Bell's palsy is idiopathic disease, and is a disease of the peripheral nerves, which are acute, and attacking the facial nerve (N.VII) that innervate all the muscles of the face, causing weakness or paralysis of one side of the face. This leads to the asymmetry of facial paralysis as well as disrupt normal function.
What are causes of Bell's Palsy and how they can make it?
The exact cause of Bell's palsy is unknown. But the disease is considered to have a relationship with viruses, bacteria, and autoimmunity. Bell's palsy include inflammatory nerves or blockade signals muscular of HSV-1 through the career of the unknown, an imbalance of immunity (stress, HIV / AIDS, trauma) or anything that directly or indirectly suppress the immune system (such as a bacterial infection of Lyme disease and otitis media , or trauma, tumors, and congenital anomalies), and anything that can cause inflammation and edema of the facial nerve (N.VII) can trigger a bell's palsy.
Etiology
There are several theories that have been proposed, namely ischemic vascular theory and the theory of viral infection.
1. Theory of ischemic vascular
This theory was put forward by Mc Groven in 1955 which states that the autonomic instability with excessive sympathetic response. This causes spasm of the arterioles and venous stasis in the lower spinal canal. This causes ischemic vasospasm and the occurrence of edema. The result is a flaccid paralysis of the peripheral muscles of facial expression serving.
2. Theory of viral infection
This theory states that some of the causes of infections that can be found in cases of facial nerve paralysis are otitis media, bacterial meningitis, Lyme disease, HIV infection, and others. In 1972 McCromick mention that on the latent phase of HSV type 1 ganglion genikulatum may undergo reactivation when the immune system decreases. The existence of reactivation of this infection causes inflammatory reactions and facial nerve edema, so the pinched nerves and nerve cell death occurs because the nerves are not getting sufficient oxygen supply. In some mild cases, there is only damage to the myelin sheath of nerve.
3. Theory of a combination
This theory was put forward by stating that the possibility Zalvan Bell's palsy is caused by an infection or reactivation of herpes simplex virus and a secondary immunological reactions or due process, causing vascular inflammation and suppression of ipsilateral peripheral nerves.
There are several theories that have been proposed, namely ischemic vascular theory and the theory of viral infection.
1. Theory of ischemic vascular
This theory was put forward by Mc Groven in 1955 which states that the autonomic instability with excessive sympathetic response. This causes spasm of the arterioles and venous stasis in the lower spinal canal. This causes ischemic vasospasm and the occurrence of edema. The result is a flaccid paralysis of the peripheral muscles of facial expression serving.
2. Theory of viral infection
This theory states that some of the causes of infections that can be found in cases of facial nerve paralysis are otitis media, bacterial meningitis, Lyme disease, HIV infection, and others. In 1972 McCromick mention that on the latent phase of HSV type 1 ganglion genikulatum may undergo reactivation when the immune system decreases. The existence of reactivation of this infection causes inflammatory reactions and facial nerve edema, so the pinched nerves and nerve cell death occurs because the nerves are not getting sufficient oxygen supply. In some mild cases, there is only damage to the myelin sheath of nerve.
3. Theory of a combination
This theory was put forward by stating that the possibility Zalvan Bell's palsy is caused by an infection or reactivation of herpes simplex virus and a secondary immunological reactions or due process, causing vascular inflammation and suppression of ipsilateral peripheral nerves.
Etiology of Bell's Palsy |
Pathophysiology
Scientists, says that in Bell's palsy, an acute inflammatory process of the facial nerve in the temporal bone, around the foramen stylomastoid. Bell's palsy is almost always occurs unilaterally. Pathophysiology is unclear, but one theory is the process of inflammation in the facial nerve that causes an increase in the diameter of the facial nerve resulting in compression of the nerve at the time through the temporal bone. Facial nerve trip out of the temporal bone through the facial canal has narrowed like a funnel shape at the exit as the mental foramen. With such unique canal formation, inflammation, ischemic demyelinated or may cause disruption of conduction. Motor impulses are delivered by the facial nerve can be a disruption in the trajectory supranuclear, nuclear and infranuklear. Supranuclear lesions can be located on the face or in the primary motor cortex on the track or pathway cortikobulbar related associations somatotropic region faces in the primary motor cortex.
Nerve Route of Bell's Palsy |
Paralysis in Bell's palsy will occur from the upper and lower facial muscles completely paralyzed. Forehead not be crimped, palpebral fissure can not be closed and eyes closed in an attempt to look eyeballs turned upward. Corners of the mouth can not be removed. Lips can not shed and platisma not be moved. Because lagophtalmos, the tears could not be distributed fairly so buried. Symptoms such as ageusia and hyperacusis accompanist does not exist, because the facial nerve is pinched at the stylomastoid foramen is no longer contained the chordae tympani fibers and fibers that innervate the stapedius muscular.
RELATED ARTICLES
• Bell's Palsy
• Clinical Manifestations of Bell's Palsy
• Bell's Palsy Diagnosis
• Medical Treatment and Therapy of Bell's Palsy
• Complications and Prognosis of Bell's Palsy
MEDICAL BOOKS ABOUT BELL'S PALSY
RELATED ARTICLES
• Bell's Palsy
• Clinical Manifestations of Bell's Palsy
• Bell's Palsy Diagnosis
• Medical Treatment and Therapy of Bell's Palsy
• Complications and Prognosis of Bell's Palsy
MEDICAL BOOKS ABOUT BELL'S PALSY