Cranial Nerves, Brain Stem Reflexes and Brain Stem Disorders Flashcards
CN I: Olfactory Nerve
Impaired smell most commonly occurs from:
mucosal swelling and inflammation during sinusitis or an URI
Permanent loss of smell may occur after severe head trauma, tumor near the olfactory lobe at the skull base (ie- meningioma)
Draw eye muscle function testing, state how you will test each muscle.
Deficit from a complete oculomotor nerve (CN III) lesion:
What occurs to the eyelid? why….
If the eyelid is manually pulled up, what is observed of the eyeball… why?
What is the only direction the pt is able to move the eye…why?
What is observed of the pupil?…what about with the pupillary light reflex? why?
Deficit from a complete oculomotor nerve (CN III) lesion:
- IPSILATERAL* EYELID: PTOSIS, due to paralysis of l_evator palpebrae superiosis muscle_
- IPSILATERAL* EYEBALL: abducted/OUTWARD deviation of eye due to unopposed lateral rectus (CN6)
- thus patient is only able to abduct the eye due to abducens nerve spared*
- IPSILATERAL PUPIL:* LARGE and UNREACTIVE to light, directly or consensually, since parasympathetic innervation of the pupil is impaired
Deficit to TROCHLEAR (CN IV) nerve:
What is the course of the CN?
What would a lesion of CN IV produce clinically?
How would the eye be impaird?
CN IV is the only nerve which exits the brain stem DORSALLY, and decussates to innervate the contralateral SUPERIOR OBLIQUE muscle
A lesion to CN IV produces SUBTLE DEFICITS that is difficult to assess clinically
*impairment downward gaze (depression of the eyeball) is best noted when the invoved eye is the adducted position*
contralateral eye involved
Lesion to CN VI abducens nerve:
What is the clinical presentation?
Affects the IPSILATERAL LR muscle –> impaired ABDUCTION of the affected eye
In binocular diplopia, an image appears ______, when the patient is either in primary position or when eyes are conjugately moving to other positions.
This is the more common type of diplopia and resolved if _______
Causes: Lesions to CNs_____ or their related extraocular muscles (NMJ disorders)
In binocular diplopia, an image appears BLURRED/DOUBLED, when the patient is either in primary position or when eyes are conjugately moving to other positions.
This is the more common type of diplopia and resolved if THE PATIENT COVERS EITHER EYE
*In severe or complete lesions to CN III, diplopia would be eliminated by the ptosis covering the eyelid*
Causes: Lesions to CNs III, IV, VI or their related extraocular muscles (NMJ disorders), brain stem lesions affecting coordinated moviement of extraocular muslces, vestibular or cerebellar systems that also can allow for smooth, reflexive eye movements
Monocular diplopia occurs when____ …
Cuases includes:
Monocular diplopia occurs when looking through ONE EYE ALONE
Rare, but can occur with with problems to the “optical system” of the eye, such as dislocated lens or detached retina or can be psychiatric disorder but NOT from neurological disease, strictly speaking.
What are the possible etiologies of nystagmus and how could you differentiate between the two major categories?
What would be one way to clinically assess what eye is the lesion occuring in?
Lesions to the vestibular system, brain stem or cerebellum–> upset the normal control or balance of conjugate eye movements –> typically produce asymmetrical nystagmus
(usually produces horizontal nystagmus, jerk TOWARDS the side of the lesion, with fast movement in the other direction)
Drug toxicity –> symmetrical nystagums, present virtually with all eye movments
What is the pathway used to have coordinated horizontal gaze: (example, to the right)
What muscles, what nuclei (and their locations) are used?
A lesion to MLF would cause what type of clinical sx?
How can you determine if this is a problem with the tract or if it is an issue with the muscle / nerve?
The RIGHT paramedian pontine reticular formation (PPRF) must activate BOTH the RIGHT abducens nucleus (CN 6) in the pons AND the LEFT oculomotor nucleus (CN3) in the midbrain = the right lateral rectus* and *left medial rectus muscles move the eyes to the right
The ASCENDING MLF leaves the RIGHT PPRF, decussates early and rised to join the LEFT oculomotor nucleus
*The left medial rectus still functions (in the above scenario), and could be tested via convergence*
What is the normal pupillary light reflex?..what is the pathway involved with this relfex?
What is the pupil’s response with optic nerve lesion?
What is the pupil’s response with a CN IIII lesion?
Light shinning into one eye causes pupil to constrict (direct) and also other eye’s pupil to constrict (consensual)
This reflex pathway involved retinal ganglion cells projecting bilaterally to the pretectal area (ROSTRAL to the superior colliculus) –> which then projects to the Edinger-WEstphal nucleus of CN IIII
With optic nerve lesion, NEITHER pupil constricts when light is shone in that eye since the affarent pathway of the reflex is impaired; yet when light is shone in the unaffected eye (and there is no other lesion), BOTH will constrict
A CN III lesion interrupts the EFFERENT part of the consensual reflex, so the effected eye will not constrict = enlarged pupil; the effected eye will never constrict when light is shone in either eye while the unaffected eye WILL constrict if light is shone in either eye
Light-near dissocation, is a dissociation between what two reflexes?
What are two common causes of this clinical syndrome?
What other syndrome may be associated with the light-near dissocation?
Dissociation of light and near reflexes / light-near dissociation occurs when the pupils are able to constrict during the near reflex (pupils constrict, lens accomodates/thickens and eyes converge) but NOT able to light stimulus
Common causes:
Dorsal Midbrain Syndrome = Parinaud’s syndrome, due to a pineal tumor compressing the dorsal midbrain and may also occur due to ischemic infarction there (@ DORSAL MIDBRAIN)
Argyll Robertson pupils in neurosphilis
Since the midbrain centers for verticle gaze may also be involved, impairment of upward gaze may accompany light-near dissocation of the pupils
Classic clinical signs of Horner’s syndrome:
Horner’s is caused by disruption of what pathway and what lesions can lead to horners?
Horners: ptosis (paralysis of the superior tarsal muscle), miosis and anhidrosis (decrease sweating in the ipsilateral face)
Occurs from a lesion disrupting the oculosympathetic pathway: long pathway that consists of three neurons in series - the first order neruons DESCENDING down the brain stem may be involved by a lateral medullary infarction (wallenberg syndrome); second order neurons originate from the intermediolateral cell column in the spinal cord at C8 to T2 levels (may be affected by a tumor as they course thorugh the apex of the lung), third order neurons arise from the s_uperior cervical sympathteic ganglion_ ascend up the internal carotid artery where they may be affected by neck trauma.
Trigeminal nerve has sensory and motor functions..if a deficit….
Where is a major area where these nerve fibers could be compressed by tumors?
Trigeminal nerve has sensory and motor functions..if a deficit is not confied to the CN V areas, it signifies that sensory deficits may be due to lesions in the contralateral thalamus or parietal lobe, or may be associated with psychiatric disorders
Tumors, particularly where they pass through bony foramina in the skull base may compress the branches of CN V OR may be affected by infection or inflammation there
A V1 territory sensory impairment plys ipsilateral involvement of CN III, IV and VI may occur from a lesion at the superior orbital fissure or nearby cavernous sinus
What is trigeminal neuralgia?
What symptoms could be experienced?
Is this seen in younger or older patients?
Is there any associated syndromes?
Treaments?
A painful syndrome of irritation or inflammation of one of the trigeminal nerve sensory branches with short circuits/misfires
Pt may experience episodic, lighting-like jabs or electrical shocks of pain usually territory V2 or V3, several times daily, provokes by talking, chewing, or touching the face + NO sensory or other CN deficits are found on neurological exam;
often seen in younger patients associated with a MS lesion at V entry into the _PONS_
In order patients, a trigeminal nerve branch is often compressed by a tortuous or kinked blood vessel (often the superior cerebellar artery) - can be surgically repositioned or padded
RX: oral anticonvulsants (carbamazepine, gabapentin or others to relieve the nerve misfiring) or procedures to destroy the nerve branch invovlement
Trigeminal’s motor role is to innervate the muslces of mastication (masseter and temporalis m)
Lesions of:
LMN –>
UMN –>
Trigeminal’s motor role is to innervate the muslces of mastication (masseter and temporalis m)
Lesions of:
LMN –> rare; atrophy and weakness in the ipsilateral m, with jaw deviating TOWARDS side of lesion
UMN –> hyper-reflexia of the jaw jerk
