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BOARD PREP > Subcortical brain stuff > Flashcards

Subcortical brain stuff Flashcards

1
Q

What is the only sense that is not processed through the thalamus?

A

smell

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2
Q

Identify the info, input, and output for the following thalamic nuclei:

ventral posterolateral nucleus

A

Info: all sensory (pain, temp, touch, prop vibration)

Input: spinothalamic, posterior column (medial lemniscus)

Output: somatosensory cortex

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3
Q

Identify the info, input, and output for the following thalamic nuclei:

ventral posteromedial nucleus

A

info: sensory face & taste
input: trigeminal & gustatory
output: somatosensory cortex

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4
Q

Identify the info, input, and output for the following thalamic nuclei:

lateral geniculate nucleus

A

info: vision
input: CNII
output: calcarine sulcus

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5
Q

Identify the info, input, and output for the following thalamic nuclei:

medial geniculate nucleu

A

info: hearing
input: superior olive and inferior colliculus of tectum
output: temporal lobe (auditry cortex)

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6
Q

Identify the info, input, and output for the following thalamic nuclei:

ventral lateral nucleus

A

info: motor
input: basal ganglia
output: motor cortex

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7
Q

What is the most common casue of thalamic syndrome?

Symptoms?

A

lacunar stroke

contralateral sensory loss (face, arm, legs) - all sensory modalitites

resolution - long-term chronic pain contralateral side but sensory exam is normal (severe pain in paroxysms or exacerbated by touch)

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8
Q

Identify the function & the resulting dysfunction froma lesion in the indicated hypothalamic area:

lateral

A

hunger

lesion: anorexia, failure to thrive in infants

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9
Q

Identify the function & the resulting dysfunction froma lesion in the indicated hypothalamic area:

ventromedial

A

satiety

lesion: hyperphagia, obesity

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10
Q

Identify the function & the resulting dysfunction froma lesion in the indicated hypothalamic area:

anterior

A

cooling

lesion: hyperthermia

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11
Q

Identify the function & the resulting dysfunction froma lesion in the indicated hypothalamic area:

posterior

A

heating

lesion: inability to thermoregulate

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12
Q

Identify the function & the resulting dysfunction froma lesion in the indicated hypothalamic area:

suprachiasmic nucleus

A

circadian rhythm

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13
Q

What are the immune substances that enter the brain and trigger a fever?

How do they do this

A
  • Enter brain
    • IL-1
    • IL-6
    • TNF
  • They then trigger prostaglandin E2 system
    • mediated by: (PLA2, COX2, prostaglandin E2 synthase)
  • this increases the anteior hypothalamus set point
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14
Q

What are the inhibitory homones released by the hypothalamus?

A
  • dopamine inhibits prolactin
  • prolactin inhibits GnRH
  • somatostatin inhibits GH
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15
Q

What part of the hypothalamus produces ADH?

Oxytocin?

A

ADH: supraoptic nucleus

Oxytocin: paraventricular nucleus

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16
Q

What is the location of a craniopharyngioma?

Symptoms?

A

rathke’s pouch

pressure on optic chiasm - bitemporal hemianopsia

pressure on hypothalamus - hypothalamic syndrome

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17
Q

What are the symptoms of hypothalamic syndrome?

A

DI (d/t loss of ADH)

Fatigue (d/t loss of CRH -> low cortisol)

obesity

loss of temperature regulation

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18
Q

What are the main functions & key components of the limbic system?

A

Function: emotion, long-term memory, smell, behavior modulation, autonomic nervous system function

components: cingulate gyrus, hippocampus, fornix, amygdala, mammilary bodies

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19
Q

What is the cause of Kluver-Bucy syndrome?

A

Damage to the amygdala (rare complication of HSV1 encephalitis)

  • Symptoms
    • hyperphagia - weight gain
    • hyperorality - examine with mouth
    • inappropriate sexual behavior - mounting inanimate objects
    • visual agnosia - inability to recognize visually presented stimuli
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20
Q

Common causes & sympotom of hippocampus lesion?

A

infarction: hippocampal branches PCA, anterior choroidal arteries

  • Symptoms
    • anterograde amnesia
    • cannot make new memories
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21
Q

What is the difference between Wernickes & Korsakoff syndromes?

They are both associated with what conditions?

A

Wernickes: acute encephalopathy

Korsakoff: chronic neurological condition (usually consequence of Wernickes)

Associated w/: alcoholism, thamine (vit B1) deficiency, atrophy of mammillary bodies

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22
Q

What is the triad seen in Wernicke’s syndrome?

Treatment?

A

visual disturabances/nystagmus

gait ataxia

confusion

often reversible w/ thiamine

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23
Q

What additional symptoms are seen in Korsakoff syndrome as opposed to Wernickes?

Treatment?

A

amnesia (recent more affected than long-term)

confabulation (make stuff up b/c can’t remember), lack of interest/concern, personality changes,

usually permanant

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24
Q

Which peduncles carry information into the cerebellum & which carrin info out?

Holding what type of information?

A
  • in:
    • middle: contralateral pons
    • inferior: ipsilateral spinal cord information (proprioception)
  • out:
    • superior: from deep cerebellar nuclei
      • to red nucleus & thalamus
25
Q

What are the two types of axons that enter the cerebellum?

How are they different?

A

climbing - from interior olivary nucleus

mossy - from everywhere else

both synapse on purkinje cells & deep nuclei

26
Q

What are the 3 deep nuclei of the cerebelum? Where do they send their information?

A

(lateral to medial)

  • Dentate
    • contralateral VA/VL nuclei of thalamus
  • interposed nucleu: globus/emboliform
    • contralateral redu nucleus
  • fastigial
    • vestibular nuclei & reticular formation
27
Q

What is the difference in symptoms between lateral & medial lesions of the cerebellum?

A
  • lateral:
    • hemispheres
    • dentate
    • extremities
  • medial:
    • floculonodular node
    • emboliform, globus, fastigial nucleus
    • trunk

both affect ipsilateral side (motor crosses twice)

28
Q

Romberg tests for what type of ataxia?

A

sensory ataxia - NOT cerebellar

patients with cerebellar ataxia will have instability even when eyes are open

29
Q

In addition to ataxia, what are the other symptoms commonly seen in cerebellar lesions?

A

hypotonia

scanning speech (irregular, slow)

dyssynergia (loss of coordinated activity) - dysmetria, intention tremor, dysdiadochokinesia

nystagmus (vertical)

nausea/vomiting

vertigo

30
Q

Ataxia telangiectasias has what type of inheritance pattern?

Mutation?

Syptoms?

A

autosomal recessive

defective ATM gene chromosome 11 (DNA hypersensitivity to ionizing radiation - failure to repair ds DNA breaks (NHEJ))

cerebellar atrophy w/in 1 yr - wheelchair by 10 yr

tenangiectasias (ear, nose, face, neck)

repeated sinus infections (immunodeficiency)

high risk cancer

31
Q

What is the name for the process of repairing double stranded DNA breaks?

A

non-homologous end joining

32
Q

What are the lab findings seen in patients with ataxia telangiectasia?

A

increased AFP

dysgammaglobinemia (low/absent IgA)

33
Q

Friedriech’s Ataxia has what type of inheritance pattern?

Mutation?

Symptoms?

A
  • autosomal recessive
  • frataxin gene chromosome 9 (needed for mitochondrial function) - increased GAA repeats
  • begins adolescence - cerebella & spinal cord degeneration
    • spinocerebellar tract
      • ataxia, dysarthria
    • dorsal columns
      • loss of position/vibration sensation
    • corticospinal tract
      • UMN weakness in lower extremities
  • hypertrophic cardiomyopathy
  • diabetes (beta cell dysfunction)
  • kyphoscoliosis
  • foot abnormalities (high arch)
34
Q

Identify the indicated structures

A
35
Q

The striatum is composed of what structures?

What about the lentiform nucleus?

A

striatum = putamen + caudate

lentiform nucleus = putamen + globus pallidus

36
Q

How do the direct and indirect pathways in the basal ganglia repectively impact the primary motor cortex?

A

direct: activates
indirect: inhibits

37
Q

The thalamus is inhibited by stimulating the cortex by what structures?

A

Globus pallidus interna & pars reticulata

38
Q

What is the role of the striatum in the direct pathway?

A

dumps GABA onto pars reticularis & globus pallidus internus

this allows the thalamus to stimulate the cortex

39
Q

What is the role of dopamine in the direct pathway?

A

when the cortex stimulates the striatum, it also stimulates the pars compacta

the pars compacta utilizes dopamine (D1 receptors) to amplify stimulation of the striatum

40
Q

What is the role of the striatum in the indirect pathway?

A

stimulates globus pallidus externus - therefore the subthalamic nucleus is free to stimulate the globus pallidus internus- which then inhibits the thalamus

41
Q

What is the role of dopamine in the indirect pathway?

A

the pars compacta stimulates D2 receptors on the striatum, which shuts it down

42
Q

What disease results from the loss of the dopamine modification pathway in the basal ganglia?

A

parkinsons

43
Q

Huntington’s affects what aspect of the basal ganglia?

A

striatum

44
Q

Hemibalism is due to damage of what part of the basal ganglia?

A

subthalamic nucleus

45
Q

Parkinsons disease is due to damage of what part of the basal ganglia?

A

substantia nigra (pars compacta & reticulata)

46
Q

Wilson’s disease can result in damage to what part of the basal ganglia?

A

globus pallidus

47
Q

What cells produce CSF?

Absorbed by what?

A

ependymal cells of choroid plexus

absorbed by villi

48
Q

Common presentign complaint & key finding in communicating hydrocephalus?

CT?

A

Headache

papilledema

dilation of ALL the ventricles

49
Q

Commnicating hydrocephauls commonly follows what condition?

What is the major concern with communicating hydrocephalus?

A

meningitis

herniation

50
Q

What is aqueductal stenosis? Presentation?

Inheritance pattern of genetic kind? Cause of non-genetic kind?

A

blocked drainage 3rd ventricle to 4th ventricle - presents as enlarging head circumference

genetic: X-linked

non-genetic: inflammation d/t intrauterine infection

51
Q

Chiari malformation II is associated with what other condition?

A

myelomeningocele (failure of spine & meninges to close around spinal cord- outside)

52
Q

What is a Dandy Walker Malformation?

A

developmental anomaly of the 4th ventricle

hypoplasia / agenesis of cerebellar vermis

(massive 4th ventricle, small cerebellum)

53
Q

3 symptoms of Dandy Walker Malformation?

A

hydrocephalus

developmental delay

motor dysfunction

54
Q

Classic finding of patients with pseudotumor cerebri (idiopathic intracranial hypertension)?

Treatment?

A

pulsatile tinnitus

rushing water/wind sound - transmission of vascular pulsations

acetazolamide

55
Q

Physical findings seen in patients with normal pressure hydrocephalus?

Classic triad?

Treatment?

A

enlarged ventricles on imaging that compress the corona radiata

normal opening pressure LP

triad: urinary incontinence, gait disturbance, dementia (wet, wobbly, wacky)

ventriculoperitoneal shunt

56
Q

Cause of Hydrocephalus ex Vacuo?

A

ventricular enlargement that occurs d/t age and the decreased mass of the cortex (esp. in alzheimers, pick disease, HIV)

the sulci increase in proportion to the increase in ventricles

57
Q

Which sinus receives CSF?

Where do all of the sinuses drain to?

A

saggital sinus

internal jugular

58
Q

Symptoms of cavernous sinus syndrome?

A

headache

swollen eyes

impairment of ocular motor nerves

Horner’s syndrome

sensory loss 1st & 2nd division trigeminal nerve

59
Q

AV malformations commonly lead to enlargement of what vein?

A

Vein of Galen

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