ll Flashcards
Neurological condition which causes the unilateral paralysis of the face.
BELL’S PALSY
is both motor and sensory, and it arises from the brainstem in between the pons and medulla. The facial nerve is also subdivided in to 5 branches.
CN VII (Facial nerve)-
There are five branches of the facial nerve which are responsible for the movement and sensation of the face, these five are:
- Temporal Branch- innervates the frontalis, orbicularis oculi and corrugator supercilli.
- Zygomatic Branch- innervates some parts of the orbicularis oculi.
- Buccal Branch- innervates the orbicularis oris, buccinators and zygomaticus muscle
- Marginal Mandibular Branch- innervates the mentalis, depressor labii inferioris and depressor anguli oris.
- Cervical Branch-innervates platysma muscle.
Name and Location of Primary Nuclei:
- Facial Motor Nucleus- Responsible for the muscles of facial expression.
- Superior Salivatory Nucleus- responsible for the salivary and lacrimal glands.
- Nucleus of Spinal Tract- responsible for the sensory at external ear and tympanic membrane.
- Nucleus Solitarius- Responsible for the sense of taste.
Movements of the muscles innervated by the facial nerve:
-Frontalis- wrinkling of the forehead and raising of eyebrows.
-Orbicularis Oculi – closing of the eyes.
-Corrugator Supercilli- frowning and vertical wrinkling of forehead.
-Orbicularis Oris- kissing pose of the lips and closing of the mouth.
-Buccinator- puffing the cheeks.
-Risorius- Smiling without the teeth showing.
-Nasalis- “flaring”/ enlarging of the nostrils.
-Mentalis- allows the lips to “pout” and chin to wrinkle.
-Zygomaticus- Elevates both corners of the mouth when smiling, shows teeth.
Platysma- Depresses both angles of the mouth.
Epidemiology of Bells Palsy
- More present in males than of the females
- Peeks from ages 20 to 40 years of age.
- Diabetic patients are most likely to develop this condition, up to four times more.
- Pregnant women are also susceptible of this condition.
- Most common acute condition which has only one nerve involved.
Etiology of Bells palsy
- Hereditary
- Swelling or inflammation of the nerve involved.
- Exposure to viral infections such as:
- Herpes Simplex
-Herpes Zoster
-Rubella
-Mumps Virus
-Cold Flue
-HFMD - Diabetes
- Acute respiratory tract infection
- Tumor which invade the temporal bone
- Fracture of the temporal bone
- Lymphocytes- mediated hypersensitivity phenomenon
- Middle ear infection
- Meningitis
TYPES/CLASSIFICATION (bells palsy)
- Unilateral noncurrent
- Unilateral recurrent
- Simultaneous bilateral
- Alternating bilateral
- Recurrent bilateral type
CLINICAL MANIFESTATION (bells palsy)
Signs and symptoms depend upon the location of lesions as follows:
Lesion1: Outside the stylomastoid Foramen
Widened palpebral fissure due to paralysis of the orbicularis palpebrum
The forehead cannot wrinkle *
The upper eyelid closes slowly *
In a complete facial paralysis, when attempt to shut the eye, closure is incomplete and the eyeball rolls upward and outward, demonstrating Bell’s phenomenon
Blinking reflex is loss on the affected side *
Saliva may dribble on the mouth
There is no deviation of the tongue or jaw
Lesion 2: In facial canal involving the chorda tympani *
Loss of taste in the anterior 2/3 of the tongue
Reduced salivation on the affected side
Lesion 3: Higher in the facial canal involving the stapedius muscle
All sign of lesion 1 and 2
Hyperacusis- painful sensitivity to loud sound
Lesion 4: Higher involving the geniculate ganglion *
All signs of 1-3 *
Pain behind and within the ear
Lesion 5: In the internal auditory meatus
Signs of Bell’s Palsy *
Deafness (CN8)
*Tinnitus
Lesion 6: at the emerges of facial nerve from pons *
Involvement of CN 5 and 8 *
May also involve CN 6,11 and 12
Marcus-Gunn or Jaw winking phenomenon-elevation of ptotic eyelid on movement of jaw to the contralateral side. *
Marin Amat Syndrome- closing of eyelids during mouth opening
Phenomenon seen in Bell’s Palsy
- Marcus Gunn Phenomenon- elevation of ptotic eyelids during movement of the jaw
- Marin- Amat Syndrome- opening of the mouth causes eye closure
- Moebius Syndrome- bilateral facial paralysis
Sign and Symptoms of Bells palsy
Acute onset unilateral upper and lower facial paralysis (over a 48-hr period)
Posterior auricular pain
Hyperacusis
Taste disturbances
Otalgia
Weakness of the facial mm.
Poor eyelid closure
Aching of the ear or mastoid
Tingling or numbness of the check/mouth
Epiphora - excessive watering of eyes
Ocular Pain
Blurred vision
Flattening of forehead and nasolabial fold on the side affected by palsy
Complication that may appear after apparent recovery: BP
State of over toning or contracture
Associated movement of synkenesis
- unilateral lacrimation on eating on due to regeneration facial nerve fibers
- hemifacial Spasm- spasm of facial muscle usually begins in orbicularis oculi
Crocodile Tears (aka Bogorads Syndrome, Gustatoclarimal reflex, Paroxysmal lacrimation)BP
confirms the presence of nerve damage and determines the severity. An _____ measure the electrical activity of a muscle in response to stimulation and the nature and speed of the conduction
DIAGNOSIS
: Laboratory Test Electromyography- BP
Dx: Imaging scan:BP
X-ray Imaging, MRI or CT scan may be needed on occasion to rule out other possible sources of pressure of the facial nerve, such as tumor or skull fracture
Facial Nerve Examination BP
A. Motor Status: test the facial muscles.
B. Reflexes: corneal(wink) conjunctiva and lid reflexes should be examined
C. Sensory Status: taste is tested as follows: sweet with sugar, sour with citric acid, bitter with quinine and salty
BP
The examination should also include:
A full neurological examination
Ear and mouth examination to exclude Ramsey–Hunt Syndrome; Herpes zoster
Ear examination
The most common is the HOUSE OF BRACKMANN for facial nerve grading: BP
Grade 1 (normal) *
Normal facial function in all area
Grade 2 (slight dysfunction) *
Gross: slight weakness noticeable on close inspection *
At rest: normal symmetry and tone
Motion: forehead-moderate to good function; eye-complete closure with minimum effort; mouthslight asymmetry
Grade 3(moderate dysfunction) *
Gross: obvious but not disfiguring difference between two sides; noticeable but not severe synkinesis, contracture and semi/hemi facial spasm *
Motion: forehead- slight to moderate movement; eye-complete closure with effort; mouth slight weak maximum effort
Grade 4(moderate severe dysfunction) *
Gross: obvious weakness and or/ disfiguring asymmetry
Motion: forehead-none; eye- incomplete closure; mouth- asymmetry with maximum effort
Grade 5 (severe dysfunction) *
Gross: only barely perceptible motion *
At rest: asymmetry *
Motion: forehead-none; eye-incomplete closure; mouth-slight movement
Grade 6 (total paralysis)
* No movement
PROGNOSIS BP
- The extent of nerve damage determines the extent of recovery. With or without treatment, most individuals begin to get better within two weeks after the initial onset of symptoms and most recover some or all facial function within six months.
- Some individuals may show moderate to severe side effects. In some cases, residual muscle weakness may last longer or may be permanent.
- Taste returns before facial strength. If taste returns within five to seven days after symptoms began, it’s more likely you will recover completely.
- It’s also more likely you will recover completely if your facial muscles were not fully paralyzed at the most severe point of the illness.
Good Prognosis signs BP
* Recovery of taste in 1st week
* Recovery of sensory function (taste) before motor function. *
Recovery of motor function, usual order of function is:
o Buccinator
o Zygomatic
o Inferior Levator
o Orbicularis occuli
o Frontalis *
Incomplete paralysis in the 1st 5-7 days *
If within after few days’ onset, EMG shows there are motor units under voluntary control in the facial mm and from CN7 remains normal or only slightly slow *
Return of voluntary motor power at the end of 3 weeks from onset
FACTORS ASSOCIATED WITH A POORER DIAGNOSIS BP
- Age greater than 60 years
- Hypertension
- Hyperacusis
- Lacrimation has decreased
- Diabetes Mellitus
- impairment of taste and complete facial weakness
- After ten years, evidence of denervation suggests a long period of recovery, which is often incomplete.
MEDICAL MANAGEMENT BP
- Corticosteroids
- Prednisone
o The standard drug used in bell palsy, is a glucocorticoid medication mostly used to suppress the immune system and decrease inflammation.
Antiviral drugs
Acyclovir and valacyclovir
Have been administered in the treatment of bell palsy in combination with prednisone or have been used alone in patients who cannot take prednisone. - Methylcellulose drops are used for affected eye
- Analgesics as required for pain
- Steroids to reduce edema of facial nerve
SURGICAL MANAGEMENT BP
Hypoglossal
o Facial nerve anastomosis to restore partial facial; Function if none has returned by 6-12 months
oFacial nerve grafting
o Facial nerve decompression
o Subocularis oculi fat lift
PHYSICAL THERAPY MANAGEMENT
for Bells Palsy
* Infrared rays and hot moist pack it has been recommended to use local superficial heat therapy for 15 minutes per session for the facial muscle prior to ES, massage or exercises, heat therapy improves local circulation and decrease skin resistance to ES, thus the lowest current intensity could be used.
* Electrical stimulation of the muscle aims to preserving muscle bulk especially in complete paralysis and it has also a physiological benefit as the patient observes muscle contraction in his face that gives him hope of recovery from facial paralysis.
*Facial massage improves circulation and may prevent contractures
Facial exercises with mirror for biofeedback- active exercise prevent muscle atrophy and improves muscle function
Sit relaxed in front of a mirror
Gently raise eyebrows, you can help the movement with finger
Draw your eyebrows together(frowning)
Wrinkle up your nose
Take a deep breath to your nose and flare nostrils
Gently try and move corners of mouth outwards
Try to smile and see if you can hold it
Lift 1 corner of the mouth and other
Is an autoimmune condition which attacks the myelin sheath of the neurons in the peripheral nervous system. The damage to the nerves causes the muscles to be weakened and sometimes paralyzed. This condition is idiopathic, the syndrome often follows infection with a virus or bacteria. GBS
GUILLAIN BARRE SYNDROME
This condition has many classifications and subtypes, namely: GBS
- Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
- Weakness and paresthesia, this type may start progressing from your legs to the trunk and onto the rest of the upper extremities.
- Most common type.
- May also decrease you reflexes.
- Acute Motor Axonal Neuropathy (AMAN)
- Milder form of the condition
- non-inflammatory disease where the axons are the ones that are targeted by the body’s immune system.
- The myelin sheath not affected.
- Affects mostly children and young adults
- Acute Motor Sensory Axonal Neuropathy (AMSAN)
- Acute onset of weakness of the distal part, loss of DTR and sensorial symptoms.
- Mostly affects the adults
- Miller-Fischer Syndrome
-Rare form of GBS
-Primarily affects the eyes, making it difficult for the patient to move it. - Damaged/impaired coordination of the limbs and unsteadiness.
-Absent of DTR
Nervous system outside the brain and spinal cord that is distributed to most parts of the body, and is responsible for motor and sensory activities (sensory receptors and motor/action conduction to the mm) and is divided into two parts. GBS
Peripheral Nervous system-
Parts of the PNS GBS
Somatic Nervous System- Regulates voluntary muscle movements.
Autonomic Nervous System regulates involuntary movement.
Neurons- Are nerve cells responsible for the conduction and relay of the information to and from the brain from the body and vice-versa, it also uses electrical signal impulses to deliver these messages and if stimulated can cause action potential.
Parts of the neuron GBS
Dendrites- Are flowerlike/ root-like structures that act as an input or receiving station of the neuron.
Cell body/Soma- Contains the nucleus and is spherical.
Axon- Acts as a bridge that is from the soma away to the distal part of the neuron that attaches to other neurons, where saltatory action happens (specifically in the myelin sheath on the axon), where impulses travel from the soma to the axon terminal to relay these messages.
-Myelin sheath- Made up of protein and fatty substances that envelops segments of the axon so that electrical impulses (saltatory conduction) travel faster, the thicker the myelin sheath the faster the conduction.
Synapse- A point where in two neurons come in contact with one another to receive or relay signals.
-
Schwann cell - produces myelin sheath in Peripheral Nervous System
Olegodendroctyes- Produces myelin sheath in the Central Nervous System.
Epidemiolog GBS
- Mostly affects Male than Females
- Distal parts are affected first
- Affects young adults to the middle-aged group ( 30 to 50 years of age)
EtiologyGBS
This condition is considered to be idiopathic.
- It is sometimes suspected to be caused by viral infection such as:
- Respiratory infection (most common, usually appears after having this)
- Gastrointestinal infection (most common, usually appears after having this)
- Human Herpes Virus Infection
- Mycoplasma pneumonia
- Polio vaccination
- Swine flu vaccine
- Rabies vaccine
CLINICAL MANIFESTATION GBS
Classic Guillain-Bare Syndrome- begins with muscle weakness and diminished reflexes of lower extremities.
● Hyporeflexia and weakness progress and may result in quadriplegia.
● Demyelination of the nerves that innervate the diaphragm and intercostal muscles result in neuromuscular respiratory failure.
● Sensory symptoms include paresthesia’s of the hands and feet and pain related to demyelination of sensory fibers
Cranial nerve demyelination can result a variety of clinical manifestations: GBS
● Optic nerve demyelination may result in blindness
● Bulbar muscle weakness related to demyelination of the glossopharyngeal and vagus nerves results in an inability to swallow or clear secretions
● Vagus nerve demyelination results in autonomic dysfunction, manifested by inability of the cardiovascular system
● The presentation is variable and may include tachycardia, bradycardia, hypertension or orthostatic hypotension.
● The symptoms of autonomic dysfunction occur and resolve rapidly.
Guillain-Barre Syndrome does not affect cognitive function or level of consciousness. While the classic clinical features include areflexia and ascending weakness. There may be a sensory presentation with progressive sensory symptoms, an atypical axonal destruction, and the Miller-Fischer variant, which includes paralysis of the ocular muscles, ataxia and areflexia.
Signs and Symptoms of GBS:
The typical patient with GBS, which in most cases will manifest as acute inflammatory demyelinating polyradiculopathy (AIDP), presents 2-4 weeks following a relatively benign respiratory or gastrointestinal illness with complaints of finger dysesthesias and proximal muscle weakness of the lower extremities. The weakness may progress over hours to days to involve the arms, truncal muscles, cranial nerves, and muscle of respiration.
Common complaints associated with cranial nerve involvement in GBS includes the following:
● Facial droop (may mimic Bell’s Palsy)
● Diplopias
● Dysarthria
● Dysphagia
● Ophthalmoplegia
● Pupillary disturbances
Clinical phases of GBS:
. Tingling on hand and feet
II. Difficulty in raising from chair
III. Areflexia, weakness, decrease DTR
IV. Respiratory monitoring
V. Mechanical ventilation
VI. Recovery/ Full activity
Most patients complain of paresthesia, numbness or similar sensory changes. Paresthesia’s generally begin in the toes and fingertips, progressing upward but generally not extending beyond the wrists or ankles. Pain associated with GBS is most sever in the shoulder girdle, back, buttocks and thighs and may occur with even the slightest movements. The pain is often described as aching or throbbing in nature.
Autonomic changes in GBS include following:
Tachycardia
● Bradycardia
● Facial flushing
● Paroxysmal hypertension
● Orthostatic hypotension
● Anhidrosis and/or diaphoresis
● Urinary retention