Neuroanatomy Flashcards
What are the 6 layers of the cortex (superficial to deep)?
Molecular (plexiform) layer
External granular layer
External pyramidal layer
Internal granular layer
Internal pyramidal layer
Multiform (fusiform) layer
(MP EG EP IG IP MF)
What are the 3 FUNCTIONAL layers of the cortex?
- Supragranular layers (I-III)
- Internal granular layer (IV)
- Infragranular layers (V & VI)
Where do intracortical connections primarily originate and terminate (layer)?
Functional: supragranular layers (I-III which are molecular/plexiform, external granular, and external pyramidal)
What are the 2 main types of intracortical connections?
Associational (intrahemispheric)
&
Commissural (to contralateral hemisphere, usu thru corpus callosum)
What does the internal granular layer do, i.e. where do its connections come from?
Receives thalamocortical connections, esp from thalamic nuclei
Most prominent in primary sensory cortices
What do the infragranular layers mostly do?
Connect cortex & subcortical regions
Where are the infragranular layers most developed?
Motor cortex
Which part of the brain has extremely small or non-existent granular layers and is aka the “agranular” cortex?
Motor cortex
What layer gives rise to all of the principal cortical efferent projections to basal ganglia, brainstem, and spinal cord?
Layer V (internal pyramidal)
Where does layer VI go?
Mostly to the thalamus
aka the multiform or fusiform layer
What’s Nelson’s syndrome?
In the setting of Cushing’s disease (ACTH) s/p bilateral adrenalectomy, but the adenoma keeps growing and secreting ACTH
Does Nelson’s syndrome have Crooke’s cells?
Crooke’s cells are found in pituitaries of Cushing’s disease, but not in the pituitary surrounding the adenomas of Nelson’s syndrome (so no)
What structures make up the diencephalon?
- Thalamus
- Hypothalamus including the Neurohypophysis
- Subthalamus
- Epithalamus
What structures make up the epithalamus?
Ant & post paraventricular nuclei
Medial & lat Habenular nuclei
Stria medullaris thalami
Posterior commissure
Pineal Body
What are 3 changes you see in mammillary bodies in Wernicke’s?
- Soft granular parenchyma (& atrophy?)
- Abnormal capillaries with microhemorrhage (slides & grossly)
- Reactive astrocytes
What are the 3 hereditary motor & sensory neuropathies?
- Charcot-Marie-Tooth
- HMSN II
- Dejerine-Sottas neuropathy
What’s the disease with onion bulbs on EM and what are they?
Charcot-Marie-Tooth
Schwann cell hyperplasia i.t.s.o repetitive de- & remyelinations
What’s the protein you should telegraph for Charcot-Marie-Tooth?
PMP22
peripheral myelin protein 22
What’s the first test you do to eval for Charcot-Marie-Tooth? and why
Single-gene testing for PMP22 duplication/deletion
PMP22 duplication (a 1.5-Mb duplication at 17p11.2 that includes PMP22) accounts for as much as 50% of all CMT
what is the most common neoplasm family that happens in the pineal region?
germ cell tumors!
(germinoma > teratoma > choriocarcinoma»_space; yolk sac & embryonal)
describe the path of the gag reflex (lol WHAT)
Touch receptors in pharyngeal mucosa (CNIX)
Solitary nucleus
Nucleus ambiguus
CNX
Muscles of palate
Brown Sequard 3 main issues with ipsi or contralateral (NOT levels, NOT tracts)
- Ipsilateral flaccid paralysis/loss of cutaneous sensation
- Ipsilateral spastic paralysis & loss of vibration sense, proprioception, & fine touch
- Contralateral loss of pain & temp
Brown Sequard issue & why it happens bc of the tracts affected (NOT levels)
- Ipsilateral flaccid paralysis d/t LMN loss (anterior corticospinal tract)
- Ipsilateral spastic paralysis d/t loss of moderation by UMN of lateral corticospinal tract; loss of vibration sense, proprioception, & fine touch d/t posterior/dorsal columns (fasciculus Gracilis (leGs) &/or fasciculus cuneatus (arms))
- Contralateral loss of pain & temp d/t spinothalamic tract
Brown Sequard ipsi/contra consequences WITH LEVELS
- Ipsi flaccid + band of sensory loss AT level of lesion
- Ipsi spastic + contra loss of vibration/proprio/fine touch BELOW level of lesion
- Contra loss of pain & temp 1-2 levels below lesion
What are the ELEVEN (ugh) structures served by the anterior choroidal artery?
- Choroid plexus (LV & 3rd vent)
- Optic chiasm & tract
- Internal capsule
- LGN
- Globus pallidus
- Tail of the caudate
- Hippo
- Amygdala
- Substantia nigra
- Red nucleus
- Crus cerebri
Which structure served by the anterior choroidal artery also has partially redundant blood supply, and where does it come from?
Posterior limb of internal capsule
Lenticulostriate arteries from MCA
What vessels can cause lateral medullary syndrome?
PICA (specifically lateral medullary segment)
Vertebral artery
What’s the eponym for lateral medullary syndrome?
Wallenberg
What are the 7 structures affected in lateral medullary syndrome?
- Vestibular nuclei
- Inferior cerebellar peduncle
- Central tegmental tract
- Lateral spinothalamic tract
- Spinal trigeminal nucleus & tract
- Nucleus ambiguus (incl vagus & glossopharyngeal nerves)
- Descending sympathetic fibers
LMS: what happens when the vestibular nuclei are infarcted?
Vomiting
Vertigo
Nystagmus
LMS: what happens when the inferior cerebellar peduncle is infarcted?
Ipsilateral ataxia, dysmetria (past pointing), dysdiadochokinesia
LMS: what happens when the central tegmental tract is infarcted?
Palatal myoclonus
LMS: what happens when the lateral spinothalamic tract is infarcted?
Contralateral loss of pain & temp from BODY (limbs & torso)
LMS: what happens when the spinal trigeminal nucleus & tract are infarcted?
ipsilateral loss of pain & temp from FACE
LMS: what happens when the nucleus ambiguus is infarcted?
Ipsilateral laryngeal, pharyngeal, & palatal hemiparalysis (dysphagia, hoarseness, diminished gag d/t efferent limb of CNX)
LMS: what happens when the descending sympathetic fibers are infarcted?
Ipsilateral Horner’s syndrome (ptosis, miosis, & anhidrosis)
What is Grinker’s myelinopathy?
Anoxic leukoencephalopathy or delayed post-hypoxic leukoencephalopathy
(white matter & BG)
Key finding in FCD Ia
Abnormal radial cortical lamination (a-b; r-t)
Key finding in FCD Ib
Abnormal tangential cortical lamination (a-b; r-t)
Key finding in FCD Ic
Abnormal radial AND tangential cortical lamination (i.e. Ia + Ib)
Key finding in FCD IIa
Dysmorphic neurons
Key finding in FCD IIb
Dysmorphic neurons AND balloon cells (b for balloon, IIb is for the 2 Ls in ballon)
Key finding in FCD IIIa
Temporal lobe, a/w hippo sclerosis
Key finding in FCD IIIb
Adjacent to glial or glioneuronal tumor
Key finding in FCD IIIc
Adjacent to vascular malformation
Key finding in FCD IIId
Adjacent to any other lesion acquired during early life (trauma, ischemic injury, encephalitis, etc)
What’s the Guillain-Mollaret triangle?
CONTRALATERAL dentate
Ipsilateral red
Ipsilateral inf olivary
What’s hypertrophic olivary degeneration (why do you get it and why is it weird)
Primary lesion in dentato-rubro-olivary pathway > Transneuronal degen of inf olivary nucleus > HYPERTROPHY of inf olivary nucleus (not atrophy!)
Where do parallel fibers come from?
Granule cells in cerebellar cortex
What do parallel fibers form?
Excitatory synapses onto dendrites of Purkinje cells & dendrites of inhib interneurons basket cells & stellate cells (molec layer)
Grumose degeneration
Degeneration of dentate nucleus of cerebellum: accumulation of granular eo material which is actually swollen/degen Purkinje axons (it looks like axonal spheroids on neurofilament or synapto IHC, just in the cerebellum