Bells Palsy
Bell's Palsy and Cranial Nerve Injuries
Bell's Palsy
AKA "idiopathic peripheral facial paralysis"
Most common peripheral paralysis of the seventh cranial nerve
Rapid and unilateral onset
Causes weakness of one half of the face, changes in taste, sensitivity to sound, and alteration in lacrimation and salivation
Affects 11-40 persons per 100,000 each year
Peak incidence usually between the ages of 15 and 50 years
Etiology includes pregnancy, postpartum periods, diabetes, hypothyroidism, familial origin, idiopathic, traumatic, neoplastic, congenital, and autoimmune causes
Pathology includes acute demyelinating disease, latent herpes viral infections, and infectious causes
Clinical manifestation includes sudden and rapid onset of unilateral facial weakness, preceding viral illness, earache, hyperacusis, tinnitus, taste disturbances, and decreased lacrimation
Lesion manifestations include facial weakness, impaired taste and salivation, hyperacusis, reduced lacrimation, and involvement of other cranial nerves
Bell's phenomenon is the upward movement of the eye on attempted closure of the lid
Synkinesis is an important sequelae of facial nerve palsy, causing abnormal involuntary facial movement
Crocodile tears, Marcus Gunn phenomenon, inverse Marcus Gunn phenomenon, and Marin-Amat phenomenon are examples of synkinesis
Crocodile tears refer to shedding of tears while eating or drinking
Marcus Gunn phenomenon is the elevation of ptotic eye in response to sucking, chewing, or mouth opening
Inverse Marcus Gunn phenomenon is the upper lid falling to cover the eye in response to sucking, chewing, or mouth opening
Marin-Amat syndrome is the upper lid falling to cover the eye in response to opening or lateral movement of the jaw
Diagnosis is based on clinical criteria and the House-Brackmann Scale
Laboratory and imaging studies are not routinely needed
Serological tests may be done to rule out Lyme disease
Electromyography and motor nerve conduction can estimate the amount of axonal loss
Ramsay-Hunt syndrome is a peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear or in the mouth
Other differential diagnoses include CNS neoplasms, stroke, HIV infection, multiple sclerosis, Guillain-Barré syndrome, Melkersson-Rosenthal syndrome, Lyme disease, otitis media, cholesteatoma, sarcoidosis, trauma to the facial nerve, and autoimmune diseases
Prognosis varies, with normal function returning within 3 weeks to 9 months
Complications include corneal dryness leading to visual loss and permanent damage to the facial nerve
Management includes protecting the cornea, corticosteroids, acupuncture, physical therapy, electrical nerve stimulation, and surgical decompression
Cranial Nerve Injuries
Olfactory nerve is located on the ventral surface of the frontal lobe and is responsible for olfaction (smell)
Anosmia is the loss of olfaction and can be caused by basilar skull fracture, CSF rhinorrhea, or halo sign
Medical Information about Cranial Nerve Injuries
Page 5
Optic Nerve
Location: Ventral surface of the frontal lobe
Central connection: Occipital lobe and Diencephalon (thalamus — Lateral Geniculate Body)
Exit: Optic Foramen
Terminates: Retina
Function: Vision (SSA)
Clinical Correlation
Central Vision Affectation:
Cataract — increase opacity of the lens
Presbyopia — impaired vision secondary to aging
Myopia — Far sightedness / Impaired near vision
Hyperopia — Near sightedness / impaired far vision
Visual Pathway
Monocular blindness
Bitemporal hemianopsia
C/L Homonymous hemianopsia
Page 6
Oculomotor Nerve
Location: Midbrain
Central connection: Midbrain
Exit: Superior orbital fissure
Terminates: superior, middle, inferior recti muscle; ciliary, sphincter muscle, levator palpebrae Superioris, inferior oblique
Function: moves the eyeball, lift the eyelid, regulate size of the pupil (GSE)
Medial rectus muscle
Adducts the eye; with its opposite partner, converges the eyes.
Superior rectus muscle
Elevates, intorts, and adducts the eye
Inferior rectus muscle
Depresses, extorts, and adducts the eye
Inferior oblique muscle
Elevates, extorts, and abducts the eye
Levator palpebrae muscle
Elevates the upper lid → Edinger—Westphal nucleus (GVE)
AKA accessory oculomotor nucleus
Parasympathetic pre-ganglionic nucleus that innervates the iris sphincter muscle and the ciliary muscle → Ciliary ganglion: (GVE)
Projects postganglionic parasympathetic fibers to the sphincter muscle of the iris (miosis) and to the ciliary muscle (accommodation)
Page 7
Trochlear Nerve
Location: Midbrain
Central connection: Posterior aspect of midbrain
Exit: Superior orbital fissure
Terminates: Superior Oblique
Function: moves the eyeball (GSE)
Abducens Nerve
Location: Pons
Central connection: Pons
Exit: Superior orbital fissure
Terminates: Lateral Rectus
Function: moves the eyeball (GSE)
Cardinal Gaze Pupillary Light Reflex
Afferent: CN2
Efferent: CN3
Direct and Consensual light
Page 8
Normal response of Pupillary Light Reflex
Direct light reflex: constriction of the pupil when light is presented on the I/L side
Consensual light reflex: constriction of the pupil when the light is presented on the C/L side
Accommodation Reflex
Afferent: CN2
Efferent: CN3
Focusses from a distant to near object
Constriction of the pupil
Thickening of the lens (constriction of ciliary muscle)
Convergence of both eyes
Trigeminal Nerve
Location: Pons
Central connection: Pons
Exit: Superior orbital fissure (V1); Foramen Rotundum (V2); Foramen Ovale (V3)
Terminates: Muscle of mastication, skin and mucus membrane of the face
Function: mastication (SVE), sensory to the face (GSA)
Divisions of CN V
V1 - Opthalmic Nerve - Sensory
V2 —- Maxillary Nerve - Sensory
V3 -—- Mandibular Nerve — Sensory and Motor*
Muscles of Mastication
Temporalis
Internal/Medial Pterygoid
Masseter
External/Lateral Pterygoid
Corneal Reflex
Afferent: CNV1 (Opthalmic Nerve)
Efferent: CN7
Page 9
Clinical Correlation
Loss of general sensation from the face and mucous membranes of the oral and nasal cavities, anterior 2/3 of tongue
Loss of the corneal reflex
Flaccid paralysis of the muscles of mastication
Deviation of the jaw to the weak side due to the unopposed action of the opposite lateral pterygoid muscle
Paralysis of the tensor tympani, leading to hyperacusis
Vestibulocochlear Nerve
Location: Pons
Central connection: Pons, Medulla, Temporal lobe
Exit: Internal Acoustic Meatus
Terminates: Organ of corti, Macula, Crista Ampularis
Function: Auditory (SSA) and Equilibrium (SSA)
Clinical Correlation
Conduction Deafness — Anatomy of The Ear Conducting system
Sensorineural Hearing Loss — CN VIII
Cortical Hearing Loss – BA 41,42 (Heschl Gyrus)
Page 10
Assessment of Vestibulocochlear Nerve
Sense of hearing: Weber vs Rinne test
Sense of balance: Equilibrium Test
Glossopharyngeal Nerve
Location: Medulla
Central connection: Medulla (posterior (dorsal) lateral sulcus
Exit: Jugular foramen
Terminates: back of the tongue, pharynx, parotid gland, carotid sinus
Function: secretion of the parotid glands (GVE), sensory to the posterior 1/3 of the tongue (SVA and GVA)
Vagus Nerve
Location: Medulla
Central connection: Medulla (posterior (dorsal) lateral sulcus
Exit: Jugular foramen
Terminates: pharynx, larynx, thoracic and abdominal viscera
Function: motor to cardiac, smooth muscles (pharynx and larynx — vocal chords) and glands (GVE); sensory to epiglottis, pharynx, larynx, epiglottis (GVA), skin of the external ear (pinna) (GSA)
Assessment of Glossopharyngeal Nerve: Sensory Function
Special sensation: Sense of taste on the posterior 1/3
General Sensation: light touch, pressure sensation on the posterior 1/3
Gag Reflex
Aka “Pharyngeal Reflex”/ “Laryngeal Reflex”
Afferent: CN 9
Efferent: CN10
Page 11: Spinal Accessory Nerve and Hypoglossal Nerve
Spinal Accessory Nerve
Location: Medulla
Central connection: Medulla (posterior (dorsal) lateral sulcus)
Exit: Jugular foramen and Foramen Magnum
Terminates:
Cranial Portion: muscles of the pharynx and larynx (connects with vagus nerve)
Spinal Portion: SCM and Trapezius
Function:
Movement of pharynx and larynx (GVE)
Shoulder and neck movement (GSE)
Clinical correlation:
Scapular Winging
Weakness of the trapezius and SCM
Hypoglossal Nerve
Location: Medulla
Central connection: Medulla (Anterior (ventral) lateral sulcus)
Exit: Hypoglossal canal
Terminates: muscles of the tongue
Function: movement of the tongue (SVE)
Muscles of the tongue:
Palatoglossus — pharyngeal plexus (CN 9 and 10)
Genioglossus — CN 12
Hyoglossus— CN 12
Styloglossus— CN 12
Hypoglossal Nerve Palsy:
Deviation of the tongue upon protrusion towards the weak side
Page 12: Peripheral and Central Vestibular System
Peripheral Vestibular System
Semicircular Canals:
Detect head acceleration
Endolymph moves freely within each canal in response to the direction of the angular head rotation
Cupula in the ampulla contains mechanosensing cilia and hair cells
Otolith Organs:
Saccule (Vertical) and utricle (Horizontal)
Detect linear acceleration and static head tilt
Sensitive to gravity
Contains calcium carbonate crystalline-structure material (otoconia)
Central Vestibular System
Brain stem processes provide primary control of many vestibular reflexes
Vestibular cortex, thalamus, and reticular formation enable the vestibular system to contribute to the integration of arousal and conscious awareness of the body, as well as to discriminate between movement of self and the environment
Page 13: Physiology and Motor Control
Tonic Firing Rate
Resting firing rate: 70 to 100 spikes/sec
Head motion through excitation or inhibition
Vestibulo-Ocular Reflex
Responsible for maintaining stability of an image on the fovea of the retina during rapid head movements
Activates eye muscles to create eye movements in the exact speed but opposite direction of head movements
Push—Pull Mechanism
Brain detects head movement and direction through comparison of inputs between the two vestibular systems
SCCs work in coplanar fashion
Increased firing rate in the SCC on the same side as head turn, and decreased firing rate in the opposite SCC
I/L (ipsilateral) leads to depolarization, C/L (contralateral) leads to hyperpolarization
Inhibitory Cutoff
Inhibition of the hair cells in the opposite labyrinth can only reduce the firing rate to zero, at which point the inhibition is cut off
Page 14: Evaluation and Identification of Symptoms
Identification of Symptoms
Dizziness: categorized as vertigo, lightheadedness, dysequilibrium, or oscillopsia
Causes of dizziness: cardiovascular system, neurologic system, vision dysfunction, psychogenic dizziness, cervicogenic dizziness, vestibular system dizziness
Vertigo: illusion of movement, episodic and indicates pathology along the vestibular pathways
Light-headedness: feeling of fainting, caused by non-vestibular factors
Dysequilibrium: sensation of being off balance, associated with vestibular and nonvestibular problems
Oscillopsia: subjective experience of motion of stationary objects, associated with VOR deficit or vestibular hypofunction
Evaluation
Identification of symptoms
Duration and circumstances of symptoms
Examination of eye movements
Observation for Nystagmus
Head Impulse Test
Head-Shaking Induced Nystagmus Test
Positional Testing
Medical Information about Cranial Nerve Injuries
Page 15
Examination of Eye Movements
Critical for defining and localizing vestibular pathology
Key tests include:
Observation for nystagmus
Head Impulse Test (examination of the VOR at high acceleration)
Head-Shaking Induced Nystagmus (HSN) test
Positional testing
Observation for Nystagmus
Two forms of nystagmus: jerk nystagmus and pendular nystagmus
Jerk nystagmus:
Consists of slow and fast components
Direction of jerk nystagmus is the direction of the fast phase
Pendular nystagmus:
Sinusoidal oscillation with slow phase in both directions and no corrective saccade
Nystagmus due to a vestibular lesion:
Slow and fast component
Direction of the nystagmus named by the direction of the fast component
Peripheral vestibular lesion:
Slow component due to relative excitation of one side of the vestibular system
Fast component generated from the parapontine reticular formation in the brain stem
Vestibular nystagmus can be suppressed in light and when visually fixating on a target
Head-Shaking Induced Nystagmus (HSN) Test
Used to examine semicircular canal function
Patient fixates on a near target while their head is manually rotated in an unpredictable direction
In a patient with a loss of vestibular function, the eyes will not move as quickly as the head rotation and will move off the target
Corrective saccade is made to reposition the eyes on the target
Page 16
Positional Testing
Used to identify whether otoconia have been displaced into the SCC, causing benign paroxysmal positional vertigo (BPPV)
Dix-Hallpike test is the most common positional test used to examine for BPPV
Direction and duration of the resultant nystagmus can help determine the type of lesion
Vestibular System Dysfunction
Peripheral Pathology:
Mechanical (Benign Paroxysmal Postural Vertigo)
Most common cause of vertigo is BPPV
BPPV occurs via cupulolithiasis and canalithiasis mechanisms
Central Nervous System Pathology:
Cerebrovascular insults, TBI, MS
Page 17
Ocular Tilt Reaction
OTR for unilateral central vestibular pathology:
Head tilting
Skew deviation of the eyes
Torsion of the eye
Intervention for BPPV
Canalith repositioning maneuver
Liberatory (Semont) maneuver
Brandt-Daroff exercises
Intervention for Unilateral Vestibular Hypofunction
Gaze Stability Exercises
Postural Stability Exercises
Habituation Exercises (Motion Sensitivity)
Page 18
Gaze Stability Exercises
Improve the VOR and other systems used for gaze stability with head motion
Retinal slip occurs when the image of an object moves off the fovea of the retina
Postural Stability Exercises
Improve balance by encouraging the development of balance strategies
Important to incorporate head movement into the exercises
Habituation Exercises (Motion Sensitivity)
Warranted when a patient with unilateral vestibular hypofunction has continual complaints of dizziness
Reduction in response to a repeatedly performed movement
Page 19
Tables: House-Brackmann Scale, Physiology and Motor Control
Medical Information about Cranial Nerve Injuries
Page 20
Clinical Correlation in PT Bell's Palsy, Cranial Nerve Injuries, Vestib Cond
Balance tests and expected results related to specific diagnosis:
BPPV (Benign Paroxysmal Positional Vertigo)
Romberg test: Negative
Acute: positive
Chronic: negative
Tandem Romberg test: Negative
Single-legged test: Negative
Acute: positive
Chronic: negative
Gait: Normal
Acute: wide-based, slow, decreased arm swing and trunk rotation
Compensated: normal
Turn head while walking: May produce slight unsteadiness
Acute: may not keep balance or slows balance, increased ataxia
Compensated: normal
UVH (Unilateral Vestibular Hypofunction)
Romberg test: Acute and chronic positive
Tandem Romberg test: Positive, eyes closed
Single-legged test: May be positive
Acute: positive
Chronic: negative
Gait: Acute: wide-based, slow, decreased arm swing and trunk rotation
Compensated: mild gait deviation
Turn head while walking: May not keep balance
Acute: may not keep balance or slows balance, increased ataxia
Compensated: normal
BVH (Bilateral Vestibular Hypofunction)
Romberg test: Acute and chronic positive
Tandem Romberg test: Positive
Single-legged test: May be unable to perform
Gait: Acute: wide-based, slow, decreased arm swing and trunk rotation
Compensated: normal
Turn head while walking: May not keep balance
Acute: may not keep balance or slows balance, increased ataxia
Compensated: normal
Common Symptoms Associated with Central versus Peripheral Vestibular Pathology
Central Vestibular Pathology
Ataxia often severe.
Abnormal smooth pursuit and abnormal saccadic eye movement tests.
SX (symptoms) usually do not include hearing loss; if so, it is often sudden and permanent fullness in ears, tinnitus.
SX might include diplopia, altered consciousness, lateropulsion.
SX of acute vertigo not usually suppressed by visual fixation.
Pendular nystagmus (eyes oscillate at equal speeds).
Peripheral Vestibular Pathology
Ataxia mild.
Smooth pursuit and saccades usually normal; positional testing may reproduce nystagmus.
SX may include hearing loss (insidious-may recover), sudden and permanent fullness in ears, tinnitus.
SX of acute vertigo usually suppressed by visual fixation.
Nystagmus will incorporate slow and fast phases (jerk nystagmus).
Pure persistent vertical nystagmus persists regardless of positional testing (persistent downbeat nystagmus in Hallpike-Dix test may indicate anterior canal BPPV).
Page 21
Postural Stability Exercises
Intervention for Bilateral Vestibular Hypofunction
Bell's Palsy, Cranial Nerve Injuries, Vestib Cond