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The main neurostomatological syndromes (neuralgias of Sphenopalatinum, Otic, Ciliary ganglions and angiotrophoneurosis) Facial pains can be the display of four processes: Trigeminal neuralgia and (rarely) Glossopharingeal neuralgia Facial forms of migraine, including cluster vascular pains Charlen and Sluder sympathalgia Psychogenic head pains Cranial neuralgias and central reasons of pain Trigeminal neuralgia It is characterized by short, intensive lancinating pain, recurring at frequent intervals and confined to one or more territories of Trigeminal nerve innervation. Trigeminal neuralgia Polyetiological disease, arising up mainly (90 % and more) in age senior 40 years. Among patients are women in 60-70 %. Frequent reasons: Mechanical compression of nerve Formation of sclerotic plate Infections in oral cavity Vascular malformations or tumors Basic lesions of brainstem Clinical features The second branch of Trigeminal nerve are usually involved – in 44 % cases, third – in 36 %, first – in 20 % cases. The repeated attacks usually arise up in the same zones of face Emotional and physical trauma can increase frequency of attacks through some time dull pain or feeling of burning appears in patients in inter attack period. Paresthesia with hypesthesia can appear only after injection-destructive treatment - signs of neuropathy Autonomic supplement of pain attack is observed less than in 1/3 patients Resistant autonomic disorders (changes of skin colour, desquamation, hypotrophy of soft tissue) can be only in patients, which had injection-destructive treatment CLINICAL MANIFESTATIONS SYMPTOMS Usually unilateral. Only 4% of patients complain on bilateral paroxysms The right side of the face is more often affected The third segment is more often affected than the second which, in turn, is more often affected than the first Brief paroxysms of intense, lancinating pain, seldom lasting longer than a minute are often triggered by cold, eating, speaking or touching the face (trigger zones) Typically, remission of pain occurs, lasting months or even years. Eventually, the pain becomes chronic Course Disease has typical remittent course Many patients do not complain on attacks months and years Disease course is with exacerbation and remission In the period of exacerbation patients answer on questions monosyllabically, barely opening slightly a mouth (the least motion of facial muscles can cause pain attack) During attacks patients stop beating The diagnosis of Trigeminal neuralgia is based on characteristic signs: Paroxysm of pain in area of face or forehead, lasting from a few seconds to 2 min localization of pain in area of one or a few branches of Trigeminal nerve Brief paroxysms of intense, lancinating pain, seldom lasting longer than a minute and absence in an inter attack period suggestion of pain from triggers zones (cold, eating, talk, washing, cleaning of teeth, speaking or touching the face ). stereotype of attacks for the same patient Distribution of trigger zones. Thus on the basis of information of somatic and neurological inspection, and if necessary instrumental, must be eliminated other reasons of head and facial pain, local processes in nasal sinuses, teeth, jaws, pharynx or basis of skull. Glossopharyngeal neuralgia Meets rarely. Typical short paroxysms of pain centered in throat or the base of the tongue, tonsils Typically triggered by swallowing (especially cold solution), cough, mastication, talk, yawning Sometimes pain irradiated in ear and neck, or only in ear (Oticalgic form) Glossopharyngeal neuralgia Triggers zones - touch to the soft palate or tonsils, sometimes by pressure on ear Attack lasts a few seconds or minutes and can be associated with bradycardia, falling BP, sometimes syncope Especially often syncope happen at neuralgia due to tumour of pharynx Disorders of sensitiveness or paresis are absent Often there are spontaneous remission from a few months to a few years Combination with Trigeminal neuralgia is possible (compression of both nerve by complete arched vessel) Differential diagnosis Sometimes a similar pain syndrome is marked at the: Tumour of pharynx (including nasopharynx), tongue, posterior cranial fosse Tonsillitis Paratonsilar abscess Hypertrophy of processus stiloideus. In last case pain increases at the turn of head Neurinoma of Glossopharyngeal nerve is observed exceptionally rarely A symptomatic neuralgia it is necessary to suspect for young people with permanent pains and symptoms of neurological deficit Treatment are same, as well as at Trigeminal neuralgia Neuralgia of Upper laryngeal nerve Characterized by paroxysmal one-sided or bilateral pain in larynx (usually at the level of upper part of Thyroid cartilage or hyoid) and corner of mandible Irradiation in eye, ears, thorax and forearm Pain is associated with hiccup, hypersalivation, cough Pains are provoked by swallowing, yawning, cough, blowing, motion of head. Some neuralgias of Upper laryngeal nerve are coursed by malformations of neck Karbamazepin (Finlepsin) and local anesthesia in hyoid thyroid membrane are effective Facial sympathalgias Is the group of the similar clinical states As a rule they have paroxysmal courses and normal state between attacks Attacks lasts from ten minutes to days (rarely) Typical is an acute, often unendurable pain in face of burning, holding apart, pressing, sometimes pulsating character The important clinical sign are autonomic signs on the side of pain: Lacrymation Conjunctival injection Rhinorrhoea from one half of nose and nasal obstruction Forehead and facial sweating Syndrome meets more frequent among men Attacks happen up acutely, mainly at nights, the sharpest pain does make a patient to move, because at peace pain becomes yet sharper Facial sympathalgias are expression two on principle different forms of pathology: 1) 2) 3) 1) 2) 3) Sympathalgic syndromes (lesion of autonomic peripheral ganglions and nerves) Nasal-ciliary neuralgia – Charlen syndrome Pterygopalatal neuralgia – Sluder syndrome Neuralgia of Large Petrosal superficial nerve – Gartner syndrome Vascular syndromes, as migraine: Cluster headache Cluster-effect (Horton histamine migraine, Garris migrainous neuralgia) Glyazer Carotid syndrome Sympathalgic syndromes, due to lesion of autonomic peripheral ganglions and nerves Pathogenesis Sympathalgic syndromes (Charlen and Sluder) are caused by pathological process of peripheral autonomic ganglions or their irritation. The aetiology is not enough clear. Herpetic rash in case of Charlen syndrome tells about herpetic ganglionitis of nasal-ciliary ganglion Etiology of Pterygopalatine sympathalgia is nasal sinus infection (in particular, in maxillary sinus) and lesion of ganglion pterygopalatine Charlen syndrome (Ciliary neuralgia) Typical attack of one-sided pain in internal corner of eye and base of the nose, in an eyeball Irradiation in a nose Rhinorrhoea and nasal obstruction Conjunctival injection, blepharospasm Pain is typically observed in internal corner of eye Usually an attack is associated with acute lacrymation, changes in frontal parts of eyeball, cornea (phenomena of keratitis or iritis) Herpetic exanthema at skin of the nose The Charlen syndrome should be differentiated with Herpetic ganglionitis of Trigeminal (Gasserii) ganglion, manifest symptoms in area of I Trigeminal branch innervation. Expressed autonomic supplement is not typical. Sluder syndrome (neuralgia of ganglion pterygopalatal) Pain is localized in base of the nose, maxilla, teeth, tongue, soft palate, ear, neck-shoulder area Then with irradiation in an eye and temple Sometimes there is reduction of muscles of soft palate (typical clatter) The attack of pain begins and finishes gradually Course of attack is quite long Certain periodicity is absent Pain is of middle severity with out motor anxiety After an attack - paresthesia in face and noise in ear are observed. Differential diagnosis Typical signs of neuralgia: one-side autonomic features. one-side oedema of face in the attack period. Differential diseases: Kvinke Angiotrophoneurotic oedema: Typical localization in lips, cheeks, bilateral oedema does not cause diagnostic difficulties Local oedema of orbit: oedema yet and pain syndrome Angiotrophic oedema in channel of Facial nerve conduce to insufficiency of Facial nerve. Recurrence of Facial neuropathy in combination with a plicate tongue, heilitis is determined as disease of Rossolimo-Melkerson-Rozental Treatment Application of autonomic tropic drugs (ganglioblockercs – Pyrroxanum) – uninnervation effect on the ganglion Antiepileptic drugs - Carbamazepinum (Tegretol, Finlepsin) Psychotropic medications - tranquilizers and antidepressants Effectively in acute period greasing a cocaine or lidocaine of middle nasal cavity Novocaine or Lidocaine blockade of autonomic ganglions Vascular syndromes Vascular syndromes meet considerably more frequent – at great part of patients with so-called Facial sympathalgias. They manifests by the attacks described before Meet more frequent for men Cluster-syndrome Horton Histamine migraine, Harris migraines neuralgia Term «Cluster headache» (CH) is most correct, as reflects the characteristic features of disease and shuts out mixing of him with a migraine Etiology The etiology is unknown. In basis of diseases are paroxysmal dilatation of branches of Carotids, deficit of sympathetic innervation of vessels with the increase (rarer decrease) of local cerebral blood circulation. Epidemiology The condition is considerably less common than migraine, perhaps 50 times less, although not so in the author's own out-patient series Approximately 80% of patients are male A family history of the condition occurs in about 2% of cases Mean age of onset is in the late twenties(20-40) Rarely, comparable cases have evolved in association with a structural brain lesion, often located around the cavernous sinus Symptoms of Cluster headache Unilateral pain (although it may transfer sides in subsequent attacks) It is orbital or peri-orbital but occasionally radiates ipsilaterally to the forehead, jaw or neck. Continuous, characteristically intense Attacks last from 15 to 180 min and usually occur once or twice a day Alcohol can trigger the pain Nausea may occur but vomiting is rare The paroxysms typically occur at the same time of the day or night. The pain is not usually pulsation but more continuous Autonomic manifestations They include the following: Lacrimation Conjunctival injection Rhinorrhoea or nasal obstruction Altered forehead sweating Homer's syndrome Horner's syndrome during an attack of cluster headache. Clinical course Typically, bouts of pain last for a few weeks, then remit but return at intervals thereafter. Chronic cluster headache is defined as a headache phase persisting beyond 12 months. Criteria for diagnosing CLUSTER HEADACHE At least five attacks fulfilling the following criteria: 1. Severe unilateral orbital, supra-orbital and/or temporal pain lasting 15-180 min untreated 2. Headache is associated with at Least one of the following signs ipsilateral to the headache: Conjunctival injection Lacrimation Nasal congestion and Rhinorrhoea Forehead and facial sweating Miosis Ptosis Eyelid edema 3. Frequency from every other day to eight each day CLUSTER HEADACHE Cluster headache is strictly unilateral and concentrated round the eye Typically it is accompanied by a number of autonomic signs Ergotamine, oxygen and sumatriptan are effective for attacks Prophylactic agents used include ergotamine, lithium and corticosteroids CHRONIC PAROXYSMAL HEMICRANIA A rare condition Predominating in women Typical very frequent, short-lived attacks of pain occur of a type similar to cluster headache Autonomic symptoms are common Indometacin, in a dose of approximately 150 mg/day, aborts the attacks within 48 h. In most patients, the attacks become chronic. IDIOPATHIC STABBING HEADACHE Defined as recurrent, very brief, stabbing pains, usually confined to the head, occurring singly or in runs. They tend to occur in subjects with migraine. They respond to regular indomethacin therapy Differential diagnosis CRANIAL ARTERIITIS Also known as temporal or giant cell arteritis. This is a granulomatous inflammation of the medium and large-sized arteries of the cranium and elsewhere. Within the cranium, the arteritis is confined to those arteries possessing an internal clastic lamina The loss of vision is the consequence of involvement of the posterior ciliary artery leading to anterior ischaemic optic neuropathy. Epidemiology The condition is rare under the age of 50 years The mean age at diagnosis is approximately 70 years The condition is slightly more common in women and almost confined to Caucasians Cranial arteritis. Superficial temporal artery biopsy showing (a)intimal thickening and medial damage and (b) giant cells with inflammatory cell infiltration in the internal elastic lamina. Symptoms of Cranial arteritis Headache, usually localized Pain on chewing (jaw claudication) General malaise Proximal muscle stiffness and pain Visual loss Clinical manifestations symptoms Headache occurs in the vast majority of patients It particularly localizes to one or other temple but may be more generalized Constant, boring, intense pain, exacerbated by contact - brushing the hair and also by exposure to cold, pain on chewing occurs (jaw claudication) Many patients feel generally unwell, with malaise, anorexia, weight loss and night sweats Stiffness and pain in the shoulder and pelvic girdle muscles (polymyalgia rheumatica) may antedate or coincide with the headache or appear as a separate entity Before persistent visual loss there may be amaurosis fugax Clinical manifestations - signs The scalp vessels are tender and thickened Pulsation is reduced more often than it is absent Scalp necrosis is rare. The optic disc is swollen and later pale Ophthalmoplegia is sometimes seen either as a sixth nerve or a pupil-sparing, third nerve palsy. Stroke incidence is low. Rarely, involvement of the aortic arch or of the mesenteric or limb vessels is symptomatic Cranial arteritis. Thickened superficial temporal artery Cranial arteritis. Fundus photograph showing ischaemic optic neuropathy in the acute phase. Therapy Corticosteroid therapy should be started immediately while biopsy is being arranged There are advocates of both high-dose and low-dose regimes initially (e.g. 60 mg or 20 mg daily of prednisolone). Eventually, patients are maintained on 7.5-10 mg daily. The condition tends to resolve after 12-24 months, when treatment can be withdrawn, though some authorities advocate long-term therapy. Cranial arteritis Cranial arteritis is an important condition to exclude in an elderly patient with a newly acquired headache The affected arteries are tender but usually still pulsatile The erythrocyte sedimentation rate is usually markedly elevated but rarely normal Corticosteroids are the drugs of choice TEMPOROMANDIBULAR JOINT DYSFUNCTION degenerative changes in the temporomandibular joint are associated with pain in the jaw sometimes referred to the ear or temple. The pain is exacerbated by chewing. Pain in a similar distribution, without evidence of joint derangement, has been attributed to abnormal activity of the jaw muscles, cither triggered by malocclusion of the jaw or the result of excessive jaw contraction in an anxious individual. Treatment is symptomatic.