Tuesday, May 15, 2012

Lupus & Trigeminal Neuralgia & Cervical Spine OA, OH MY!

Do You Happen To Have Lupus(SLE)or another AI Disorder and Trigeminal Neuralgia?
Do You Have Cervical Spine Osteoarthritis or a Neck Injury?
If you do, YOU ARE NOT ALONE!  There's dozens of us out there!  Let's band together to learn about possible treatments and find physicians who specialize in these rare conditions!  We want to hear YOUR story!!!

Do You Have Trigeminal Neuralgia?
Do You Have Geniculate Neuralgia?
Do You Have or Have You Ever Had Burning Mouth Syndrome?
Have You Had Bells Palsy?
Do You or Have You Ever Had Distortions With Taste and/or Smell?
Do You Have Torticollis Spasms or Cervical Dystonia?
Do You Have Lupus?
Do You Have Frequent Infections, like Herpes Simplex?

Without knowing why we have the conditions, how will we be treated for it?

Here are some known causes for cranial neuralgias:
  1. Blood vessels pressing on the root of the trigeminal nerve
  2. Pressure on the trigeminal nerve from multiple sclerosis or a tumor
  3. Multiple sclerosis causing damage to the myelin sheath protecting nerves
  4. Damage to the cervical spine: inflammatory processes causing disc herniations and bony spurs causing pressure on cranial nerve XI, (the accessory nerve) is known to cause torticollis spasms
  5. Tumors, lesions or cancer in the brainstem
  6. Postherpatic Neuralgia: herpes zoster shingles virus reactivation complications
  7. Physical damage to the nerve - this may be the result of injury, a dental or surgical procedure, or infection.
  8. Cervical spinal surgery can cause damage to associated nerves, for example hemofacial spasms.
  9. Family history (genes, inherited) - 4.1% of patients with unilateral trigeminal neuralgia (affects just one side of the face) and 17% of those with bilateral trigeminal neuralgia (affects both sides of the face) have close relatives with the disorder. Compared to a 1 in 15,000 risk in the general population, 4.1% and 17% indicate that inheritance is probably a factor. 
  10.  Vitamin B Defiency
  11.  Hypothyroism 
  12.  Most scientists believe that in Bells Palsy, a condition of cranial nerve 7 that a viral infection such as viral meningitis or the common cold sore virus - herpes simplex - causes the disorder. They believe that the facial nerve swells and becomes inflamed in reaction to the infection, causing pressure within the Fallopian canal and leading to an infarction (the death of nerve cells due to insufficient blood and oxygen supply). In some mild cases (where recovery is rapid), there is damage only to the myelin sheath of the nerve. The myelin sheath is the fatty covering-which acts as an insulator-on nerve fibers in the brain.(info from national institute of neurological disorders)
  13. Intracranial dolichoectasias:  In cases involving the Basilar Artery, (VBD) the pathogenesis arises from direct compression of the cranial nerves.  Symptoms include hemofacial spasm, trigeminal neuralgia and paresis. As the arrangement of the connective tissue is disturbed, the vessel wall is no longer able to hold its original conformation
  14. Cranial Nerve Palsies from Oral Cancer
  15. Cavernous Sinus Syndrome 
  16. Diabetic Neuropathy 
  17. Sjogren's Syndrome (mixed connective tissue disease) See http://www.lupusuk.org.uk/latest-news/102-sjogrens-syndrome-systemic-features 
  18. Vasculitis and Nerve Compression Syndromes (from the National Institute of Neurological Disorders and Stroke)

Possible non-confirmed causes for cranial neuralgias:
  1. Systemic lupus erythematosus and other autoimmune disease can cause inflammation causing damage to the myelin sheath protecting nerves
  2. Herpes simplex 1 Virus reactivation in cranial nerve ganglions
  3. Inflammation from cervical injury or severe osteoarthritis causing damage to the trigeminal nerve and multiple cranial nerves
  4. Connective tissue disease can cause damage to the carotid artery and vertibral vasilar artery which puts pressure on the cranial nerves

The discs that form the cervical area are made from connective tissue, which undergoes gradual disc degeneration-or spondylolysis as it is formally called- due to small injuries that do not represent a great discomfort, but over time may provoke more serious injuries that do cause immediate pain and dysfunction.
And how does this process occur? As we grow old, our discs start loosing the water and its sock absorbing ability. The first thing that happens in a neck disc is the appearance of tears in the outer ring or annulus with no visible symptoms at all and gets healed forming scar tissue. Scar tissues are weak tissues that make the disc more prone to wear.

The continuous wearing of the disc starts reducing the gap between each vertebra, producing a collapse that affects the facet joints (bony knobs) on the back of the column. Since bones can not fit properly, there is produced a pressure on the articular cartilage that may result in osteoarthritis.

When ache pain becomes chronic, it is referred as mechanical Wry Neck due to the fact that our neck gets worse every time we move our neck, which is possible by means of the mechanical parts of the neck that allow the neck to twist and bend. This pain seems to be originated by the inflammation of the facet joints and the disc degeneration. When the inflammation grows, our neck muscles respond with spasms in an attempt to stop the movement of the cervical area. 

You can realize you are suffering from a cervical condition if you present:

-    Moderate to acute Wry Neck
-    Headaches
-    Numbness, pain and slow reflexes in shoulders, arms and hands
-    Decrease motion of neck, numbness
-    Walking problems

Nevertheless, it is a physician the ones who can establish a secure diagnose of your condition after a series of examinations that include a physical examination, X-rays, Magnetic Resonance Imaging (MRI), Computer Assisted Tomography (CAT Scan), Electromyogram (EMG), Myelography (Myelogram), Bone Scan and laboratory tests.
Motor innervation occurs through the glossopharyngeal nerve (IX), the vagus nerve (X), the allied spinal accessory nerve (XI), and the recurrent laryngeal nerve. Sensory innervation in the oropharynx section occurs as a result of the glossopharyngeal nerve (IX), with the vagus nerve (X) providing for the nasopharynx and the hypopharynx/laryngopharynx. As the sensory fibers from the glossopharyngeal nerve (IX) and the vagus nerve (X) enter the brainstem they are bundled together and terminate in the trigeminal nucleus. The trigeminal nerve (CN5) is responsible for creating a complete sensory map of the face and mouth with pain, touch, temperature and position signals all processed through this nerve. Accordingly, trigeminal neuralgia as a result of disc herniation, disc bulging, spondylolisthesis and spinal kyphosis or slippage, amongst other conditions, can be responsible for serious problems with the innervation of the face, jaw, and pharynx. Facial pain, jaw pain, neck pain, problems with chewing and swallowing, a sensation of a lump in the throat, and muscular spasms in the face, jaw, and neck can all result from compression of the cervical spinal nerves.

Cervical Spinal Nerves

The hypopharynx’s uppermost point is at the hyoid bone, which lies at approximately the same level as the 4th-6th cervical vertebrae. The pharynx is innervated by a number of nerves with their roots in the cervical spine. Damage to these nerve pathways can result in problems with the correct functioning of all three sections with ramifications for proper control of the separation of the larynx and oesophagus. Faults in innervation, both motor and sensory, in this area may prevent the two pathways functioning properly.

Intracranial dolichoectasias
From Wikipedia, the free encyclopedia
The term dolichoectasia means elongation and distension. It is used to characterize arteries throughout the human body which have shown significant deterioration of their tunica intima (and occasionally the tunica media), weakening the vessel walls and causing the artery to elongate and distend.
Most commonly caused by hypertension, continued stress on the walls of the artery will degrade the vessel wall by damaging and loosening the collagen and elastin meshwork which comprises the intima. Similarly, hypercholesterolemia or hyperlipidemia can also provide sufficient trauma to the vessel wall resulting in dolichoectasia. As the arrangement of connective tissue is disturbed, the vessel wall is no longer able to hold its original conformation and begins to unravel due to the continued hypertension. High blood pressure mold and force the artery to now take on an elongated, tortuous course to better withstand the higher pressures.
Most commonly affected is the Vertebral Basilar Artery (Vertebral Basilar Dolichoectasia or Vertebrobasillar Dolichoectasia). The Internal Carotid Artery is also at high risk to be affected. Patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) are more likely to be subject to dolichoectasias. Dolichoectasias are most common in elderly females.
In cases involving the Basilar Artery (VBD), the pathogenesis arises from direct compression of different cranial nerves.

Fig. 1: Dolichoectasia of the suprasellar segment of the left internal carotid artery with compression of the optic chiasm

Fig. 2
Additionally, ischemic effects on the brain stem and cerebellar hemispheres as well as symptoms related to hydrocephalus are common. Direct cranial nerve compression can lead to isolated cranial nerve dysfunction, usually associated with a normal-sized basilar artery that is tortuous and elongated. Cranial nerve dysfunction most commonly involves the VII cranial nerve and the V cranial nerve. Multiple cranial nerve dysfunction is far more likely to occur if there is dilation (ectasia) associated with a tortuous and elongated basilar artery. Cranial nerves affected in descending order of frequency include: VII, V, III, VIII, and VI.
Internal Carotid Artery dolichoectasia is particularly interesting because the artery normally already contains one hairpin turn. Seen in an MRI as two individual arteries at this hairpin, a carotid artery dolichoectasia can progress so far as to produce a second hairpin turn and appear as three individual arteries on an MRI. In the case of a dolichoectasia of the Internal Carotid Artery (ICD), the pathogenesis is primarily related to compression of the Optic Nerves at the Optic Chiasma.  (fig 1 and 2)
Signs and Symptoms
  • Progressive Visual Field Defect
A combination of lifestyle modifications and medications can be used for the treatment of dolichoectasias.
2. MedPix

Quote From The Cleveland Clinic, Center For Disease Management On     LUPUS & CRANIAL NEUROPATHIES

Bridget Wright,   Swati Bharadwaj,   Abby Abelson

 Neuropathies can be peripheral, autonomic, or cranial. Wrist drops and foot drops occasionally result from peripheral nerve vasculitis. Besides an electromyogram (EMG), a nerve biopsy could also be obtained. For EMG-positive peripheral neuropathy, initial treatment is typically higher doses of prednisone, especially in patients with sensorimotor loss, along with neurontin or tricyclic antidepressants. Steroid-sparing agents such as imuran may be used thereafter. If the EMG is negative, neurontin or a tricyclic antidepressant should suffice. With cranial neuropathies, the mainstay of treatment is higher doses of prednisone.

Cranial Nerve Functions
Disorder of sensory and/or motor function of a specific cranial nerve(s).
Diagnostic criteria:
Syndrome corresponding to specific nerve function:
  1. Olfactory nerve: Loss of sense of smell, distortion of smell, and loss of olfactory discrimination
  2. Optic nerve: Decrease or loss of visual acuity, diminished color perception, afferent pupillary defect and visual field deficits
  3. Oculomotor nerve: Ptosis of the upper eyelid and inability to rotate eye upward, downward, or inward (complete lesion), and/or dilated nonreactive pupil and paralysis of accommodation (interruption of parasympathetic fibers only)
  4. Trochlear nerve: Extorsion and weakness of downward movement of affected eye
  5. Abducens nerve: Weakness of eye abduction
  6. Trigeminal nerve: Paroxysm of pain in lips, gums, cheek, or chin initiated by stimuli in trigger zone (trigeminal neuralgia) and sensory loss of the face or weakness of jaw muscles
  7. Facial nerve: Unilateral or bilateral paralysis or facial expression muscles, impairment of taste, and hyperacusis (painful sensitivity to sounds)
  8. Vestibulo-cochlear nerve: Deafness, tinnitus (cochlear), dizziness and/or vertigo (vestibular)
  9. Glossopharyngeal nerve: Swallowing difficulty, deviation of soft palate to normal side, anesthesia of posterior pharynx and/or glossopharyngeal neuralgia (unilateral stabbing pain in root of tongue and throat, triggered by coughing, sneezing, swallowing, and pressure on ear tragus)
  10. Vagus nerve: Soft palate droop, loss of the gag reflex, hoarseness, nasal voice, and/or loss of sensation at external auditory meatus.
  11. Accessory nerve: Weakness and atrophy of sternocleidomastoid muscle and upper part of trapezius muscle.
  12. Hypoglossal nerve: Paralysis of one side of tongue with deviation to the affected side
  • Skull fracture
  • Tumor: meningioma, carcinomatous meningitis, aneurysm
  • Infection: herpes zoster, neuroborreliosis, syphilis, mucormycosis
  • Miller Fisher syndrome
  • Nutritional: thiamine deficiency
  • Metabolic: diabetes mellitus
  • Inflammatory: multiple sclerosis
  • Ischemic: giant cell arteritis, brainstem stroke
  • Infiltrative: sarcoid

I am not a medical professional, so please do not substitute this medical information for seeing your physician or specialist.  :)

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