Thalamus, Hypothalamus, Limbic B&B Flashcards
what white matter tract is found directly next to the thalamus, and what is the clinical importance of this?
internal capsule - many thalamic lesions will damage these fibers, resulting in motor dysfunction/ hemiparesis
relay station for all sensations except smell
thalamus - sensory relay, consciousness, sleep, alertness
what are the 5 most important thalamic nuclei and their functions?
- ventral posterolateral (VPL): sensory relay
- ventral posteromedial (VPM): sensory face and taste relay
- lateral geniculate nucleus (LGN): vision relay (Lateral for Light)
- medial geniculate nucleus (MGN): hearing relay (Medial for Music)
- ventral lateral (VL): motor relay
what is the input and output of the ventral posterolateral (VPL) thalamic nuclei?
input: all sensory from spinothalamic tract, posterior column medial lemnisucs
output: somatosensory cortex
which thalamic nuclei takes input from the spinothalamic tract and medial lemniscus, and sends output to the somatosensory cortex?
ventral posterolateral (VPL) nuclei
what is the input and output of the ventral posteromedial (VPM) thalamic nuclei?
input: trigeminal (sensory face) and gustatory (taste) fibers
output: somatosensory cortex
which thalamic nuclei takes input from the trigeminal (sensory face) and gustatory (taste) fibers, and sends output to the somatosensory cortex?
ventral posteromedial (VPM) nuclei
what is the input and output of the lateral geniculate nucleus (LGN) of the thalamus?
input: CN II (optic)
output: calcarine sulcus
which thalamic nuclei takes input from CN II, and where does it send it?
lateral geniculate nucleus: input from CN II, output to calcarine sulcus
what is the input and output of the medial geniculate nucleus (MGN) of the thalamus?
input: hearing from superior olive and inferior colliculus of tectum
output: auditory cortex of temporal lobe
which thalamic nuclei takes input from the superior olive and inferior colliculus of tectum, and where does it send it?
medial geniculate nucleus (MGN): hearing input from superior olive and inferior colliculus of tectum, output to auditory cortex of temporal lobe
what is the input and output of the ventral lateral (VL) thalamic nuclei?
input: motor from basal ganglia
output: motor cortex
which thalamic nuclei relays to the motor cortex, and where does it get its input?
ventral lateral (VL) nuclei: takes motor input from basal ganglia, sends output to motor cortex
what type of stroke most often causes thalamic syndrome, and how does it present?
lacunar stroke —> complete sensory loss on contralateral side (face, arms, legs - all sensory modalities) because all sensation relays through thalamus (so this is the only place where this could happen)
Resolution can lead to long-term chronic pain on contralateral side (sensory exam will appear normal)
if a patient presents with complete sensory loss on one side of their body (face, arms, legs - all sensory modalities), where must the injury have occurred and why?
thalamic syndrome, most often due to lacunar stroke
all sensations (except smell) relay through thalamus - therefore, this is only location that could cause complete loss on contralateral side
what are the 4 major functions of the hypothalamus?
- autonomic control (SNS/PNS)
- temperature regulation
- water balance
- pituitary control
what are the 5 major hypothalamic areas and their functions?
- lateral - hunger
- ventromedial - satiety
- anterior - cooling [AC]
- posterior - heating
- suprachiasmatic nucleus - circadian rhythm
what would occur from a lesion of the lateral vs ventromedial hypothalamus?
lateral: drives hunger, lesion —> anorexia, failure to thrive in infants [Less hungry]
ventromedial: drives satiety, lesion —> hyperphagia, obesity [Very hungry]
what would occur from a lesion of the anterior vs posterior hypothalamus?
anterior = cooling (AC), lesion —> hyperthermia
posterior = heating, lesion —> inability to thermoregulate
which area of the hypothalamus controls circadian rhythm?
suprachiasmatic nucleus
what is the role of the hypothalamus in fever? describe
- IL-1, IL-6, TNF (pyrogenic) enter brain
- stimulate prostaglandin E2 synthesis via arachidonic acid pathway (mediated by PLA2, COX-2, prostaglandin E2 synthase)
- increases set point of anterior hypothalamus (“AC”)
if temperature reaches too high (hyperpyrexia), may cause permanent brain damage (must cool down patient)!!
what kind of drugs can be used to treat patients with hyperpyrexia due to damage to the anterior hypothalamus?
IL-1/IL-6/TNF enter brain —> stimulate prostaglandin E2 synthesis —> increase set point of anterior hypothalamus (cooling system, “AC”)
rx: NSAIDs, Tylenol (block PGE2 synthesis)
what 8 hormones does the hypothalamus secrete?
- TRH —> TSH
- CRH —> ACTH
- GHRH —> GH
- GNRH —> FSH, LH
- dopamine —> decrease prolactin
- somatostatin —> decrease GH
- ADH - released by posterior pituitary
- oxytocin - released by posterior pituitary
which nuclei of the hypothalamus secrete ADH and oxytocin, respectively?
supraoptic nuclei —> ADH
paraventricular nuclei —> oxytocin
synthesized by hypothalamus, released by neurohypophysis (posterior pituitary)
which part of the hypothalamus does leptin act on?
leptin: secreted by adipocytes, signals satiety
leptin INHIBITS the lateral hypothalamus (hunger center), and STIMULATES the ventromedial hypothalamus (satiety center)
from what do craniopharyngioma originate?
craniopharyngioma: rare tumor from Rathke’s pouch
puts pressure on optic chiasm (bitemporal hemianopia) and hypothalamus (hypothalamic syndrome)
how does hypothalamic syndrome present? (4)
- diabetes insipidus via loss of ADH
- fatigue via loss of CRH (low cortisol)
- obesity via damage to ventromedial nuclei (satiety center)
- loss of temperature regulation via damage to anterior (AC) and posterior (heat) nuclei
what are the 5 major functions of the limbic system?
- emotion
- long-term memory
- smell
- behavior modulation
- autonomic nervous system
what are the 5 structures of the limbic system?
- cingulate gyrus
- hippocampus
- fornix
- amygdala
- mammillary bodies
Kluver-Bucy Syndrome
damage to bilateral amygdala —> hyperphagia, hyperorality, inappropriate sexual behavior, visual agnosia
rare complication of HSV1 encephalitis
Kluver-Bucy Syndrome is a rare complication of…
damage to bilateral amygdala —> hyperphagia, hyperorality, inappropriate sexual behavior, visual agnosia
rare complication of HSV1 encephalitis
Pt with PMH of HSV1 encephalitis presents with weight gain and inability to recognize visually presented objects. They were recently let go from their job for inappropriate sexual behavior. What is going on, and where is the damage?
Kluver-Bucy Syndrome: damage to bilateral amygdala —> hyperphagia, hyperorality, inappropriate sexual behavior, visual agnosia
rare complication of HSV1 encephalitis
what type of memory loss occurs with damage to the hippocampus? how does this typically occur?
anterograde amnesia - cannot make new memories
very sensitive to hypoxic damage! (infarction to hippocampal branches of PCA or anterior choroidal arteries)
The hippocampus is very sensitive to hypoxic damage, which can result in anterograde amnesia. Where would the infarction occur to cause this? (2)
infarction to hippocampal branches of posterior cerebral artery (PCA) or anterior choroidal arteries
what is Wernicke vs Korsakoff syndrome?
Wernicke syndrome = acute encephalopathy, reversible
Korsakoff syndrome = chronic neurologic condition, permanent
both associated with thiamine (B1) deficiency and alcoholism —> damage to thalamic nuclei
atrophy of mammillary bodies is common finding (~80% for both)
about 80% of patients with Wernicke-Korsakoff Syndrome have atrophy of…
mammillary bodies
Wernicke syndrome = acute encephalopathy
Korsakoff syndrome = chronic neurologic condition
both associated with thiamine (B1) deficiency and alcoholism —> damage to thalamic nuclei
how does Wernicke’s syndrome vs Korsakoff syndrome present?
Wernicke triad: visual disturbances/ nystagmus, gait ataxia, confusion - symptoms reversible with thiamine (B1)!
Korsakoff: amnesia (recent > remote memories), confabulation (bc they can’t remember), lack of interest/concern, personality changes - permanent
You’re rotating in the ED. On your first day of rotation, you see a patient who presents with nystagmus, gait ataxia, and confusion. The patient is treated and sent home the following day. On your last day of rotation, the same patient comes in presenting with amnesia and confabulation, and you note personality changes.
What is going on with is patient?
patient is alcoholic with thiamine (B1) deficiency
first visit: Wernicke triad: visual disturbances/ nystagmus, gait ataxia, confusion - symptoms reversible with thiamine (B1)!
last visit: Korsakoff: amnesia (recent > remote memories), confabulation (bc they can’t remember), lack of interest/concern, personality changes - permanent, patients who have had Wernicke Syndrome several times before
imaging will likely (80%) show atrophy of mammillary bodies
Pt comes into the ED with gait ataxia, nystagmus, and confusion, and you suspect Wernicke Syndrome. How can you test for Wernicke Syndrome, and how will you treat them?
Wernicke can be precipitated by giving glucose without thiamine, because thiamine is a co-factor for glucose metabolism —> glucose will worsen a thiamine deficiency
alcoholics presenting to ED are given ”banana bag”: IV infusion of thiamine, folic acid, and magnesium sulfate
what’s contained in a “banana bag”?
IV infusion of thiamine, folic acid, and magnesium sulfate
given to alcoholics presenting to the ED who may have Wernicke-Korsakoff Syndrome (associated with thiamine/B1 deficiency)
A patient presents to the ED with confusion, gait ataxia, and visual disturbances. You’re preceptor suggests giving them glucose to aid in your diagnosis. Why?
Wernicke Syndrome can be precipitated by giving glucose without thiamine, because thiamine is a co-factor for glucose metabolism —> glucose will worsen a thiamine deficiency
what are the functions of the limbic system? (4)
Homeostasis (hypothalamus)
Olfaction (olfactory cortex)
Memory (hippocampus)
Emotions (amygdala)
HOME!
what are the components of the Circuit of Papez for memory? (7 stops along the way)
- hippocampal formation (subiculum)
- fornix (main output of hippocampus)
- mammillary bodies
- mammillothalamic tract
- anterior thalamic nucleus
- cingulate gyrus
- entorhinal cortex
- back to hippocampal formation
where are the amygdala and hippocampus anatomically located, respectively?
amygdala - anterior to hippocampus
hippocampus - base of inferior horn of lateral ventricles
which 2 thalamic nuclei are associated with the limbic system, and what are their respective roles?
- dorsomedial nucleus - part of emotion pathway
- anterior nucleus - part of memory pathway
what are the components of the reward pathway of the limbic system?
aka mesolimbic dopamine pathway: ventral tegmental area (in midbrain) —> nucleus accumbens (ventral striatum)
what sorts of disorders are associated with lesions to the following locations:
a. cingulate gyrus
b. nucleus accumbens
c. dorsolateral prefrontal cortex
a. cingulate gyrus - mood disorders
b. nucleus accumbens - addiction
c. dorsolateral prefrontal cortex - impaired working memory
for what types of memories is the hippocampus NOT needed? (3)
- very old memories
- motor memories
- non-declarative implicit memories
only widespread damage to cortex has effect on storage of memories
however, hippocampal formation is required to create new memories (anterograde) or access recent memories (retrograde)
contrast the functions of the following nuclear groups of the amygdala:
a. medial nuclei
b. basolateral nuclei
c. central nuclei
Medial nuclei: Connect to olfactory bulb and cortex.
Basolateral nuclei: Well-developed in humans. Receives direct sensory input from the thalamus and sensory cortices. Connects to orbital and prefrontal cortex.
Central nuclei: are the output nuclei - They project to the hypothalamus and brainstem
in which 2 areas of the cortex does emotional regulation occur?
- ventromedial prefrontal cortex
- orbitofrontal cortex
