Cranial Nerves Flashcards
Why do you not use ammonia to test for olfaction?
it can be recognized by nasal epithelium and does not require an intact olfactory pathway.
cranial nerve nuclei are found mainly where?
at the level of the brainstem
sensory nuclei develop within the dorsal/alar plate (of neuro tube), motor nuclei develop within the basal plate
in the hindbrain, the alar plate lies lateral to the basal plate in the floor of the 4th ventricle
Is CN I a peripheral nerve?
not really. its a central nervous system tract terminating in the olfactory bulb
How do you perceive a particular smell?
true olfactory nerves (second order ganglion nerve cells) terminate in the mucous membrane that lines the nasal cavity. to perceive a smell, molecules must dissolve into the mucous overlying the cribriform plate and supply chemical stimulation to the nerve endings at that location.
anosmia
complete loss of smell
usually not indicative of a cortical lesion, but mainly associated with viral infections, allergic rhinitis, aging, or head trauma, rhinorrhea (CSF drainage), and backwash meningitis
sense of smell may return eventually
lesion of what gyrus can cause hallucinations of smell?
lesion of the uncinate gyrus of the anterior temporal lobe
hallucinations of smell can be associated with deja vu
termed uncinate fits or seizures
hyposmia
decreased sense of smell
hyperosmia
increased sense of smell
parosmia
perversion of smell
cacosmia
abnormally disagreeable smell
anosmia in both nostrils
common causes: blocked nasal passage, common cold (MC), trauma, and a relative loss with normal aging.
Is CN I a true nerve?
No, its a fiber tract of the brain.
Is CN II a true nerve?
no, it is a fiber tract of the brain
Meyers loop?
fan-like radiating portion of optic nerve that curves around the inferior horn of the lateral ventricle
geniculocalcarine tract?
contains 4th order neurons of optic tract from the LGN and passes to the occipital (calcarine) cortex
Central connections of optic nerve
- from pretectal region –> Edinger westphal nucleus via posterior commisure
- from superior colliculi –> other cranial and spinal nuclei via tectobulbar and tectospinal tracts
- from occipital cortex–> other cortical and subcortical areas
Pretectal area of CN II
simple and consensual light reflexes
connections from superior colliculi from CN II
involuntary musculoskeletal refexes
reflex movements of the eye and head after optic stimulation
genniculocalcarine tract (from LGN) from CN II
visual perception
through the tectobulbar and tectospinal tracts of CN II
through cranial and spinal nuclei–> involuntary reflexes (ex. accomodation)
through pontine nuclei–> corticopontine tract–> postural reflexes
macula
retinal area of central vision
fovea centralis
small central pit composed of closely packed cones, where vision is sharpest and color discrimination most acute.
rods and cones of retina react specifically to what?
physical light
Cones are responsible for what?
sharp vision and color discrimination
rods are responsible for what?
low intensity light vision and night vision
retrobulbar neuritis
lesion of optic nerve or tract
MC cause is multiple sclerosis
optic or bulbar neuritis
lesion which includes various forms of retinitis
papilledema (AKA “choked disc”)
commonly seen symptom of increased intracranial pressure due to brain tumors, abscesses, hemorrhage, hypertension, and other causes
optic atrophy
decreased visual acuity and change in color of optic dis to light pink, white, or gray
primary optic atropy
caused by processes that involve the optic nerve and do not produce papilledema
secondary optic atrophy
a sequal of papilledema
primary (simple) optic atrophy
may be due to tabes dorsalis, multiple sclerosis, or hereditary
secondary optic atrophy
may be due to neuritis, glaucoma, or increased intracranial pressure
Foster Kennedy Syndrome
may be caused by tumors at the base of the frontal lobe and is characterized by ipsilateral blindness and anosmia (with atrophy of optic and olfactory nerve) and contralateral papilledema
amaurotic familial idiocy (AKA Tay-Sachs disease)
cerebromacular degeneration with severe mental deficiency occurring in Jewish families and is associated with blindness, optic atrophy, and dark cherry red spot in place of the macula lutea
Argyll Robertson pupil
reacts only to accommodation
neither a direct or indirect reaction to light
occurs mostly as a diabetic complication
Holmes-Adie Syndrome
tonic pupillary reaction and the absence of one or more tendon reflexes. pupil is said to be “myotonic”, with a very slow, almost imperceptible contraction to light and in near vision, a slower dilation upon removal of the stimuli.
People with this syndrome have an abnormal sensitivity to weak solution (~25% methacholine): instilled into the conjunctival sac is demonstrable in affected eyes; tonic pupils constrict, whereas pupils of normal eyes remain unaffected (ADLER-SCHEIE TEST)
heterotropia
deviation of bilateral eye alignment
Exotropia
deviation of eyes outward/lateral
Esotropia
deviation of eyes inward/medial
hypertropia
deviation of eyes upward
hypotropia
deviation of eyes downward
yoked movement
the medial longitudinal fasciculus (MLF) primary function is to coordinate eye movements by interconnecting the nuclei of CN III, IV, and VI
