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Flashcards in Neuro4 Deck (39):

What is the classic triad of symptoms associated with Horner syndrome?

(1) ptosis (drooping of the eyelid; superior tarsal muscle)
(2) miosis (pupil constriction)
(3) anhydrosis (absence of sweating) and flushing of affected side of the face


How many neurons are involved in the pathway from the hypothalamus to the eye that is involved in horner syndrom? what is the pathway?


1st - hypothalamus to intermediolateral column of spinal cord (lateral horns)
2nd - lateral horns to superior cervical ganglion
3rd - ganglion to :
(a) pupil
(b) smooth muscles of eyelid
(c) sweat glands of forehead and face

**the 2nd neuron is the preganglionic sympathetic neuron; the 3rd neuron is the postganglionic neuron


Above what level would we expect a lesion to cause Horner syndrome?

Horner syndrome is associated with a lesion of the spinal cord above T1


What information does the ophthalmic division of the trigeminal nerve carry? (V1)

(5 places)

V1 carries sensory information from:

--the scalp and forehead
--upper eyelid
--conjunctiva and cornea (corneal reflex)
--the nose and nasal mucosa
--the frontal sinuses


What fibers does the oculomotor nerve carry with it?

--motor efferents that innervate most of the extraocular eye muscles
--parasympathetic preganglionic fibers that synapse on the postganglionic nerves in the ciliary ganglion. (These will synapse on the pupillary sphincter muscle


What is the organization of fibers in the oculomotor nerve?

The motor efferents are located centrally, and the parasympathetic preganglionic fibers are located peripherally

(Motor-Medial, Parasympathetic-Peripheral)


How would a lesion of the oculomotor nerve present?

--loss of direct and consensual pupillary light reflex
--loss of accommodation and convergence
--loss of extraocular eye movement, adduction in particular --> diplopia on horizantal gaze


Hemifacial anesthesia would result from lesion to what?



Hemifacial anhydrosis would result from lesion to what?

--Descending hypothalamic fibers, above T1
--The sympathetic chain (e.g., superior cervical ganglion)


Hemifacial weakness would result from lesion to what?

Facial nerve


Can INO (internuclear opthalmoplegia) be a symptom of an oculomotor nerve palsy?

No. INO is a specific diagnosis; it is caused by lesion of the medial longitudinal fasciculus (MLF), which formed by neuronal axons that extend from the abducens nucleus, decussate, and synapse on the oculomotor nucleus on the opposite side.

INO results in patients who cannot adduct an eye on horizantal gaze --> horizantal diplopia. This is a shared symptom with a CNIII palsy. However, in INO, patients would not have ptosis or pupil abnormalities (mydriasis)


Where is the substantia nigra located?

In the midbrain, between the crus cerebri and the red nucleus


What are the common symptoms associated with Parkinson disease?


Tremor (e.g., pill-rolling tremor)
Rigidity ("cogwheel" rigidity)
Akinesia (or bradykinesia)
Postural instability
Shuffling gait

**TRA are the "classic" triad


What is the histopathologic hallmark of Parkinson disease?

--Lewy bodies: round, eosinophilic, intracytoplasmic inclusions seen in dopaminergic nigrostriatal neurons

--loss of dopaminergic neurons (i.e., depigmentation) of the substantia nigra pars compacta


What are Lewy bodies composed of?



What two diseases are associated with Lewy bodies?

(1) Parkinson disease
(2) Lewy body dementia


How can Lewy body dementia and Parkinson disease be differentiated clinically? (3)

(1) Dementia is a common feature *late* in the disease in Parkinson's, whereas early-onset dementia is suggestive of Lewy body disease.

(2) Lewy body disease is also characterized by hallucinations (not present in Parkinsons)

(3)cortical Lewy bodies present in Lewy body disease (only found in substantia nigra in Parkinson's)


What histologic feature is associated with Creutzfeldt-Jakob disease (CJD)?

spongiform changes


Adult Polycystic Kidney Disease

Autocomal dominant genetic disorder characterized by bilaterally enlarged kidneys with multiple cyts.

Associated with Berry aneurysms in the circle of Willis, which can bleed and produce a subarachnoid hemorrhage


Location of lesion in Wernicke aphasia

superior temporal gyrus


Location of lesion in Broca aphasia

Inferior frontal gyrus


Location of lesion in Conduction aphasia

Arcuate fasciculus


Type of aphasia?

Fluent: Yes
Comprehends: No
Repeats: No



Type of aphasia?

Fluent: NO
Comprehends: Yes
Repeats: No



Type of aphasia?

Fluent: Yes
Comprehends: Yes
Repeats: No



Why can symptoms in a patient with a subdural hematoma present later (even several days to weeks) than a person with an epidural hematoma?

The bleeding in a subdural hematoma originates from bridging veins, which are under venous pressure, giving more time for blood to accumulate before symptoms arise.

Unlike the subdural hematoma, the epidural hematoma is under high arterial pressure (middle meningeal artery), and has limited outflow space (confined to area within suture lines). This results in rapid compression of the brain and production of symptoms.


Classic presentation of an epidural hematoma? (5 steps)

(1) trauma
(2) immediate loss of consciousness (from initial impact)
(3) recovery/transient lucid period
(4) declining consciousness
(5) even coma from brain stem compression (if untreated)


Diffuse (cortical) atrophy with prominent sulci might be indicative of?

Alzheimer Disease

Other anatomical findings in this disease include prominent atrophy in the hippocampal region


Evidence of intraventricular blood might be indicative of?

Subarachnoid hemorrhage


What is the classic presentation/patient hx of a subdural hemorrhage?

(1) trauma
(2) clinical presentation days later (late onsent)
(3) older patient
(4) obtunded patient (diminished consciousness)


72 year old patient found lying in her bed unresponsive. She was in good condition 2 hours prior. She has a history of Alzheimer disease, no evidence of fall or trauma. CT shows a large intraparenchymal hemorrahge centered in the left parietal lobe. What might we suspect?

Amyloid angiopathy


What is amyloid angiopathy?

Amyloid deposition in the walls of cerebral blood vessels in Alzheimers patients. Amyloid makes the vessels weak and prone to rupture; can make Alzheimers patients prone large lobar hemorrhages usually centered in the parietal lobe


72 year old patient found lying in her bed unresponsive. She was in good condition 2 hours prior. She has a history of Alzheimer disease, no evidence of fall or trauma. CT shows a large intraparenchymal hemorrahge centered in the left parietal lobe.

Why wouldn't this be due to a subdural hematoma (and what about the case would put subdural hematoma on the differential)?

Alzheimers patients are more susceptible to subdural hematomas due to brain atrophy, which stretches the bridging veins, making them more prone to rupture.

However, subdural hematomas are typically associated with trauma, and do not cause intraparenchymal hemorrhage. Subdural hematomas also have symptoms that are slow-onset. In this case, her symptoms developed rapidly.


72 year old patient found lying in her bed unresponsive. She was in good condition 2 hours prior. She has a history of Alzheimer disease, no evidence of fall or trauma. CT shows a large intraparenchymal hemorrahge centered in the left parietal lobe.

What would put Charcot-Bouchard aneurysm on the list, and why would it not be suspected in this case?

Charcot-Bouchard aneurysms can lead to sudden onset intraparenchymal hemorrhage.

However, Charcot-Bouchard aneurysms are not associated with lobar hemorrhages, and are typically seen in patients with severe hypertension.


What is the most common cause of intraparenchymal hemorrhage?

(systemic) Hypertension


What three conditions besides hypertension may be associated with intraparenchymal hemorrhage?

(1) amyloid angiopathy
(2) vasculitis
(3) neoplasm


45 yo man with a hx of uncontrolled hypercholesterolemai and hypertension presents to the ED after collapsing at home, and passes. Autopsy reveals massive intracerebral hemorrage filling the ventricles. What the most likely location of the hemorrhage?

Basal ganglia and internal capsule


What is the most common site of (massive) intraparenchymal bleed (due to hypertenstion)?

The basal ganglia and internal capsule


What would be the classic basic pathology of intraparenchymal hemorrhage in the basal ganglia and internal capsule due to hypertension?

Rupture of Charcot-Bouchard aneurysm of lenticulostriate vessels.

--> lenticulostriate vessels are branches of the middle meningeal artery