NR 603 Week 1- Compare & Contrast Assignment(V1)-
Trigeminal Neuralgia & Giant Cell Arteritis
During week one, the comparisons of Trigeminal Neuralgia and Giant Cell Arteritis is
discussed. These diseases have similar and dissimilar signs and symptoms. This discussion will
compare and contrast areas on presentation, pathophysiology, assessment, diagnosis, and
treatment of both issues. Overall, a thorough history and physical exam will be needed to
determine a definitive diagnosis.
Trigeminal neuralgia (TN) presents as a chronic condition invading the trigeminal nerve.
This nerve carries sensation impulses from the face to the brain. Slightly affected sensations can
trigger a sudden experience of excruciating pain. The pain attacks can last for a short period or
can progress to more frequent periods of agonizing pain. There are many treatment options, and
the patient will not have to suffer from pain (Zakrzewska & Linskey, 2016).
Giant cell arteritis (GCA) is also known as temporal arteritis. GCA is an inflammation of
the artery lining most often in the temples of the head. This disease like TN can cause sudden
pain and tenderness in the head, scalp, and jaw. GCA, unlike TN, can lead to vision problems
ultimately causing blindness left untreated (Roberts & Clifford, 2017).
The pathophysiology for TN is unknown but can be related to abnormalities in the
afferent neurons of the trigeminal nerve. Researchers believe that symptoms are contributed to
nerve compression and damage can create hyperexcitability along the axons. This
hyperexcitability leads to the jolt of pain experienced by the patient (Vasappa, Kapur, &
Krovvidi, 2016).
More specifically, TN is thought to be demyelination of the trigeminal nerve root where
the pathway meets the pons. The A-β fibers, which control touch sensations, and the β fibers, which control touch sensations, and the A-β fibers, which control touch sensations, and the δ and C
fibers, which control pain sensation, lie close to each other. The fiber compressions and
demyelination nearby initiates an ephaptic cross-β fibers, which control touch sensations, and the talk between them. (Vasappa, Kapur, &
Krovvidi, 2016).
The pathophysiology of GCA is different than TN because it a disease caused by
inflammation not demyelination of nerves. Inflation is considered vasculitis and can be
localized, multifocal, or widespread. In GCA the elasticity of the arteries in the temporal,
cranial or carotid systems is affected. Mononuclear cells will infiltrate and attack the arteries
involved disrupts the elasticity. The artier becomes thickened and occludes the lumen (Roberts
& Clifford, 2017).
Trigeminal Neuralgia & Giant Cell Arteritis
During week one, the comparisons of Trigeminal Neuralgia and Giant Cell Arteritis is
discussed. These diseases have similar and dissimilar signs and symptoms. This discussion will
compare and contrast areas on presentation, pathophysiology, assessment, diagnosis, and
treatment of both issues. Overall, a thorough history and physical exam will be needed to
determine a definitive diagnosis.
Trigeminal neuralgia (TN) presents as a chronic condition invading the trigeminal nerve.
This nerve carries sensation impulses from the face to the brain. Slightly affected sensations can
trigger a sudden experience of excruciating pain. The pain attacks can last for a short period or
can progress to more frequent periods of agonizing pain. There are many treatment options, and
the patient will not have to suffer from pain (Zakrzewska & Linskey, 2016).
Giant cell arteritis (GCA) is also known as temporal arteritis. GCA is an inflammation of
the artery lining most often in the temples of the head. This disease like TN can cause sudden
pain and tenderness in the head, scalp, and jaw. GCA, unlike TN, can lead to vision problems
ultimately causing blindness left untreated (Roberts & Clifford, 2017).
The pathophysiology for TN is unknown but can be related to abnormalities in the
afferent neurons of the trigeminal nerve. Researchers believe that symptoms are contributed to
nerve compression and damage can create hyperexcitability along the axons. This
hyperexcitability leads to the jolt of pain experienced by the patient (Vasappa, Kapur, &
Krovvidi, 2016).
More specifically, TN is thought to be demyelination of the trigeminal nerve root where
the pathway meets the pons. The A-β fibers, which control touch sensations, and the β fibers, which control touch sensations, and the A-β fibers, which control touch sensations, and the δ and C
fibers, which control pain sensation, lie close to each other. The fiber compressions and
demyelination nearby initiates an ephaptic cross-β fibers, which control touch sensations, and the talk between them. (Vasappa, Kapur, &
Krovvidi, 2016).
The pathophysiology of GCA is different than TN because it a disease caused by
inflammation not demyelination of nerves. Inflation is considered vasculitis and can be
localized, multifocal, or widespread. In GCA the elasticity of the arteries in the temporal,
cranial or carotid systems is affected. Mononuclear cells will infiltrate and attack the arteries
involved disrupts the elasticity. The artier becomes thickened and occludes the lumen (Roberts
& Clifford, 2017).
