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In: Dyck PJ 1mg finasteride otc hair loss news, Thomas PK buy cheap finasteride 5 mg line hair loss cure 2013, Griffin JP, Low PA, Podusl JF (eds) Peripheral neuropathies. Saunders, Philadelphia, pp 836–868 Scherer H (1986) Nervus vestibulocochlearis. In: Schmidt D, Malin JC (eds) Erkrankungen der Hirnnerven. Thieme, Stuttgart, pp 186–218 67 Glossopharyngeal nerve Genetic testing NCV/EMG Laboratory Imaging Biopsy + Branchial motor: stylopharyngeus muscle. Quality Visceral motor: otic ganglion, fibers to stimulate the parotid gland. General sensory: posterior one third of the tongue, skin of the external ear, and the internal surface of the tympanic membrane. Special sensory: taste, from the posterior third of the tongue. The nuclei consist of: the nucleus ambiguus, inferior salivatory nucleus, and Anatomy nucleus solitarius. The nerve emerges from the medulla oblongata at the dorsal border of the inferior olive. A dural isthmus separates the nerve from the vagus nerve. It leaves the cranial vault through the jugular foramen (jointly with the vagus and accessory nerves), and passes in the upper neck between the carotid artery and jugular vein. Then it passes superficially to the internal carotid artery behind the styloid process. The nerve follows the posterior inferior part of the stylopharyn- geus muscle, between the constrictors of the pharynx, and finally reaches the deep hypoglossus muscle. Its extracranial course includes several ganglia (superior and petrous ganglia). Lesions can cause minor swallowing difficulties, disturbance of taste, glos- Symptoms sopharyngeal neuralgia (rare: pain behind the angle of the jaw, deep within the ear and throat). Abnormal lacrimation (“crocodile tears”) may occur, but may also be a complication of Bell’s palsy with lesions proximal to the geniculate ganglion. Taste on the soft palate, pharynx, fauces, and posterior third of tongue is Signs disturbed. Salivary production of the parotid gland can be reduced. Acute sectioning bilaterally may cause hypertension. Lesions are rarely isolated, and more often associated with vagus nerve lesions. Pathogenesis Topographical: Brainstem: vascular brainstem lesions (e. Meningitis, “polyneuritis cranialis”, AIDP Exit from the cranial vault: jugular foramen syndrome (with CN X, XI; Vernet’s syndrome) caused by: chordoma, fracture of base of skull, neuroma, metastasis. Neck (iatrogenic): carotid operations, resection of aneurysms, neck dissection ear nose and throat (ENT and neurosurgical procedures). Metabolic: Amyloid-deposition Porphyria Toxic: Nitrofurantoin Tetanus toxin Vascular: Brainstem lesions Infectious: Diphtheria Herpes zoster Polio Inflammatory and immune mediated: AIDP Cryoglobulinemia Miller Fisher syndrome Periarteritis nodosa Sarcoid Serum sickness SLE Neoplastic: Leptomeningeal carcinomatosis Leukemia Myeloma Vagal rootlet neuroma Surgery: Tonsillectomy (rare) Trauma: Basal fracture of skull Association with neuropathies: AIDP Diphtheria Paraneoplastic 69 Glossopharyngeal neuralgia is a rare occurrence, much less frequent than trigeminal neuralgia. Pain radiates into the ear, pharynx, neck and the base of the tongue. Diagnosis is made by examination, and subsequent imaging and laboratory Diagnosis tests that may be helpful in identifying suspected causes. Bulbar muscular disorders Differential diagnosis Motor neuron disorders Myasthenia gravis Pain: trigeminal neuralgia For neuralgia: amytriptyline, carbamazepine, gabapentin Therapy Kumral E, Afsar N, Kirbas D, et al (2002) Spectrum of medial medullary infarction: clinical References and magnetic resonance imaging findings. J Neurol 249: 85–93 Newsom-Davies J, Thomas PK, Spalding JMK (1984) Diseases of the ninth, tenth, eleventh, and twelfth cranial nerves. In: Dyck PJ, Thomas PK, Bunge R (eds) Peripheral neuropathy.

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More complex discharges from the motor unit are fascicula- tions discount finasteride 5 mg with visa female hair loss in male pattern, myokymia purchase 1mg finasteride with mastercard hair loss in men xxy, neuromyotonia, and the discharges of muscle-cramps and tetany. CRDs stem from electrically linked muscle fibers, firing in a synchro- nous pattern. These MUAPs have a variable duration, depending on the method of assessment (concentric needle, monopolar, or single fiber technique), and depend on the muscle and the age of the patient. At mild contraction the duration is usually in the range of 5 to 15 ms, has up to four phases, and an amplitude between 300–3000 µV. For the assessment of MUAPs, duration is more constant and reliable than amplitude. Maximum contraction produces overlapping MUAPs, called an interference pattern under normal conditions. The spectrum of pathologic abnormalities ranges from individual MUAPs firing in neurogenic conditions, to a full interference pattern with low amplitude in myopathies. Types of pathological discharges: Fasciculations resemble MUAPs in configuration, but have an irregular dis- charge pattern. They may be linked with a visible or palpable muscle twitch. They can be benign, or occur as part of a neuromuscular condition and are notably increased in ALS. CRDs (“bizarre high frequency discharges”) are caused by groups of adjacent muscle fibers discharging with ephaptic spread from one fiber to another. They are usually seen in chronic neurogenic and myopathic disease processes. They typically begin and end abruptly, and have a frequency of 5–100 Hz. The frequency does not change and contrasts with the waning and waxing pattern of myotonia. Myotonic discharges are induced by mechanical provocation (needle, percus- sion). They are independent repetitive discharges of muscle fibers at rates of 20 to 80 Hz. The amplitude and frequency wane characteristically. They occur in myotonic dystrophy, myotonia congenita, paramyotonia congenita, hyperkalemic periodic paraly- sis, acid maltase deficiency, and myotubular myopathy. Neuromyotonia are bursts of multiple spikes, discharging in high frequency (up to 300 Hz). The frequency remains constant, but the amplitude slowly decreas- es. Sometimes groups of normal appearing MUAPs are called neuromyotonia, but may also be classified as myokymia. Myokymia is a burst of motor unit potentials (resembling normal MUAPs), and appearing in groups separated by intervals of silence. Focal myokymia is often associated with radiation damage. Cramp discharges are involuntary muscle discharges, consisting of multiple MUAPs that originate from an involuntary tetanic contraction. EMG techniques Automated or semi-automated methods are available on most new EMG machines. Decomposition techniques can extract single MUAPs from an interference pattern. For analysis of the interference pattern, a turn ampli- tude system is available in most programs – Single fiber (SF) EMG is performed with a special needle (SFEMG-needle), a special filter setting, and special analysis programs. The SFEMG technique permits the study of the fiber density and the time relationship between discharges of fibers.

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Pathogenesis The pathogenesis of paraneoplastic neuropathies is unclear generic 1 mg finasteride with mastercard hair loss gastric sleeve, but is believed to be the result of numerous auto-antibodies associated with cancer cheap 5mg finasteride amex hair loss in men kilts. The sen- sorimotor type has been associated with anti-CV2 antibodies. Demyelinating forms are more highly associated with lymphoma and Hodgkin’s disease. Sensory neuronopathy is related to anti-Hu and other anti-neuronal antibodies, in the context of small cell lung cancer. Diagnosis Nerve conduction velocities reveal sensory axonal loss with absent SNAPs. Anti-Hu antibodies, especially in cases of lung cancer, may be detectable. Biopsies are rarely indicated, except for presumed vasculitic neuropathy. Differential diagnosis Concommitant metabolic diseases, malnourishment, and weight loss have to be considered. Chemotherapeutic neuropathy is a common possibility. The syndrome of sensory neuronopathy is not exclusively paraneoplastic, but may also be idiopathic or associated with Sjogren’s syndrome. Therapy No treatments are available for the sensory/motor, demyelinating, and auto- nomic syndromes. For sensory neuropathies and neuronopathies immunmodulatory therapies have been suggested and range from steroids to intravenous gammaglobulin, plasmapheresis, and immunosuppression. The neuropathies may respond to immunotherapy and anti-neoplastic treat- Prognosis ments. Subacute sensory neuronopathy usually remains in a plateau phase, responding poorly to therapy. Camdessanche JP, Antoine JC, Honnorat J, et al (2002) Paraneoplastic peripheral neuro- References pathy associated with anti Hu antibodies. Brain 125: 166–175 Chinn JS, Schuffler MD (1988) Paraneoplastic visceral neuropathy as a cause of severe gastrointestinal motor dysfunction. Gastroenterology 95: 1279–1286 Grisold W, Drlicek M (1999) Paraneoplastic neuropathy. Curr Opin Neurol 12: 617– 625 Krarup C, Crone C (2002) Neurophysiological studies in malignant disease with particular reference to involvement of peripheral nerves. J Neurol 249: 651–661 Storstein A, Vedeler C (2001) Neuropathy and malignancy: a retrospective survey. J Neurol 248: 322–327 276 Motor neuropathy or motor neuron disease syndrome Genetic testing NCV/EMG Laboratory Imaging Biopsy ++ + Anatomy/distribution Anterior horn cells degenerate, which leads to concomitant degeneration of long tracts. Symptoms The degree and course of motor impairment can be variable, but generally there is weakness. Clinical syndrome/ Motor neuron disease syndrome is associated with several cancer conditions signs and can exhibit different combinations of lower and upper motor neuron signs. One type associated with anti-Hu antibodies is relentlessly progressive and involves mostly lower motor neurons and encephalopathy. Another lower motor neuron syndrome is associated with lymphoma. A syndrome of upper and lower motor neuron signs resembling ALS is linked to numerous tumors (lymphoma, ovarian, uterine, breast, non-small cell lung cancer). Finally, an upper motor neuron syndrome has been reported with breast cancer. Pathogenesis The existence of paraneoplastic motor neuron disease is controversial. Some feel that this is an occurrence of two separate common disorders in one patient. Evidence for the existence of paraneoplastic motor neuron disease is based on the presence of antibodies to antigens shared by neurons and tumors, the responsiveness of some motor neuron disease to successful cancer treatment, and occurrence of motor neuron disease in patients exhibiting other well- characterized paraneoplastic syndromes. Diagnosis Diagnosis of a paraneoplastic motor neuron disease can be suggested by a lower motor neuron syndrome in association with cancer. Differential diagnosis Polyneuropathy or ALS coinciding with cancer. Therapy While some have reported regression of nervous system disease with treatment of cancer and immune therapy, generally treatments are not effective.