CN, Brainstem Reflexes & Brainstem Disorders Flashcards
1
Q
Olfactory Nerve (CN 1)
A
- lesion produces anosmia (loss of the sense of smell, either total [severe head trauma-nerve branches sheared/torn where they pass through the bony cribiform plate] or partial.)
- most common: sinusitis (associated mucosal swelling and inflammation) or URI
- head trauma can shear n. branches in cribiform plate
- rare: orbitofrontal (near the olfactory lobe) tumors; eg meningioma
2
Q
Oculomotor (CN3), Trochlear (CN4), and Abducens (CN 6)
A
- SO4, LR6, all the rest 3; extraocular muscles
- test with drawing letter “H”
- lesions produce diplopia which is BINOCULAR
- binocular diplopia=single image vision when either eye is covered
- monocular diplopia=double images when one eye is covered, from psychiatric disease or ocular pathology (e.g. dislocated lens)
- right CN 3 (Oculomotor N) lesion:
- severe ptosis (ipsilateral drooping eyelid entirely covers the eye)-due to paralysis of the levator palpebrae superioris muscle
- large pupil, unreactive to light (parasympathetic innervation of the pupil is impaired)
- outward deviation (AB-duct the eye) from lateral rectus action (LR6 is spared)
- CN 4; SO4 (Trochlear N) lesion:
- weakness of R. SO muscle (AD-ducted right eye does not fully depress)
- only CN which exists the BS dorsally, decussated to innervate contralat SO
- Test: Down.IN (AD-ducted)
- right CN 6; LR6 (ABducens N) lesion
- affects ipsi LR, imapirs AB-duction of affected eyeball
3
Q
Pupillary Disorders: Pupillary Light Reflex
A
- Lesion in R Optic CN 2
- light in R. eye, no response in L or R
- Light in L. eye, both constrict
- Problem: afferent pt (CN2) of reflex of R eye (efferent is CN3-pupillo constrictors)
- Rationale: light in L. eye works because
- Lesion in R. CN 3
- A right CN3 lesion interrupts the efferent part (pupillo constrictors) of this consensual reflex, so the enlarged right pupil never constricts when light is shined in either eye.
- left pupil constricts with light shined in either eye.
- AOP (afferent optic) + EOCULOM (efferent occulomotor)
4
Q
IR. Down.IN. Test: Down.OUT
MR. IN. Test: IN.IN
LR6. Test: OUT.OUT
SR. Up.IN Test: UpOUT
IO. Up.OUT. Test: UpIN
SO4. Down.OUT. Test: Down.IN
A
5
Q
Eye Movement Disorders-Binocular diplopia
A
- Normal binocular vision depends on equivalent areas of the retina of each eye perceiving the same visual stimulus.
- If the eyeballs are not perfectly aligned in primary position (“looking straight ahead”) or when conjugately moving to other positions, a visual image may appear blurred or doubled (binocular diplopia).
- Binocular diplopia is the more common type of diplopia and resolves if the patient covers either eye.
- It can be caused by lesions of cranial nerves 3,4,6, or their related extraocular muscles (or NMJs therein).
- severe or complete oculomotor nerve lesion-diplopia would be eliminated by the ptosis covering the involved eye.
- lesions involving these brain stem or cerebellar connections could also cause diplopia.
6
Q
Eye Movement Disorders-Monocular diplopia
A
- relatively rare and occurs when looking with one eye alone.
- may occur from a problem in the “optical system” of an eye-such as a dislocated lens or detached retina, –OR– may be related to a psychiatric disorder, but NOT from neurological disease, strictly speaking.
7
Q
Eye Movement Disorders-Nystagmus
A
- Patients complaining of diplopia may also be noted to have nystagmus
- Nystagmus= repetitive, oscillatory, jerky eye movements.
- can be physiological –OR– normally induced (as when suddenly stopping someone rotating in a swivel chair).
- Pathological or abnormal nystagmus occurs with lesions of the vestibular system, brain stem, or cerebellum which upset the normal control or balance of conjugate eye movements.
- Such lesions typically produce asymmetrical nystagmus, more prominent with certain eye movements or positions.
- nystagmus caused by drug toxicity usually is symmetrical and present with virtually all eye movements or positions.
8
Q
Eye Movement Disorders-Internuclear ophthalmoplegia (INO)/MLF syndrome
A
- paralysis of extraocular muscles (“ophthalmoplegia”) from a lesion between the nuclei (“internuclear”) involved with lateral gaze (oculomotor and abducens nuclei).
- lesion interrupts the ascending medial longitudinal fasciculus (MLF)
- To have coordinated horizontal gaze rightward, for example: the right paramedian pontine reticular formation (PPRF) must activate both the right abducens nucleus in the pons and the left oculomotor nucleus in the midbrain, so that the right lateral rectus (LR6) and left medial rectus muscles (CN3) move the eyes to the right.
- ascending MLF leaves the right PPRF, decussates early and rises to join the left oculomotor nucleus.
- A lesion along the main left-sided course of the MLF here (en route from pons to midbrain) produces:
- paralysis of adduction of the left eye
- WITH: nystagmus of the abducting right eye (see Fig. 3).
- A lesion along the main left-sided course of the MLF here (en route from pons to midbrain) produces:
- left medial rectus still functions (both eyes adduct/converge when looking closely at an object
-
most common causes of MLF lesions:
- multiple sclerosis in younger patients
- ischemic infarction in older patients.
9
Q
Normal Pupillary Light Reflex
A
- elicited by shining light into one eye, causing its pupil to constrict (direct response) and constriction of the other eye (consensual response).
- This reflex pathway involves:
- retinal ganglion cells projecting bilaterally to the pretectal area (rostral to the superior colliculus)
- which then projects to the EWN of CN III.
- Ex: a L. optic nerve lesion impairs the afferent part of this consensual reflex=neither pupil constricts when light is shined into the left eye, BUT both pupils constrict when light is shined into the right eye.
10
Q
Pupillary Disorders-RAPD (relative afferent pupillary defect)
A
- may occur from a partial optic nerve or retinal lesion.
- Both pupils may initially constrict to light, but after moving the light source from the normal to the abnormal eye (“swinging flashlight test”), pupillary dilatation occurs because of relatively reduced afferent input at the affected eye.
- If one were to observe both eyes simultaneously, the light stimulus produces direct and consensual pupillary constriction, but to a lesser degree when the affected eye is stimulated.
11
Q
Pupillary Disorders-Near Reflex
A
- occurs when viewing a nearby object; is 3-fold:
- pupillary constriction
- lens accomodation (“thickening”)
- convergence of the eyes
- dissociation of light and near reflexes (light-near dissociation)
- combo:
- selective disruption of the pupillary light reflex rapthway at the pretectal area
- -BUT- connections for the near reflex are preserved
- =pupils only constrict during the near reflex, but NOT to a light stimulus
- Classic causes:
- dorsal midbrain (Parinaud’s) syndrome
- classicaly=pineal tumor compressing the dorsal MB
- may also occur form an ischemic infarction (at the dorsal MB)
- Argyll Robertson pupils in neurosyphilis
- dorsal midbrain (Parinaud’s) syndrome
- may also involve impairment of upward gaze
- combo:
12
Q
Pupillary Disorders-Horner’s Syndrome
A
- cause: lesion disrupting the oculosympathetic pathway
- classic triad:
- miosis (a smaller, constricted pupil which dilates poorly in darkness)
- anhidrosis (decreased sweating in the ipsilateral face since sweat glands have sympathetic innervation)
- mild ptosis (paralysis of the superior tarsal muscle); subtle and mild in comparison to the more obvious ptosis from an oculomotor (CN III) nerve lesion
- oculosympathetic pathway is relatively long and consists of three neurons in series.
- First- order neurons descending down the BS may be involved by a lateral medullary infarction (Wallenberg syndrome).
- Second-order neurons originating from the intermediolateral cell column in the spinal cord at C8 to T2 levels may be affected by a tumor as they course through the apex of the lung.
- Third-order neurons arising from the superior cervical sympathetic ganglion ascend up the internal carotid artery where they may be affected by neck trauma.
13
Q
Trigeminal Nerve (CN V)
A
- The trigeminal nerve has sensory and motor functions.
- Sensation over the face + anterior scalp is conveyed to the BS by 3 divisions/branches:
- V-1 (ophthalmic); V-1 sensory deficit over the forehead should also involve the anterior scalp
- V-2 (maxillary)
- V-3 (mandibular); V-3 sensory deficit should NOT involve the corner of the jaw or the neck.
- These branches may be compressed by:
- tumors-particularly where they pass through bony foramina in the skull base
- infection or inflammation
- sensory deficits not confined to the trigeminal nerve territory may be due to:
- lesions in the contralateral thalamus or parietal lobe
- psychiatric disorders.
- Trigeminal branch sensory deficits may accompany other cranial nerve lesions (combos).
- A V-1 territory sensory impairment + ipsilateral involvement of cranial nerves III, IV and VI may occur from a lesion at the superior orbital fissure or nearby cavernous sinus.
-
Trigeminal neuralgia = painful syndrome of irritation or inflammation of one of the trigeminal nerve sensory branches which “short circuits” or “misfires.”
- CP: episodic, lightning-like jabs or “electrical shocks” of pain usually in the territory of V-2 or V-3, several times daily
- provoked by talking, chewing or touching the face.
- MS lesion at the trigeminal nerve entry region into the pons = cause in younger patients.
-
older patients, a trigeminal nerve branch is often compressed by a tortuous or kinked blood vessel (often the superior cerebellar artery)
- Tx:
- surgically repositioned or padded
- oral anticonvulsants: carbamazepine, gabapentin to relieve the nerve “misfiring”
- procedures to destroy the nerve branch involved.
- Tx:
- CP: episodic, lightning-like jabs or “electrical shocks” of pain usually in the territory of V-2 or V-3, several times daily
- The trigeminal nerve also innervates the muscles of chewing or mastication—the masseter and temporalis muscles.
- LMN lesion of the trigeminal motor nerve is rare, produces atrophy + weakness in these ipsilateral muscles
- CP: jaw deviating toward the side of the lesion.
- Both ipsilateral and contralateral UMN in the motor cortex control the trigeminal motor nerve on one side
- Unilateral UMN lesion does NOT produce any jaw deviation or severe weakness.
- Bilateral UMN lesions may cause hyper-reflexia of the jaw jerk (since it is a muscle stretch reflex)
- LMN lesion of the trigeminal motor nerve is rare, produces atrophy + weakness in these ipsilateral muscles
14
Q
**Facial Nerve (CN 7)**
A
- Each facial nerve, originating from its facial nucleus in the pons, innervates the ipsilateral facial muscles.
- LMN facial paralysis involves the nucleus or nerve of CN VII and causes a relatively severe paralysis of the entire ipsilateral half of the face. This would be the isolated finding with a lesion at or near the stylomastoid foramen (Lesion 1).
- Lesion 2A-IPSI facial paralysis + impaired taste over the anterior 2/3 of the tongue=chorda tympani branch of the facial nerve is also involved
- Lesion 2B-slightly more proximal lesion also involves the facial nerve branch to the stapedius muscle.
- stapedius muscle acts to dampen middle ear ossicle movements in the presence of loud sounds
- CP of stapedius mu denervation: an unpleasant sensitivity to sound (hyperacusis) .
- Lesion 3- at the internal auditory meatus (cerebellopontine angle) would create all the deficits as in lesion 2B + hearing impairment and tinnitus, from involvement of the adjacent CN VIII.
- often from an acoustic neuroma-a tumor arising from CN VIII.
- Lesion 4-near the facial (CN7) nucleus in the pons, such as a small ischemic infarction, would create ipsi weakness of lateral gaze, from involvement of the adjacent PPRF.
- In addition to tumors or trauma causing lesions of CN VII in its course outside the pons, a very common syndrome is Bell’s palsy (idiopathic facial nerve paralysis).
- CP: pt may awaken to suddenly notice severe paralysis of one side of the face, sometimes with ipsilateral hyperacusis and impaired taste.
- Path: Herpes simplex or other viruses may cause this inflammation
- Tx: short course of oral corticosteroid medication hastens recovery from the presumed facial nerve inflammation where it travels through the temporal (petrous) bone.
- anti-viral medication may also be part of the tx.
- Prognosis: most patients recover fully after a few wks.
- Facial paralysis may also occur with lesions of the UMN that control the facial (CN VII) nucleus.
- The part of the CN VII nucleus which innervates the upper face or forehead is controlled by UMN (corticobulbar tract fibers) originating both ipsilaterally and contralaterally
- the rest of the CN VII nucleus is controlled only by contralateral UMN
- Thus, facial paralysis from an UMN lesion causes a relatively milder paralysis of only the lower part of the contralateral face, sparing the forehead.
15
Q
Glossopharyngeal (CN IX) and Vagus (CN X) Nerves
A
- taste, visceral afferent, and visceral efferent functions cannot be tested clinically.
- Both nerves innervate pharyngeal and laryngeal muscles, so lesions can cause impairments of speech or swallowing (difficult to test each nerve separately).
- decreased or absent gag reflex (difficult to evaluate due to pt varaibility) when touching one side of the pharynx suggests a glossopharyngeal nerve lesion on that side.
-
Elevation of the palatal arch when asking the patient to say “ah”- reflects vagal nerve function.
- LMN lesion of vagal nerve branches innervating the palate causes ipsilateral drooping/sagging of the palatal arch with the uvula pointing toward the other (normal) side.
- LMN lesion of vagal nerve branches innervating the larynx causes hoarseness from ipsilateral paralysis of vocal cord muscles.
