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Trigeminal neuralgia: An enigma

Author: Dr. Altaf Malik H Department of Oral and Maxillofacial Govt. Dental College, Srinagar. Co-authors: Dr. Ajaz Shah A , Associate Professor and Chief, Department of Oral and Maxillofacial Govt. Dental College, Srinagar. Dr. Suhail Latoo Lecturer Department of Pathology and Oral Microbiology, Govt. Dental College, Srinagar. Dr. Manzoor Ahmad Malik J & K Health Services, SDH Banipora < / strong> Dr. Rubeena Tabasum Resident C. Hospital D, Srinagar. Dr. Shazia Qadir Department of Oral and Maxillofacial Govt. Dental College, Srinagar. Definition Trigeminal neuralgia (TN - tic) is a disorder of the fifth cranial (trigeminal) nerve that causes episodes of intense, throbbing pain of electric shock, as in areas where facial nerve branches are distributed - lips, eyes, nose, scalp, forehead, the upper jaw and lower jaw. In 1900, in a reference article, Cushing reported a method of removal Total trigeminal ganglion to treat TN. In 1912, Osler described TN as follows: In patients with advanced TN paroxysms in rapid succession and without assignable cause, and in the intervals, the patient may never be completely painless. They are initiated by almost any kind of external stimulus, eg an air stream, and the movement of facial muscles or tongue while speaking, contact with the skin, especially on points where pain seems to originate, and the act of swallowing, especially when the pain involves the area of the lining of the distribution of the nerve. This is not a self-limited disease. In some cases, the neuralgia reached such frightening intensity that makes the patient's life intolerable. In the past suicide was not a rare consequence.

Pathophysiology: Usually no structural lesion is present, although many researchers agree that the vascular compression, arterial or venous loops usually at the entrance of the trigeminal nerve in the pons is essential to the pathogenesis of idiopathic variety. This compression of the trigeminal nerve focal demyelination. Since the exact pathophysiology remains controversial, TN may have a central and / or peripheral etiology. CAUSES

It is not always possible to determine what causes trigeminal pain. However, several possibilities exist. nerve compression root> / strong>. The compression of the nerve root is now often regarded as the essential cause of classical trigeminal neuralgia. However, other opinions exist yet. In this case, a small blood vessel clip the root of the trigeminal nerve. The spasms may be due to the pulsation of blood vessel compressing the nerve even more. damage to the myelin sheath . Damage to the myelin sheath may cause pain of trigeminal. This type of damage usually occurs within the context of multiple sclerosis (MS). In a simple manner, the damage can be regarded as a kind of short-circuit the way it is presented in picture 2 (not included here, as I have no scanner, sorry ...). Normally, sensations of pain and heat are transmitted by different neural pathways. The myelin sheath of nerves isolates of these roads from each other. If myelin is damaged, different signals are mixed and thus identified as the nerve pain is something that would, for example, normally the impression of a light touch. Other . Accidents unsuccessfully dental work, or various infections can damage the trigeminal nerve. In this case, the mechanism of damage is probably similar to that of patients with MS. The chickenpox virus, which causes herpes zoster, can sometimes cause severe pain in the trigeminal. The pain is particularly difficult to treat. problems functional . Functional problems in the joints or bones of the face are often regarded as the cause of atypical facial pain. The bones of the jaw can press the nerve, and compression is perceived as pain. This pain then causes tension in the muscles of the face, causing the nerve to be squeezed even more tightly. It can be very difficult to break this vicious circle. reasons psychological . "The psychological reasons" are often cited as the underlying cause of atypical face pain. There is no doubt that psychological factors influence the patient's tolerance of pain and how he or she relates to it. Unfortunately, doctors often use these reasons as a kind of psychological weapon, and not attempt to address the real problem that causes pain. Chronic pain is certainly a person angry and depressed, and secondly there is no reason to assume that anger and depression are the cause of pain. frequency: United States: < ; / strong> According to Penman in 1968, the prevalence of TN is approximately 107 men and 200 women for 1 million people. Mauskop states that about 40,000 patients in the United States suffer from this disease at some point. The incidence is 4-5/100, 000. Rushton and Olafson found that about 1% of patients with multiple sclerosis (MS) develop TN, while Jensen et al reported that 2% of patients with TN have MS.

mortality / morbidity: TN is not associated with a shortened life. However, the morbidity associated with chronic and recurrent pain of the face can be substantial if the condition is not adequately controlled. People can choose to limit activities that precipitate pain, such as chewing or even lose weight in extreme circumstances. TN may evolve into a chronic pain syndrome, and patients may suffer from depression and loss from daily operation.

Race: No risk factors have been identified racial. Gender: The male-female ratio is 2:3. "/ P> Age: Age of onset is usually 60-70 years: thus, advanced age is a major risk factor. Patients who present with the disease when aged 20-40 years are more likely to suffer from demyelinating lesion in the pons secondary to MS. MS and hypertension are two risk factors found in epidemiological studies.

Criteria: Classical trigeminal neuralgia meets certain, quite specifically defined criteria. < spasmodic pain / strong>. The pain is short spasmodic attacks. It is often described as resembling electric shocks. A typical attack lasts only a few seconds. Several attacks can, however, succeed in minutes. The pain is, at worst, completely paralyzing. Location . Pain is usually very locally in the area of the trigeminal nerve does not radiate into other areas. The pain is almost always on one side of the face. Trigger Point . called trigger points are typical of trigeminal neuralgia. These are points in the face that if touched, even slightly, will trigger an attack of pain. These points can be located in the lips, on the side of the jaw, under the eye, eyelid, or anywhere where the trigeminal nerve happens. Trigger activities . If an activity causes a trigger point to be touched, it can launch an attack. For example, eating can become almost impossible. Weight loss is common in people with trigeminal neuralgia. Shaving, makeup, and even talking can become difficult. In certain cases, even a gust of wind can be enough to launch an attack. An attack can, however, also start without provocation. Discounts . reductions known, or painless periods, are typical of classic TN. This period can begin completely unpredictable and last for a few days to several weeks or months. In this case, the pain is completely absent and life does not feel in any way abnormal. Without the medical care of pain, however, generally appear again sooner or later. CLINICAL History: TN Clinical presentation appears as a throbbing unilateral facial pain that is triggered by similar activities or chewing or touching affected areas on the face. Patients can locate their pain accurately. The pain is not confined exclusively to one of three divisions of the nerve but most often along the line of demarcation is the maxillary and mandibular nerves or parts of the mandible and ophthalmic nerve. Among patients, 60% complained of throbbing pain shooting from the corner of the mouth to the angle of the jaw. Twitching of the pain of the upper lip or the canine eye and eyebrow, sparing the orbit itself, are experienced by 30% of patients. This distribution is the division between the first and second parts of the nerve. According to Patten, less than 5% of patients have ophthalmic involvement. Strictly unilateral, the disorder affects the right side of the face five times more often than the left. The pain is characteristic of stringent quality paroxysmal and lancinating. It starts with a sensation of electric shocks in an affected area, then quickly crescendos in less than 20 seconds to unbearable malaise felt deep in the face, often twisted expression of the patient. The pain begins to fade within seconds, giving way to a burning pain of a few seconds to several minutes. During crises, patients may face, hence the term tic douloureux. The number of attacks can vary from less than one per day, a dozen or more per hour, up to several hundred per day. Clearances fully reduced between attacks, even when they are severe and frequent. Thus TN is an exception to the rule that nerve injuries usually produce symptoms of constant pain and allodynia. If the pain is particularly common, patients can be difficult to consider at the height of an attack. A valuable clue for diagnosis is the onset of pain to certain activities. Patients carefully avoid rubbing your face or shaving a relaxation area, unlike other facial pain syndromes, in which they face massage or apply heat or ice. According to Sands, trigger zones, or areas of increased sensitivity, are present in half of patients and are often near the nose or mouth. In chewing, talking, smiling, or drink hot or cold liquids may initiate TN pain. Touching, shaving, brushing teeth, blowing the nose, or meet the cold air from a car window can also give rise to pain. Unlike migraine pain, people rarely suffer TN attacks during sleep, which is a key point in history. Patients with MS and TN have complaints similar to those of the idiopathic variety, except they have a much younger age (often <40 years). Some have atypical facial pain, without triggering areas, and without access memory nagging unease. As indicated above, AMT is not uncommon in MS, but it is rarely the first manifestation. In general, it occurs in advanced stages of MS. Natural history and prognosis after a first accident, the disease may remit for months and even years. Subsequently, attacks could become more frequent, more easily triggered, more disabling and may require medication long term. Patients may find immediate relief and satisfied with a single drug, most commonly carbamazepine. However, over the years, they may need a second or third drug to control breakthrough episodes and, finally, may need surgery. Procedures simpler, less invasive are generally well tolerated, but provide only short term relief. At this stage, other operations and perhaps more invasive may be required, and with these procedures, the risk of the negative effect of increasing off anesthesia dolorosa. Thus, the long-term prognosis of this disorder is variable. According to Fromm et al, some patients may have a syndrome neuralgia pretrigeminal for a period of several weeks or even years before symptoms develop customary TN. They complain of unrelenting pain sinuses or teeth that lasts for hours, triggered by movement of the jaw or drink. Not surprisingly, their first seek dental care. Some find benefit from baclofen or carbamazepine.

physics: In idiopathic TN, the results of neurologic examination were normal. sensation of face, masseter bulk and strength and corneal reflexes should be intact. No sensory loss is less checked immediately after an explosion of pain. Any area of permanent numbness excludes the diagnosis. The corneal reflex also must be intact. The loss of this reflex also excludes the diagnosis of idiopathic TN, unless a previous section of the trigeminal nerve was performed. The diagnosis of idiopathic TN is tenable only if no physical signs of the fifth nerve dysfunction are present. All the jaw or facial weakness or trouble swallowing suggests another etiology. In patients with MS or a structural lesion and TN, loss of sensitivity is often found during the examination. Any objective abnormality on neurological examination to exclude the diagnosis of idiopathic TN.

other considerations diagnosis are relevant TN. other pain syndromes including lancinating paroxysmal head less often glossopharyngeal neuralgia (GN) and occipital neuralgia (ON) syndromes. GN causes pain in the tonsillar fossa, posterior pharynx, and ear and may be initiated by coughing, yawning, or swallowing cold liquids. During acute attacks of this disease, which is frequently associated with underlying disease, the patient may be unable to speak and tries to avoid moving the lips or tongue. A sudden involuntary when attempting to reach the affected side of the face is diagnostic. ON causes pain in the posterior region of the head. Thus, the distribution of NT easily distinguished. Confusion arises only if the patient can not provide a clear history. According to Goadsby and Lipton, syndromes, paroxysmal hemicrania usually lasts a few seconds, similar to TN, but occur in and around the eye. Intense unilateral conjunctival injection and lacrimation signal an autonomous element, which further distinguishes this condition. This condition does not respond to carbamazepine. Migraine and cluster headaches may produce unilateral pain, but are not triggered by movement or contact with the face, nor do they respond quickly to carbamazepine. According Turp and Gobetti, atypical facial pain usually extends beyond the distribution of the fifth cranial nerve, is rarely triggered, and presents a constant relentless discomfo