60
what is alexia caused by?
damage to left visual cortex + damage to splenium of corpus callosum (carries axons from right visual cortex to angular gyrus)
61
what is writing mediated by? what are these areas supplied by?
Broca's area and Wernicke's area, both supplied by MCA
62
what is the Romberg's sign? how can they compensate, and what does that mean?
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
what causes "word deafness"?
absence of auditory cortex or its input via auditory radiations
64
what is "word deafness"?
inability to recognize words as language
65
what is spinal shock? what do patients present with?
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
do people recover from spinal shock? why does this happen?
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
what is Brown-Sequard syndrome?
spinal cord hemisection with unknown incidence (trauma, herniated disc, etc.) -can affect symmetrical sides or any other "half" divisions
68
what can damage to the hypothalamic-reticulo-spinal tract cause?
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
what is syringomyelia? what is it caused by?
development of fluid-filled cavity (syrinx) w/in spinal cord | -50% of cases due to obstruction of CSF circulation (Arnold-Chiari malformation)
70
what is Arnold-Chiari malformation I?
cerebellar tonsils that are abnormally shaped and downwardly displaced below level of foramen magnum

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