Paralysis. Medical search

A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)

Complete or severe weakness of the muscles of respiration. This condition may be associated with MOTOR NEURON DISEASES; PERIPHERAL NERVE DISEASES; NEUROMUSCULAR JUNCTION DISEASES; SPINAL CORD DISEASES; injury to the PHRENIC NERVE; and other disorders.

Congenital or acquired paralysis of one or both VOCAL CORDS. This condition is caused by defects in the CENTRAL NERVOUS SYSTEM, the VAGUS NERVE and branches of LARYNGEAL NERVES. Common symptoms are VOICE DISORDERS including HOARSENESS or APHONIA.

A heterogenous group of inherited disorders characterized by recurring attacks of rapidly progressive flaccid paralysis or myotonia. These conditions have in common a mutation of the gene encoding the alpha subunit of the sodium channel in skeletal muscle. They are frequently associated with fluctuations in serum potassium levels. Periodic paralysis may also occur as a non-familial process secondary to THYROTOXICOSIS and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1481)

Severe or complete loss of facial muscle motor function. This condition may result from central or peripheral lesions. Damage to CNS motor pathways from the cerebral cortex to the facial nuclei in the pons leads to facial weakness that generally spares the forehead muscles. FACIAL NERVE DISEASES generally results in generalized hemifacial weakness. NEUROMUSCULAR JUNCTION DISEASES and MUSCULAR DISEASES may also cause facial paralysis or paresis.

A common condition characterized by transient partial or total paralysis of skeletal muscles and areflexia that occurs upon awakening from sleep or less often while falling asleep. Stimuli such as touch or sound may terminate the episode, which usually has a duration of seconds to minutes. This condition may occur in normal subjects or be associated with NARCOLEPSY; CATAPLEXY; and hypnagogic HALLUCINATIONS. The pathophysiology of this condition is closely related to the normal hypotonia that occur during REM sleep. (From Adv Neurol 1995;67:245-271)

Paralysis caused by a neurotropic toxin secreted by the salivary glands of ticks.

An autosomal dominant familial disorder which presents in infancy or childhood and is characterized by episodes of weakness associated with hyperkalemia. During attacks, muscles of the lower extremities are initially affected, followed by the lower trunk and arms. Episodes last from 15-60 minutes and typically occur after a period of rest following exercise. A defect in skeletal muscle sodium channels has been identified as the cause of this condition. Normokalemic periodic paralysis is a closely related disorder marked by a lack of alterations in potassium levels during attacks of weakness. (Adams et al., Principles of Neurology, 6th ed, p1481)

A diminution of the skeletal muscle tone marked by a diminished resistance to passive stretching.

Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)

An acute infectious disease of humans, particularly children, caused by any of three serotypes of human poliovirus (POLIOVIRUS). Usually the infection is limited to the gastrointestinal tract and nasopharynx, and is often asymptomatic. The central nervous system, primarily the spinal cord, may be affected, leading to rapidly progressive paralysis, coarse FASCICULATION and hyporeflexia. Motor neurons are primarily affected. Encephalitis may also occur. The virus replicates in the nervous system, and may cause significant neuronal loss, most notably in the spinal cord. A rare related condition, nonpoliovirus poliomyelitis, may result from infections with nonpoliovirus enteroviruses. (From Adams et al., Principles of Neurology, 6th ed, pp764-5)

A hypermetabolic syndrome caused by excess THYROID HORMONES which may come from endogenous or exogenous sources. The endogenous source of hormone may be thyroid HYPERPLASIA; THYROID NEOPLASMS; or hormone-producing extrathyroidal tissue. Thyrotoxicosis is characterized by NERVOUSNESS; TACHYCARDIA; FATIGUE; WEIGHT LOSS; heat intolerance; and excessive SWEATING.

A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of SKELETAL MYOCYTES. Defects in the SCN4A gene, which codes for the alpha subunit of this sodium channel, are associated with several MYOTONIC DISORDERS.

A family of invertebrate RNA viruses in the order Picornavirales.

Severe or complete loss of motor function in the lower extremities and lower portions of the trunk. This condition is most often associated with SPINAL CORD DISEASES, although BRAIN DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; and MUSCULAR DISEASES may also cause bilateral leg weakness.

Abnormally high potassium concentration in the blood, most often due to defective renal excretion. It is characterized clinically by electrocardiographic abnormalities (elevated T waves and depressed P waves, and eventually by atrial asystole). In severe cases, weakness and flaccid paralysis may occur. (Dorland, 27th ed)

A syndrome characterized by the acute onset of unilateral FACIAL PARALYSIS which progresses over a 2-5 day period. Weakness of the orbicularis oculi muscle and resulting incomplete eye closure may be associated with corneal injury. Pain behind the ear often precedes the onset of paralysis. This condition may be associated with HERPESVIRUS 1, HUMAN infection of the facial nerve. (Adams et al., Principles of Neurology, 6th ed, p1376)

Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation.

Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc.

Severe or complete loss of motor function in all four limbs which may result from BRAIN DISEASES; SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; or rarely MUSCULAR DISEASES. The locked-in syndrome is characterized by quadriplegia in combination with cranial muscle paralysis. Consciousness is spared and the only retained voluntary motor activity may be limited eye movements. This condition is usually caused by a lesion in the upper BRAIN STEM which injures the descending cortico-spinal and cortico-bulbar tracts.

Branches of the vagus (tenth cranial) nerve. The recurrent laryngeal nerves originate more caudally than the superior laryngeal nerves and follow different paths on the right and left sides. They carry efferents to all muscles of the larynx except the cricothyroid and carry sensory and autonomic fibers to the laryngeal, pharyngeal, tracheal, and cardiac regions.

Paralysis of an infant resulting from injury received at birth. (From Dorland, 27th ed)

A species of ENTEROVIRUS which is the causal agent of POLIOMYELITIS in humans. Three serotypes (strains) exist. Transmission is by the fecal-oral route, pharyngeal secretions, or mechanical vector (flies). Vaccines with both inactivated and live attenuated virus have proven effective in immunizing against the infection.

A live vaccine containing attenuated poliovirus, types I, II, and III, grown in monkey kidney cell tissue culture, used for routine immunization of children against polio. This vaccine induces long-lasting intestinal and humoral immunity. Killed vaccine induces only humoral immunity. Oral poliovirus vaccine should not be administered to immunocompromised individuals or their household contacts. (Dorland, 28th ed)

The motor nerve of the diaphragm. The phrenic nerve fibers originate in the cervical spinal column (mostly C4) and travel through the cervical plexus to the diaphragm.

A serotype of botulinum toxins that has specificity for cleavage of SYNAPTOSOMAL-ASSOCIATED PROTEIN 25.

A bis-quaternary steroid that is a competitive nicotinic antagonist. As a neuromuscular blocking agent it is more potent than CURARE but has less effect on the circulatory system and on histamine release.

Restoration, reconstruction, or improvement of a defective or damaged LARYNX.

The musculofibrous partition that separates the THORACIC CAVITY from the ABDOMINAL CAVITY. Contraction of the diaphragm increases the volume of the thoracic cavity aiding INHALATION.

Toxic proteins produced from the species CLOSTRIDIUM BOTULINUM. The toxins are synthesized as a single peptide chain which is processed into a mature protein consisting of a heavy chain and light chain joined via a disulfide bond. The botulinum toxin light chain is a zinc-dependent protease which is released from the heavy chain upon ENDOCYTOSIS into PRESYNAPTIC NERVE ENDINGS. Once inside the cell the botulinum toxin light chain cleaves specific SNARE proteins which are essential for secretion of ACETYLCHOLINE by SYNAPTIC VESICLES. This inhibition of acetylcholine release results in muscular PARALYSIS.

A form of inherited long QT syndrome (or LQT7) that is characterized by a triad of potassium-sensitive periodic paralysis, VENTRICULAR ECTOPIC BEATS, and abnormal features such as short stature, low-set ears, and SCOLIOSIS. It results from mutations of KCNJ2 gene which encodes a channel protein (INWARD RECTIFIER POTASSIUM CHANNELS) that regulates resting membrane potential.

Prolonged failure of muscle relaxation after contraction. This may occur after voluntary contractions, muscle percussion, or electrical stimulation of the muscle. Myotonia is a characteristic feature of MYOTONIC DISORDERS.

Examination, therapy or surgery of the interior of the larynx performed with a specially designed endoscope.

Drugs that interrupt transmission at the skeletal neuromuscular junction without causing depolarization of the motor end plate. They prevent acetylcholine from triggering muscle contraction and are used as muscle relaxants during electroshock treatments, in convulsive states, and as anesthesia adjuvants.

A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.

Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles.

A group of genetic disorders of the KIDNEY TUBULES characterized by the accumulation of metabolically produced acids with elevated plasma chloride, hyperchloremic metabolic ACIDOSIS. Defective renal acidification of URINE (proximal tubules) or low renal acid excretion (distal tubules) can lead to complications such as HYPOKALEMIA, hypercalcinuria with NEPHROLITHIASIS and NEPHROCALCINOSIS, and RICKETS.

The intentional interruption of transmission at the NEUROMUSCULAR JUNCTION by external agents, usually neuromuscular blocking agents. It is distinguished from NERVE BLOCK in which nerve conduction (NEURAL CONDUCTION) is interrupted rather than neuromuscular transmission. Neuromuscular blockade is commonly used to produce MUSCLE RELAXATION as an adjunct to anesthesia during surgery and other medical procedures. It is also often used as an experimental manipulation in basic research. It is not strictly speaking anesthesia but is grouped here with anesthetic techniques. The failure of neuromuscular transmission as a result of pathological processes is not included here.

A pair of cone-shaped elastic mucous membrane projecting from the laryngeal wall and forming a narrow slit between them. Each contains a thickened free edge (vocal ligament) extending from the THYROID CARTILAGE to the ARYTENOID CARTILAGE, and a VOCAL MUSCLE that shortens or relaxes the vocal cord to control sound production.

The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and SALIVARY GLANDS, and convey afferent information for TASTE from the anterior two-thirds of the TONGUE and for TOUCH from the EXTERNAL EAR.

A disease caused by potent protein NEUROTOXINS produced by CLOSTRIDIUM BOTULINUM which interfere with the presynaptic release of ACETYLCHOLINE at the NEUROMUSCULAR JUNCTION. Clinical features include abdominal pain, vomiting, acute PARALYSIS (including respiratory paralysis), blurred vision, and DIPLOPIA. Botulism may be classified into several subtypes (e.g., food-borne, infant, wound, and others). (From Adams et al., Principles of Neurology, 6th ed, p1208)

The sudden collapse and disappearance or diminution of a colony of organisms.

The synapse between a neuron and a muscle.

Viruses infecting insects, the largest family being BACULOVIRIDAE.

Neurons which activate MUSCLE CELLS.

A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.

Pathologic conditions which feature SPINAL CORD damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord.

A syndrome associated with inflammation of the BRACHIAL PLEXUS. Clinical features include severe pain in the shoulder region which may be accompanied by MUSCLE WEAKNESS and loss of sensation in the upper extremity. This condition may be associated with VIRUS DISEASES; IMMUNIZATION; SURGERY; heroin use (see HEROIN DEPENDENCE); and other conditions. The term brachial neuralgia generally refers to pain associated with brachial plexus injury. (From Adams et al., Principles of Neurology, 6th ed, pp1355-6)

Recording of the changes in electric potential of muscle by means of surface or needle electrodes.

Traumatic injuries to the RECURRENT LARYNGEAL NERVE that may result in vocal cord dysfunction.

An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)

Inflammation of the spinal cord. Relatively common etiologies include infections; AUTOIMMUNE DISEASES; SPINAL CORD; and ischemia (see also SPINAL CORD VASCULAR DISEASES). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction.

A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.

Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).

A variety of neuromuscular conditions resulting from MUTATIONS in ION CHANNELS manifesting as episodes of EPILEPSY; HEADACHE DISORDERS; and DYSKINESIAS.

Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.

A vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases. (From Wyngaarden et al., Cecil Textbook of Medicine, 19th ed, p2251)

An unnaturally deep or rough quality of voice.

The largest cartilage of the larynx consisting of two laminae fusing anteriorly at an acute angle in the midline of the neck. The point of fusion forms a subcutaneous projection known as the Adam's apple.

Vaccines used to prevent POLIOMYELITIS. They include inactivated (POLIOVIRUS VACCINE, INACTIVATED) and oral vaccines (POLIOVIRUS VACCINE, ORAL).

Diseases characterized by MYOTONIA, which may be inherited or acquired. Myotonia may be restricted to certain muscles (e.g., intrinsic hand muscles) or occur as a generalized condition.

Traumatic injuries to the facial nerve. This may result in FACIAL PARALYSIS, decreased lacrimation and salivation, and loss of taste sensation in the anterior tongue. The nerve may regenerate and reform its original pattern of innervation, or regenerate aberrantly, resulting in inappropriate lacrimation in response to gustatory stimuli (e.g., "crocodile tears") and other syndromes.

Diseases of the twelfth cranial (hypoglossal) nerve or nuclei. The nuclei and fascicles of the nerve are located in the medulla, and the nerve exits the skull via the hypoglossal foramen and innervates the muscles of the tongue. Lower brain stem diseases, including ischemia and MOTOR NEURON DISEASES may affect the nuclei or nerve fascicles. The nerve may also be injured by diseases of the posterior fossa or skull base. Clinical manifestations include unilateral weakness of tongue musculature and lingual dysarthria, with deviation of the tongue towards the side of weakness upon attempted protrusion.

A tubular organ of VOICE production. It is located in the anterior neck, superior to the TRACHEA and inferior to the tongue and HYOID BONE.

A condition characterized by transient weakness or paralysis of somatic musculature triggered by an emotional stimulus or physical exertion. Cataplexy is frequently associated with NARCOLEPSY. During a cataplectic attack, there is a marked reduction in muscle tone similar to the normal physiologic hypotonia that accompanies rapid eye movement sleep (SLEEP, REM). (From Adams et al., Principles of Neurology, 6th ed, p396)

A genus of poisonous snakes of the subfamily Elapinae of the family ELAPIDAE. They comprise the kraits. Twelve species are recognized and all inhabit southeast Asia. They are considered extremely dangerous. (Moore: Poisonous Snakes of the World, 1980, p120)

Inherited myotonic disorders with early childhood onset MYOTONIA. Muscular hypertrophy is common and myotonia may impair ambulation and other movements. It is classified as Thomsen (autosomal dominant) or Becker (autosomal recessive) generalized myotonia mainly based on the inheritance pattern. Becker type is also clinically more severe. An autosomal dominant variant with milder symptoms and later onset is known as myotonia levior. Mutations in the voltage-dependent skeletal muscle chloride channel are associated with the disorders.

A condition characterized by recurrent episodes of daytime somnolence and lapses in consciousness (microsomnias) that may be associated with automatic behaviors and AMNESIA. CATAPLEXY; SLEEP PARALYSIS, and hypnagogic HALLUCINATIONS frequently accompany narcolepsy. The pathophysiology of this disorder includes sleep-onset rapid eye movement (REM) sleep, which normally follows stage III or IV sleep. (From Neurology 1998 Feb;50(2 Suppl 1):S2-S7)

Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.

A central respiratory stimulant with a brief duration of action. (From Martindale, The Extra Pharmocopoeia, 30th ed, p1225)

Disorders of one or more of the twelve cranial nerves. With the exception of the optic and olfactory nerves, this includes disorders of the brain stem nuclei from which the cranial nerves originate or terminate.

Difficulty and/or pain in PHONATION or speaking.

Traumatic injuries to the LARYNGEAL NERVE.

Insect members of the superfamily Apoidea, found almost everywhere, particularly on flowers. About 3500 species occur in North America. They differ from most WASPS in that their young are fed honey and pollen rather than animal food.

The resection or removal of the innervation of a muscle or muscle tissue.

Muscles of facial expression or mimetic muscles that include the numerous muscles supplied by the facial nerve that are attached to and move the skin of the face. (From Stedman, 25th ed)

Diseases characterized by injury or dysfunction involving multiple peripheral nerves and nerve roots. The process may primarily affect myelin or nerve axons. Two of the more common demyelinating forms are acute inflammatory polyradiculopathy (GUILLAIN-BARRE SYNDROME) and POLYRADICULONEUROPATHY, CHRONIC INFLAMMATORY DEMYELINATING. Polyradiculoneuritis refers to inflammation of multiple peripheral nerves and spinal nerve roots.

Mechanical compression of nerves or nerve roots from internal or external causes. These may result in a conduction block to nerve impulses (due to MYELIN SHEATH dysfunction) or axonal loss. The nerve and nerve sheath injuries may be caused by ISCHEMIA; INFLAMMATION; or a direct mechanical effect.

Diseases of the cervical (and first thoracic) roots, nerve trunks, cords, and peripheral nerve components of the BRACHIAL PLEXUS. Clinical manifestations include regional pain, PARESTHESIA; MUSCLE WEAKNESS, and decreased sensation (HYPESTHESIA) in the upper extremity. These disorders may be associated with trauma (including BIRTH INJURIES); THORACIC OUTLET SYNDROME; NEOPLASMS; NEURITIS; RADIOTHERAPY; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, pp1351-2)

A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.

The use of peripheral nerve stimulation to assess transmission at the NEUROMUSCULAR JUNCTION, especially in the response to anesthetics, such as the intensity of NEUROMUSCULAR BLOCKADE by NEUROMUSCULAR BLOCKING AGENTS.

A general term indicating inflammation of the BRAIN and SPINAL CORD, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and ENCEPHALITIS in the literature.

Contractile tissue that produces movement in animals.

A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)

An aspect of cholinesterases.

Respiratory muscles that arise from the lower border of one rib and insert into the upper border of the adjoining rib, and contract during inspiration or respiration. (From Stedman, 25th ed)

A family of small RNA viruses comprising some important pathogens of humans and animals. Transmission usually occurs mechanically. There are nine genera: APHTHOVIRUS; CARDIOVIRUS; ENTEROVIRUS; ERBOVIRUS; HEPATOVIRUS; KOBUVIRUS; PARECHOVIRUS; RHINOVIRUS; and TESCHOVIRUS.

A set of twelve curved bones which connect to the vertebral column posteriorly, and terminate anteriorly as costal cartilage. Together, they form a protective cage around the internal thoracic organs.

An idiopathic syndrome characterized by one or more of the following; recurrent orofacial swelling, relapsing facial paralysis, and fissured tongue (lingua plicata). The onset is usually in childhood and relapses are common. Cheilitis granulomatosa is a monosymptomatic variant of this condition. (Dermatol Clin 1996 Apr;14(2):371-9; Magalini & Magalini, Dictionary of Medical Syndromes, 4th ed, p531)

Branches of the VAGUS NERVE. The superior laryngeal nerves originate near the nodose ganglion and separate into external branches, which supply motor fibers to the cricothyroid muscles, and internal branches, which carry sensory fibers. The RECURRENT LARYNGEAL NERVE originates more caudally and carries efferents to all muscles of the larynx except the cricothyroid. The laryngeal nerves and their various branches also carry sensory and autonomic fibers to the laryngeal, pharyngeal, tracheal, and cardiac regions.

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

A genus of the family PICORNAVIRIDAE whose members preferentially inhabit the intestinal tract of a variety of hosts. The genus contains many species. Newly described members of human enteroviruses are assigned continuous numbers with the species designated "human enterovirus".

Antitumor and immunotherapeutic effects of activated invasive T lymphoma cells that display short-term interleukin 1alpha expression. (1/1176)

Expression of cytokines in malignant cells represents a novel approach for therapeutic treatment of tumors. Previously, we demonstrated the immunostimulatory effectiveness of interleukin 1alpha (IL-1alpha) gene transfer in experimental fibrosarcoma tumors. Here, we report the antitumor and immunotherapeutic effects of short-term expression of IL-1alpha by malignant T lymphoma cells. Activation in culture of T lymphoma cells with lipopolysaccharide-stimulated macrophages induces the expression of IL-1alpha. The short-term expression of IL-1alpha persists in the malignant T cells for a few days (approximately 3-6 days) after termination of the in vitro activation procedure and, thus, has the potential to stimulate antitumor immune responses in vivo. As an experimental tumor model, we used the RO1 invasive T lymphoma cell line. Upon i.v. inoculation, these cells invade the vertebral column and compress the spinal cord, resulting in hind leg paralysis and death of the mice. Activated RO1 cells, induced to express IL-1alpha in a short-term manner, manifested reduced tumorigenicity: approximately 75% of the mice injected with activated RO1 cells remained tumor free. IL-1 was shown to be essential for the eradication of activated T lymphoma cells because injection of activated RO1 cells together with IL-1-specific inhibitors, i.e., the IL-1 receptor antagonist or the M 20 IL-1 inhibitor, reversed reduced tumorigenicity patterns and led to progressive tumor growth and death of the mice. Furthermore, activated RO1 cells could serve as a treatment by intervening in the growth of violent RO1 cells after tumor take. Thus, when activated RO1 cells were injected 6 or 9 days after the inoculation of violent cells, mortality was significantly reduced. IL-1alpha, in its unique membrane-associated form, in addition to its cytosolic and secreted forms, may represent a focused adjuvant for potentiating antitumor immune responses at low levels of expression, below those that are toxic to the host. Further assessment of the immunotherapeutic potential of short-term expression of IL-1alpha in activated tumor cells may allow its improved application in the treatment of malignancies. (+info)

Common peroneal nerve palsy: a clinical and electrophysiological review. (2/1176)

In a series of 70 patients (75 cases of common peroneal nerve palsy) the common causes were trauma about the knee or about the hip, compression, and underlying neuropathy. A few palsies occurred spontaneously for no apparent reason. The prognosis was uniformly good in the compression group; recovery was delayed but usually satisfactory in patients who had suffered stretch injuries. In the acute stage, when clinical paralysis appears to be complete, electrophysiological studies are a useful guide to prognosis. They may also indicate an underlying neuropathy and they detect early evidence of recovery. The anatomical peculiarities of the common peroneal nerve are noted and aspects of the clinical picture, management, and prognosis of palsy are discussed. (+info)

Incidence of deep vein thrombosis and leg oedema in patients with strokes. (3/1176)

In a series of 26 patients with strokes 13 had deep vein thrombosis (DVT) in the leg, demonstrated by fibrinogen scanning. In 10 patients the thrombosis was in the paralysed leg but the degree of paralysis was unrelated to the tendency to develop DVT, which usually occurred about the third day. Leg oedema in 10 patients was unrelated to the DVT. (+info)

A five-year assessment of controlled trials of in-patient and out-patient treatment and of plaster-of-Paris jackets for tuberculosis of the spine in children on standard chemotherapy. Studies in Masan and Pusan, Korea. Fifth report of the Medical Research Council Working Party on tuberculosis of the spine. (4/1176)

In two centres in Korea 350 patients with a diagnosis of tuberculosis of the thoracic and/or lumbar spine were allocated at random: in Masan to in-patient rest in bed (IP) for six months followed by out-patient treatment or to ambulatory out-patient treatment (OP) from the start; in Pusan to out-patient treatment with a plaster-of-Paris jacket (J) for nine months or to ambulatory treatment without any support (No J). All patients recieved chemotherapy with PAS with isoniazid for eighteen months, either supplemented with streptomycin for the first three months (SPH) or without this supplement (PH), by random allocation. The main analysis of this report concerns 299 patients (eighty-three IP, eighty-three OP, sixty-three J, seventy No J; 143 SPH, 156 PH). Pre-treatment factors were similar in both centres except that the patients in Pusan had, on average, less extensive lesions although in a greater proportion the disease was radiographically active. One patient (J/SPH) died with active spinal disease and three (all No J/SPH) with paraplegia. A fifth patient (IP/PH) who died from cardio respiratory failure also had pulmonary tuberculosis. Twenty-three patients required operation and/or additional chemotherapy for the spinal lesion. A sinus or clinically evident abscess was either present initially or developed during treatment in 41 per cent of patients. Residual lesions persisted in ten patients (four IP, two OP, one J, three No J; six SPH, four PH) at five years. Thirty-two patients had paraparesis on admission or developing later. Complete resolution occurred in twenty on the allocated regimen and in eight after operation or additional chemotherapy or both. Of the remaining four atients, all of whom had operation and additional chemotherapy, three died and one still had paraparesis at five years. Of 295 patients assessed at five years 89 per cent had a favourable status. The proportions of the patients responding favourably were similar in the IP (91 per cent) and OP (89 per cent) series, in the J (90 per cent) and No J (84 per cent) series and in the SPH (86 per cent) and PH (92 per cent) series. (+info)

Hypoglossal nerve injury as a complication of anterior surgery to the upper cervical spine. (5/1176)

Injury to the hypoglossal nerve is a recognised complication after soft tissue surgery in the upper part of the anterior aspect of the neck, e.g. branchial cyst or carotid body tumour excision. However, this complication has been rarely reported following surgery of the upper cervical spine. We report the case of a 35-year-old woman with tuberculosis of C2-3. She underwent corpectomy and fusion from C2 to C5 using iliac crest bone graft, through a left anterior oblique incision. She developed hypoglossal nerve palsy in the immediate postoperative period, with dysphagia and dysarthria. It was thought to be due to traction neurapraxia with possible spontaneous recovery. At 18 months' follow-up, she had a solid fusion and tuberculosis was controlled. The hypoglossal palsy persisted, although with minimal functional disability. The only other reported case of hypoglossal lesion after anterior cervical spine surgery in the literature also failed to recover. It is concluded that hypoglossal nerve palsy following anterior cervical spine surgery is unlikely to recover spontaneously and it should be carefully identified. (+info)

Isolated dysarthria due to extracerebellar lacunar stroke: a central monoparesis of the tongue. (6/1176)

OBJECTIVES: The pathophysiology of dysarthria can preferentially be studied in patients with the rare lacunar stroke syndrome of "isolated dysarthria". METHODS: A single study was carried out on seven consecutive patients with sudden onset of isolated dysarthria due to single ischaemic lesion. The localisation of the lesion was identified using MRI. The corticolingual, cortico-orofacial, and corticospinal tract functions were investigated using transcranial magnetic stimulation. Corticopontocerebellar tract function was assessed using 99mTc hexamethylpropylene amine oxime-single photon emission computerised tomography (HMPAO-SPECT) in six patients. Sensory functions were evaluated clinically and by somatosensory evoked potentials. RESULTS: Brain MRI showed the lesions to be located in the corona radiata (n=4) and the internal capsule (n=2). No morphological lesion was identified in one patient. Corticolingual tract function was impaired in all patients. In four patients with additional cortico-orofacial tract dysfunction, dysarthria did not differ from that in patients with isolated corticolingual tract dysfunction. Corticospinal tract functions were normal in all patients. HMPAO-SPECT showed no cerebellar diaschisis, suggesting unimpaired corticopontocerebellar tract function. Sensory functions were not affected. CONCLUSION: Interruption of the corticolingual pathways to the tongue is crucial in the pathogenesis of isolated dysarthria after extracerebellar lacunar stroke. (+info)

Awareness during anesthesia: a closed claims analysis. (7/1176)

BACKGROUND: Awareness during general anesthesia is a frightening experience, which may result in serious emotional injury and post-traumatic stress disorder. We performed an in-depth analysis of cases from the database of the American Society of Anesthesiologists Closed Claims Project to explore the contribution of intraoperative awareness to professional liability in anesthesia. METHODS: The database of the Closed Claims Project is composed of closed US malpractice claims that have been collected in a standardized manner. All claims for intraoperative awareness were reviewed by the reviewers to identify patterns of causation and standard of care. Logistic regression analysis was used to identify independent patient and anesthetic factors associated with claims for recall during general anesthesia compared to other general anesthesia malpractice claims. RESULTS: Awareness claims accounted for 79 (1.9%) of 4,183 claims in the database, including 18 claims for awake paralysis, i.e., the inadvertent paralysis of an awake patient, and 61 claims for recall during general anesthesia, ie., recall of events while receiving general anesthesia. The majority of awareness claims involved women (77%), younger than 60 yr of age (89%), American Society of Anesthesiologists physical class I-II (68%), who underwent elective surgery (87%). Most (94%) claims for awake paralysis represented substandard care involving errors in labeling and administration, whereas care was substandard in only 43% of the claims for recall during general anesthesia (P < 0.001). Claims for recall during general anesthesia were more likely to involve women (odds ratio [OR] = 3.08, 95% confidence interval [CI] = 1.58, 6.06) and anesthetic techniques using intraoperative opioids (OR = 2.12, 95% CI = 1.20, 3.74), intraoperative muscle relaxants (OR = 2.28, 95% CI = 1.22, 4.25), and no volatile anesthetic (OR = 3.20, 95% CI = 1.88, 5.46). CONCLUSIONS: Deficiencies in labeling and vigilance were common causes for awake paralysis. Claims for recall during general anesthesia were more likely in women and with nitrous-narcotic-relaxant techniques. (+info)

Golli-induced paralysis: a study in anergy and disease. (8/1176)

The Golli-MBP transcription unit contains three Golli-specific exons as well as the seven exons of the classical myelin basic protein (MBP) gene and encodes alternatively spliced proteins that share amino acid sequence with MBP. Unlike MBP, which is a late Ag expressed only in the nervous system, Golli exon-containing gene products are expressed both pre- and postnatally at many sites, including lymphoid tissue, as well as in the central nervous system. To investigate whether Golli-MBP peptides unique to Golli would result in neurological disease, we immunized rats and observed a novel neurological disease characterized by mild paralysis and the presence of groups of lymphocytes in the subarachnoid space but not in the parenchyma of the brain. Disease was induced by Th1-type T cells that displayed an unusual activation phenotype. Primary stimulation in vitro induced T cell proliferation with increased surface CD45RC that did not become down-regulated as it did in other Ag-stimulated cultures. Secondary stimulation of this CD45RChigh population with Ag, however, did not induce proliferation or IL-2 production, although an IFN-gamma-producing population resulted. Proliferation could be induced by secondary stimulation with IL-2 or PMA-ionomycin, suggesting an anergic T cell population. Cells could adoptively transfer disease after secondary stimulation with IL-2, but not with Ag alone. These responses are suggestive of a chronically stimulated, anergic population that can be transiently activated to cause disease, fall back into an anergic state, and reactivated to cause disease again. Such a scenario may be important in chronic human disease. (+info)

1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.

Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.

Respiratory paralysis can manifest in different ways depending on the underlying cause and severity of the condition. Some common symptoms include:

1. Difficulty breathing: Patients may experience shortness of breath, wheezing, or a feeling of suffocation.
2. Weakened cough reflex: The muscles used for coughing may be weakened or paralyzed, making it difficult to clear secretions from the lungs.
3. Fatigue: Breathing can be tiring and may leave the patient feeling exhausted.
4. Sleep disturbances: Respiratory paralysis can disrupt sleep patterns and cause insomnia or other sleep disorders.
5. Chest pain: Pain in the chest or ribcage can be a symptom of respiratory paralysis, particularly if it is caused by muscle weakness or atrophy.

Diagnosis of respiratory paralysis typically involves a physical examination, medical history, and diagnostic tests such as electroencephalogram (EEG), electromyography (EMG), or nerve conduction studies (NCS). Treatment options vary depending on the underlying cause but may include:

1. Medications: Drugs such as bronchodilators, corticosteroids, and anticholinergics can be used to manage symptoms and improve lung function.
2. Respiratory therapy: Techniques such as chest physical therapy, respiratory exercises, and non-invasive ventilation can help improve lung function and reduce fatigue.
3. Surgery: In some cases, surgery may be necessary to correct anatomical abnormalities or repair damaged nerves.
4. Assistive devices: Patients with severe respiratory paralysis may require the use of assistive devices such as oxygen therapy, ventilators, or wheelchairs to help improve their quality of life.
5. Rehabilitation: Physical therapy, occupational therapy, and speech therapy can all be helpful in improving function and reducing disability.
6. Lifestyle modifications: Patients with respiratory paralysis may need to make lifestyle changes such as avoiding smoke, dust, and other irritants, getting regular exercise, and managing stress to help improve their condition.

* Type 1: Hypokalemic Periodic Paralysis (Hyperkalemia-induced muscle weakness)
* Type 2: Hyperkalemic Periodic Paralysis (K+ channels dysfunction, leading to muscle weakness)
* Type 3: Peripheral nerve damage causing FPPA
* Type 4: Central nervous system damage causing FPPA

Slide 3: Causes of Familial Periodic Paralysis (FPPA)

* Genetic mutations in SCN4A, KCNA1, and other genes involved in ion channel function
* Abnormalities in the expression and function of ion channels
* Autosomal dominant or recessive inheritance pattern

Slide 4: Symptoms of Familial Periodic Paralysis (FPPA)

* Muscle weakness or paralysis, often triggered by changes in diet, physical activity, or other environmental factors
* Weakness of the lower extremities more pronounced than the upper extremities
* Muscle cramps and twitching
* Abdominal pain
* Nausea and vomiting

Slide 5: Diagnosis of Familial Periodal Paralysis (FPPA)

* Clinical evaluation, including patient history and physical examination
* Electromyography (EMG) to assess muscle activity and diagnose FPPA
* Genetic testing to identify genetic mutations associated with FPPA
* Blood tests to measure potassium levels and rule out other conditions

Slide 6: Treatment of Familial Periodic Paralysis (FPPA)

* Potassium supplements to maintain normal potassium levels
* Avoiding triggers such as stress, cold temperature, and certain medications
* Physical therapy to improve muscle strength and function
* Pain management with analgesics and other medications as needed

Slide 7: Prognosis of Familial Periodic Paralysis (FPPA)

* FPPA is a chronic condition with no cure, but with proper management, patients can lead relatively normal lives
* The prognosis varies depending on the severity and frequency of attacks, as well as the presence of any complications
* Early diagnosis and treatment can improve the quality of life for patients with FPPA

Slide 8: Current Research in Familial Periodic Paralysis (FPPA)

* Genetic research to better understand the underlying causes of FPPA and develop new treatments
* Studies on the effectiveness of new medications and therapies for FPPA
* Investigation into the potential use of stem cells for treating FPPA

Slide 9: Current Challenges in Familial Periodic Paralysis (FPPA)

* Limited awareness and understanding of FPPA among healthcare professionals and the general public
* Lack of effective treatments for severe cases of FPPA
* Limited availability of specialized care and support for patients with FPPA

Slide 10: Conclusion

* Familial periodic paralysis (FPPA) is a rare and complex condition that affects both children and adults
* Early diagnosis and proper management are critical to improving the quality of life for patients with FPPA
* Ongoing research offers hope for new treatments and therapies, but more work needs to be done to increase awareness and understanding of this condition.

The main symptoms of facial paralysis are:

1. Weakness or numbness in the facial muscles
2. Drooping or sagging of one side of the face
3. Twitching or spasms in the facial muscles
4. Difficulty smiling, frowning, or expressing emotions
5. Difficulty closing the eye on the affected side
6. Dry mouth or difficulty swallowing
7. Pain or discomfort in the face or head.

The diagnosis of facial paralysis is based on a combination of clinical examination, imaging studies such as MRI or CT scans, and other tests to determine the underlying cause. Treatment options for facial paralysis depend on the underlying cause and may include medications, surgery, physical therapy, and other interventions to address any associated symptoms.

There are several types of facial paralysis, including:

1. Bell's palsy: A condition that causes weakness or paralysis of the muscles on one side of the face, usually due to nerve damage.
2. Facial spasm: A condition characterized by involuntary twitching or contractions of the facial muscles.
3. Hemifacial spasm: A condition that causes weakness or paralysis of half of the face due to nerve compression.
4. Trauma-related facial paralysis: Caused by injury or trauma to the face or head.
5. Tumor-related facial paralysis: Caused by a tumor that compresses or damages the nerves responsible for facial movement.
6. Stroke-related facial paralysis: Caused by a stroke that affects the nerves responsible for facial movement.
7. Neurodegenerative diseases such as Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS).
8. Infection-related facial paralysis: Caused by infections such as Lyme disease, meningitis, or encephalitis.
9. Post-viral facial paralysis: Caused by a viral infection that affects the nerves responsible for facial movement.

Treatment for facial paralysis depend on the underlying cause and may include medications, surgery, physical therapy, and other interventions to address any associated symptoms.

Sleep paralysis typically occurs when the body is in a state of rapid eye movement (REM) sleep, a stage of sleep characterized by vivid dreams and increased brain activity. In REM sleep, the body is paralyzed to prevent acting out dreams, but in sleep paralysis, the paralysis persists even after the individual has awoken.

There are several factors that may contribute to sleep paralysis, including:

1. Sleep deprivation: Lack of sleep or disruptions in normal sleep patterns can increase the risk of sleep paralysis.
2. Genetics: Sleep paralysis may run in families, suggesting that there may be a genetic component to the condition.
3. Sleep disorders: Certain sleep disorders, such as narcolepsy or sleep apnea, may increase the risk of sleep paralysis.
4. Mental health: Sleep paralysis may be more common in individuals with mental health conditions such as anxiety or depression.
5. Substance use: Alcohol and certain medications may disrupt sleep patterns and increase the risk of sleep paralysis.

There is no specific treatment for sleep paralysis, but there are several strategies that may help reduce the frequency and severity of episodes. These include:

1. Improving sleep habits: Establishing a regular sleep schedule, avoiding caffeine and alcohol before bedtime, and creating a relaxing sleep environment can help promote better sleep and reduce the risk of sleep paralysis.
2. Reducing stress: Practicing stress-reducing techniques such as meditation or yoga may help reduce the risk of sleep paralysis.
3. Treating underlying sleep disorders: If sleep paralysis is occurring as a result of a sleep disorder, treating the underlying condition may help resolve the problem.
4. Medication: In some cases, medication may be prescribed to help regulate sleep patterns and reduce the risk of sleep paralysis.
5. Cognitive-behavioral therapy (CBT): CBT may be helpful in managing the anxiety and fear associated with sleep paralysis.

If you are experiencing recurrent sleep paralysis, it is important to speak with a healthcare professional to rule out any underlying medical conditions and develop a treatment plan.

Tick paralysis is most commonly seen in children and young adults, and it is more prevalent during the spring and summer months when ticks are most active. The condition is usually diagnosed based on a combination of clinical symptoms and laboratory tests, such as blood tests or lumbar puncture.

Treatment of tick paralysis typically involves antibiotics to eradicate the infection, as well as supportive care to manage symptoms such as muscle weakness, paralysis, and respiratory failure. In severe cases, hospitalization may be necessary to provide intensive care.

Prevention of tick paralysis includes avoiding areas with high grass and leaf litter, wearing protective clothing and insect repellents when outdoors, and checking for ticks after spending time outdoors. Removing ticks promptly can also help prevent the spread of infection.

Overall, tick paralysis is a rare but potentially serious condition that can be caused by tick bites. Prompt diagnosis and treatment are essential to prevent long-term neurological damage or death.

The main symptoms of HyperKPP are recurrent episodes of muscle weakness or paralysis, usually triggered by changes in potassium levels or other factors such as stress, exercise, or certain medications. These episodes can last from a few minutes to several hours and can affect any part of the body, including the legs, arms, face, and respiratory muscles.

During an episode, patients may experience muscle weakness, paralysis, and twitching, as well as abnormal heart rhythms and palpitations. They may also have difficulty speaking, swallowing, or breathing. In severe cases, HyperKPP can lead to respiratory failure and other complications.

There is no cure for HyperKPP, but medications such as acetazolamide and sodium citrate can help manage symptoms and prevent episodes. Patients with HyperKPP must avoid triggers such as stress, exercise, and certain medications, and maintain a balanced diet and regular potassium intake to control symptoms. In severe cases, a pacemaker or an implantable cardioverter-defibrillator (ICD) may be necessary to regulate the heart rhythm.

HyperKPP is a rare disorder that affects approximately 1 in 100,000 people worldwide. It can be difficult to diagnose, as the symptoms can be similar to other conditions such as hypokalemic periodic paralysis or other muscle disorders. However, genetic testing and a thorough medical history can help confirm the diagnosis.

Overall, HyperKPP is a rare and complex disorder that requires careful management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle modifications, many patients with HyperKPP are able to lead active and fulfilling lives.

Hypotonia is a state of decreased muscle tone, which can be caused by various conditions, such as injury, disease, or disorders that affect the nervous system. It is characterized by a decrease in muscle stiffness and an increase in joint range of motion. Muscle hypotonia can result in difficulty with movement, coordination, and balance.

There are several types of muscle hypotonia, including:

1. Central hypotonia: This type is caused by dysfunction in the central nervous system and results in a decrease in muscle tone throughout the body.
2. Peripheral hypotonia: This type is caused by dysfunction in the peripheral nervous system and results in a selective decrease in muscle tone in specific muscle groups.
3. Mixed hypotonia: This type combines central and peripheral hypotonia.

Muscle hypotonia can be associated with a variety of symptoms, such as fatigue, weakness, poor coordination, and difficulty with speech and swallowing. Treatment options vary depending on the underlying cause of the condition and may include physical therapy, medication, and lifestyle modifications.

Muscle hypotonia is a common condition that can affect people of all ages, from children to adults. Early diagnosis and treatment are important to help manage symptoms and improve quality of life. If you suspect you or your child may have muscle hypotonia, consult with a healthcare professional for proper evaluation and treatment.

The normal range for potassium levels in the blood varies depending on age, gender, and other factors, but generally it is between 3.5 and 5.5 mEq/L (milliequivalents per liter).

Hypokalemia can be caused by a variety of factors such as diarrhea, vomiting, certain medications (diuretics, laxatives), kidney disease or malfunctioning of the parathyroid glands.

There are three main forms of poliomyelitis:

1. Non-paralytic polio, which causes symptoms such as fever, headache, and sore throat, but does not lead to paralysis.
2. Paralytic polio, which can cause partial or complete paralysis of the muscles in the limbs, trunk, and respiratory system. This form is more severe and can be fatal.
3. Post-polio syndrome, which occurs in some individuals years after they have recovered from a paralytic polio infection. It is characterized by new muscle weakness, pain, and fatigue.

Poliomyelitis was once a major public health problem worldwide, but widespread immunization campaigns have led to a significant decline in the number of cases. The World Health Organization (WHO) has set a goal of eradicating polio by 2018.

Treatment for poliomyelitis typically focuses on managing symptoms and supporting respiratory function. In severe cases, hospitalization may be necessary to provide intensive care, such as mechanical ventilation. Physical therapy and rehabilitation are also important in helping individuals recover from paralysis.

Prevention is key to controlling the spread of poliomyelitis. This includes vaccination with the oral poliovirus vaccine (OPV), which has been shown to be safe and effective in preventing polio. In addition, good hygiene practices, such as washing hands regularly, can help reduce the risk of transmission.

The most common cause of thyrotoxicosis is an overactive thyroid gland, known as hyperthyroidism. This can be caused by a variety of factors, including:

* Graves' disease: An autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone.
* Toxic multinodular goiter: A condition in which one or more nodules in the thyroid gland become overactive and produce excessive amounts of thyroid hormone.
* Thyroid adenoma: A benign tumor of the thyroid gland that can cause hyperthyroidism.
* Thyroid cancer: A malignant tumor of the thyroid gland that can cause hyperthyroidism.

Symptoms of thyrotoxicosis can vary depending on the severity of the condition and the individual affected, but may include:

* Weight loss
* Increased heart rate
* Anxiety
* Sweating
* Tremors
* Nervousness
* Fatigue
* Heat intolerance
* Increased bowel movements
* Muscle weakness

Thyrotoxicosis can be diagnosed through a series of tests, including:

* Blood tests: To measure thyroid hormone levels in the blood.
* Thyroid scan: To visualize the thyroid gland and identify any nodules or tumors.
* Ultrasound: To evaluate the structure of the thyroid gland and detect any abnormalities.

Treatment for thyrotoxicosis depends on the underlying cause, but may include:

* Medications to reduce thyroid hormone production.
* Radioactive iodine therapy to destroy part or all of the thyroid gland.
* Surgery to remove part or all of the thyroid gland.

It is important to note that untreated thyrotoxicosis can lead to complications such as heart problems, osteoporosis, and eye problems, so it is important to seek medical attention if symptoms persist or worsen over time.

Paraplegia is classified into two main types:

1. Complete paraplegia: Total loss of motor function in both legs and pelvis.
2. Incomplete paraplegia: Some degree of motor function remains in the affected limbs.

Symptoms of paraplegia can include weakness, paralysis, numbness, or tingling sensations below the level of the spinal cord injury. Loss of bladder and bowel control, sexual dysfunction, and changes in sensation (such as decreased sensitivity to touch and temperature) are also common.

Diagnosis typically involves a physical examination, medical history, neurological tests such as reflexes and muscle strength, and imaging studies like X-rays or MRIs to determine the underlying cause of paraplegia. Treatment depends on the specific cause of the condition and may include medications, rehabilitation therapy, and assistive devices such as braces, canes, or wheelchairs.

Causes of Hyperkalemia:

1. Kidney dysfunction: When the kidneys are not able to excrete excess potassium, it can build up in the bloodstream and lead to hyperkalemia.
2. Medications: Certain drugs, such as ACE inhibitors, potassium-sparing diuretics, and NSAIDs, can increase potassium levels by blocking the excretion of potassium in the urine.
3. Diabetic ketoacidosis: High levels of potassium can occur in people with uncontrolled diabetes who have diabetic ketoacidosis.
4. Acute kidney injury: This condition can cause a rapid increase in potassium levels as the kidneys are unable to remove excess potassium from the blood.
5. Heart disease: Potassium levels can rise in people with heart failure or other cardiac conditions, leading to hyperkalemia.

Symptoms of Hyperkalemia:

1. Muscle weakness and fatigue
2. Abnormal heart rhythms (arrhythmias)
3. Palpitations
4. Constipation
5. Nausea and vomiting
6. Abdominal cramps
7. Fatigue
8. Confusion
9. Headaches
10. Weakness in the legs and feet

Treatment of Hyperkalemia:

The treatment of hyperkalemia depends on the underlying cause and the severity of the condition. Some of the common methods for lowering potassium levels include:

1. Diuretics: These medications help remove excess fluid and electrolytes, including potassium, from the body.
2. Calcium gluconate: This medication can help stabilize cardiac function and reduce the risk of arrhythmias.
3. Insulin and glucose: Giving insulin and glucose to someone with diabetic ketoacidosis can help lower potassium levels by increasing glucose uptake in the cells.
4. Hemodialysis: This is a process that uses a machine to filter waste products, including excess potassium, from the blood.
5. Potassium-binding resins: These medications can bind to potassium ions in the gut and prevent their absorption into the bloodstream.
6. Sodium polystyrene sulfonate (Kayexalate): This medication can help lower potassium levels by binding to excess potassium in the gut and causing it to be eliminated in the stool.
7. Activated charcoal: This medication can help bind to potassium ions in the gut and prevent their absorption into the bloodstream.

In severe cases of hyperkalemia, hospitalization may be necessary to monitor and treat the condition. In some instances, dialysis may be required to remove excess potassium from the blood. It is important to note that the treatment for hyperkalemia should only be done under the guidance of a healthcare professional, as some medications or procedures can worsen the condition if not properly managed.

The term "Bell's palsy" was coined by Sir Charles Bell in 1829, and it is named after him. The condition is caused by damage to the facial nerve, which can be due to a variety of factors such as viral infections, autoimmune disorders, trauma, or tumors.

Bell's palsy can cause a range of symptoms including:

* Weakness or paralysis of the facial muscles on one side of the face
* Drooping or weakness of the eyelid or corner of the mouth
* Difficulty closing the eye or smiling
* Dryness or excessive tearing of the eye
* Increased sensitivity to sound or touch on the affected side
* Pain or discomfort in the face, jaw, or ear

Bell's palsy can be diagnosed by a neurologist based on symptoms and physical examination. Imaging tests such as MRI or CT scans may be ordered to rule out other conditions that can cause similar symptoms.

There is no cure for Bell's palsy, but various treatments can help manage the symptoms. These may include:

* Medications to reduce inflammation and pain
* Physical therapy to improve facial function and appearance
* Surgery to repair or remove damaged nerve tissue
* Corticosteroid injections to reduce swelling and inflammation

The prognosis for Bell's palsy is generally good, with most people experiencing a full recovery within a few weeks to months. However, some people may experience long-term symptoms or complications such as permanent nerve damage or eye dryness.

Some examples of Facial Nerve Diseases include:

* Bell's Palsy: A condition that causes weakness or paralysis of the facial muscles on one side of the face, often resulting in drooping or twitching of the eyelid and facial muscles.
* Facial Spasm: A condition characterized by involuntary contractions of the facial muscles, which can cause twitching or spasms.
* Progressive Bulbar Palsy (PBP): A rare disorder that affects the brain and spinal cord, leading to weakness and wasting of the muscles in the face, tongue, and throat.
* Parry-Romberg Syndrome: A rare condition characterized by progressive atrophy of the facial muscles on one side of the face, leading to a characteristic "smile" or "grimace."
* Moebius Syndrome: A rare neurological disorder that affects the nerves responsible for controlling eye movements and facial expressions.
* Trauma to the Facial Nerve: Damage to the facial nerve can result in weakness or paralysis of the facial muscles, depending on the severity of the injury.

These are just a few examples of Facial Nerve Diseases, and there are many other conditions that can affect the facial nerve and cause similar symptoms. A comprehensive diagnosis and evaluation by a healthcare professional is necessary to determine the specific underlying condition and develop an appropriate treatment plan.

Quadriplegia can be classified into two types:

1. Complete quadriplegia: This is when all four limbs are paralyzed and there is no movement or sensation below the level of the injury.
2. Incomplete quadriplegia: This is when some movement or sensation remains below the level of the injury, but not in all four limbs.

The symptoms of quadriplegia can vary depending on the underlying cause and severity of the condition. They may include:

* Loss of movement in the arms and legs
* Weakness or paralysis of the muscles in the arms and legs
* Decreased or absent sensation in the arms and legs
* Difficulty with balance and coordination
* Difficulty with walking, standing, or sitting
* Difficulty with performing daily activities such as dressing, grooming, and feeding oneself

The diagnosis of quadriplegia is typically made through a combination of physical examination, medical history, and imaging studies such as X-rays or MRIs. Treatment for quadriplegia depends on the underlying cause and may include:

* Physical therapy to improve strength and mobility
* Occupational therapy to learn new ways of performing daily activities
* Assistive devices such as braces, walkers, or wheelchairs
* Medications to manage pain, spasticity, or other symptoms
* Surgery to repair or stabilize the spinal cord or other affected areas.

Overall, quadriplegia is a severe condition that can significantly impact a person's quality of life. However, with appropriate treatment and support, many people with quadriplegia are able to lead active and fulfilling lives.

There are different types of OP, including:

1. Erb's Palsy: A condition that occurs when the nerves in the neck are damaged during delivery, leading to weakness or paralysis of the arm and shoulder muscles.
2. Brachial Plexus Birth Palsy (BPBP): A condition that occurs when the nerves in the upper group of the brachial plexus (a network of nerves in the neck and shoulder) are damaged during delivery, leading to weakness or paralysis of the arm and hand muscles.
3. Posterior Cord Syndrome: A condition that occurs when the nerves in the lower back are damaged during delivery, leading to weakness or paralysis of the legs, bladder, and bowel function.
4. Central Cord Syndrome: A condition that occurs when the nerves in the spinal cord are damaged during delivery, leading to weakness or paralysis of the muscles in the trunk, arms, and legs.

The symptoms of OP can vary depending on the type and severity of the condition, but may include:

* Weakness or paralysis of specific muscle groups
* Difficulty with movement and coordination
* Loss of sensation in certain areas of the body
* Bladder and bowel dysfunction
* Decreased reflexes

OP can be diagnosed through a physical examination, nerve conduction studies, and imaging tests such as MRI or EMG. Treatment for OP typically involves physical therapy, occupational therapy, and other supportive measures to help improve muscle strength and function. In some cases, surgery may be necessary to relieve pressure on the affected nerves or to repair damaged tissue.

Preventing OP is important, and this can involve:

* Proper use of obstetric forceps or vacuum extraction during delivery
* Avoiding excessive traction or pressure on the baby's head or body during delivery
* Monitoring fetal heart rate and using appropriate interventions if there are signs of distress
* Encouraging a safe and healthy pregnancy and delivery, with proper prenatal care and avoiding risk factors such as smoking, alcohol use, and high blood pressure.

The most common symptoms of enterovirus infections include:

* Diarrhea
* Vomiting
* Fever
* Abdominal pain
* Headache
* Fatigue

In some cases, enterovirus infections can lead to more severe complications, such as:

* Hand, foot, and mouth disease (HFMD)
* Aseptic meningitis
* Encephalitis
* Myocarditis

Enteroviruses are highly contagious and can be spread through:

* Close contact with an infected person
* Contaminated food and water
* Insect vectors

There is no specific treatment for enterovirus infections, but symptoms can be managed with supportive care, such as hydration, rest, and pain relief. Antiviral medications may be used in severe cases.

Prevention measures include:

* Good hygiene practices, such as frequent handwashing
* Avoiding close contact with people who are sick
* Properly preparing and storing food and water
* Avoiding sharing items that come into contact with the mouth, such as utensils and drinking glasses.

The symptoms of Andersen Syndrome can vary in severity and may include:

1. Heart rhythm disturbances (arrhythmias)
2. Abnormal heart rate
3. Fainting spells (syncope)
4. Seizures
5. Weakness or paralysis of the face, arms, or legs
6. Vision problems
7. Hearing loss
8. Developmental delays and intellectual disability
9. Craniofacial abnormalities
10. Short stature

Andersen Syndrome is usually diagnosed through a combination of clinical evaluation, electrophysiology studies, and genetic testing. Treatment is aimed at managing the symptoms and may include medications to regulate the heart rhythm, anticonvulsants for seizure control, and physical therapy to improve muscle strength and coordination. In some cases, implantation of a cardioverter-defibrillator (ICD) may be necessary to prevent sudden death.

Andersen Syndrome is an autosomal dominant disorder, which means that a single copy of the mutated gene is enough to cause the condition. It can be inherited from one affected parent or can occur spontaneously due to a new mutation. The syndrome affects both males and females equally and can affect individuals of all ages, including children and adults.

Overall, Andersen Syndrome is a rare and complex disorder that requires careful management and monitoring by a team of healthcare professionals. With appropriate treatment, individuals with this condition can lead fulfilling lives despite the challenges posed by the syndrome.

There are two main types of myotonia:

1. Thomsen's disease: This is an inherited form of myotonia that affects the muscles of the face, neck, and limbs. It is caused by mutations in the CLCN1 gene and can be severe, causing difficulty with speaking, swallowing, and breathing.
2. Becker's muscular dystrophy: This is a form of muscular dystrophy that affects both the skeletal and cardiac muscles. It is caused by mutations in the DMPK gene and can cause myotonia, muscle weakness, and heart problems.

The symptoms of myotonia can vary depending on the severity of the condition and may include:

* Muscle stiffness and rigidity
* Spasms or twitches
* Difficulty with movement and mobility
* Fatigue and weakness
* Cramps
* Muscle wasting

Myotonia can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electromyography (EMG) and muscle biopsy. There is no cure for myotonia, but treatment options may include:

* Physical therapy to improve movement and mobility
* Medications to relax muscles and reduce spasms
* Lifestyle modifications such as avoiding triggers and taking regular breaks to rest
* Surgery in severe cases to release or lengthen affected muscles.

It is important to note that myotonia can be a symptom of other underlying conditions, so proper diagnosis and management by a healthcare professional is essential to determine the best course of treatment.

There are several types of ophthalmoplegia, including:

1. External ophthalmoplegia: This type affects the muscles that control lateral and vertical movements of the eyes.
2. Internal ophthalmoplegia: This type affects the muscles that control rotational movements of the eyes.
3. Superior oblique paresis: This type affects the superior oblique muscle, which controls downward and outward movements of the eye.
4. Inferior oblique paresis: This type affects the inferior oblique muscle, which controls upward and outward movements of the eye.

Symptoms of ophthalmoplegia may include difficulty moving the eyes, double vision, droopy eyelids, and blurred vision. Treatment options depend on the underlying cause of the condition and may include physical therapy, prism lenses, or surgery.

There are several types of RTA, including:

1. Type 1 RTA: This is caused by a defect in the genes that code for the proteins involved in acid secretion in the renal tubules.
2. Type 2 RTA: This is caused by damage to the renal tubules, such as from exposure to certain drugs or toxins.
3. Type 4 RTA: This is caused by a deficiency of the hormone aldosterone, which helps regulate electrolyte levels in the body.

Symptoms of RTA can include:

* Nausea and vomiting
* Abdominal pain
* Fatigue
* Weakness
* Dehydration
* Increased heart rate
* Decreased urine production

RTA can be diagnosed through blood tests that measure the pH levels in the body, as well as tests that assess kidney function and electrolyte levels. Treatment for RTA typically involves correcting any underlying causes, such as stopping certain medications or addressing electrolyte imbalances. In some cases, medications may be prescribed to help regulate acid levels in the body.

Prevention of RTA includes maintaining proper hydration, avoiding exposure to harmful substances, and managing any underlying medical conditions that may increase the risk of developing RTA. Early detection and treatment can help prevent complications and improve outcomes for individuals with RTA.

1. Foodborne botulism: This type of botulism is caused by eating foods that have been contaminated with the bacteria. Symptoms typically begin within 12 to 72 hours after consuming the contaminated food and can include double vision, droopy eyelids, slurred speech, difficulty swallowing, and muscle weakness.
2. Infant botulism: This type of botulism occurs in infants who are exposed to the bacteria through contact with contaminated soil or object. Symptoms can include constipation, poor feeding, and weak cry.
3. Wound botulism: This type of botulism is caused by the bacteria entering an open wound, usually a deep puncture wound or surgical incision.

Botulism is a rare illness in the United States, but it can be deadly if not treated promptly. Treatment typically involves supportive care, such as mechanical ventilation and fluids, as well as antitoxin injections to neutralize the effects of the toxin. Prevention measures include proper food handling and storage, good hygiene practices, and avoiding consumption of improperly canned or preserved foods.

Some common examples of spinal cord diseases include:

1. Spinal muscular atrophy: This is a genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement. It can cause muscle weakness and wasting, as well as other symptoms such as respiratory problems and difficulty swallowing.
2. Multiple sclerosis: This is an autoimmune disease that causes inflammation and damage to the protective covering of nerve fibers in the spinal cord. Symptoms can include vision problems, muscle weakness, balance and coordination difficulties, and cognitive impairment.
3. Spinal cord injuries: These can occur as a result of trauma, such as a car accident or a fall, and can cause a range of symptoms including paralysis, numbness, and loss of sensation below the level of the injury.
4. Spinal stenosis: This is a condition in which the spinal canal narrows, putting pressure on the spinal cord and nerve roots. Symptoms can include back pain, leg pain, and difficulty walking or standing for long periods.
5. Tumors: Benign or malignant tumors can grow in the spinal cord, causing a range of symptoms including pain, weakness, and numbness or tingling in the limbs.
6. Infections: Bacterial, viral, or fungal infections can cause inflammation and damage to the spinal cord, leading to symptoms such as fever, headache, and muscle weakness.
7. Degenerative diseases: Conditions such as amyotrophic lateral sclerosis (ALS) and primary lateral sclerosis (PLS) can cause progressive degeneration of the spinal cord nerve cells, leading to muscle weakness, twitching, and wasting.
8. Trauma: Traumatic injuries, such as those caused by sports injuries or physical assault, can damage the spinal cord and result in a range of symptoms including pain, numbness, and weakness.
9. Ischemia: Reduced blood flow to the spinal cord can cause tissue damage and lead to symptoms such as weakness, numbness, and paralysis.
10. Spinal cord infarction: A blockage in the blood vessels that supply the spinal cord can cause tissue damage and lead to symptoms similar to those of ischemia.

It's important to note that some of these conditions can be caused by a combination of factors, such as genetics, age, lifestyle, and environmental factors. It's also worth noting that some of these conditions can have a significant impact on quality of life, and in some cases, may be fatal.

Brachial plexus neuritis is a condition that affects the brachial plexus, a network of nerves that runs from the spine down to the shoulder and arm. It occurs when the nerves in this region become inflamed or damaged, leading to pain and weakness in the arm and hand.

The condition can be caused by a variety of factors, including injury, infection, or compression of the nerves. It is more common in young adults and may be associated with certain medical conditions, such as diabetes, thyroid disease, or Lyme disease.

Symptoms of brachial plexus neuritis may include pain, numbness, tingling, and weakness in the arm and hand. The condition can also cause difficulty with gripping or grasping objects, and may affect fine motor skills such as writing or buttoning a shirt.

Treatment for brachial plexus neuritis typically involves physical therapy, pain management, and addressing any underlying medical conditions. In some cases, surgery may be necessary to relieve compression or damage to the nerves. With appropriate treatment, most people with brachial plexus neuritis are able to recover significant function in their arm and hand over time.

Recurrent laryngeal nerve injuries refer to damage or trauma to the recurrent laryngeal nerve, which is a branch of the vagus nerve that supplies motor and sensory functions to the larynx (voice box) and other structures in the neck and throat. These injuries can occur due to various causes such as surgery, trauma, or degenerative conditions.

Types of Recurrent Laryngeal Nerve Injuries:

There are several types of recurrent laryngeal nerve injuries, including:

1. Traumatic injury: This type of injury occurs due to direct blows or penetrating wounds to the neck or throat.
2. Ischemic injury: This type of injury occurs due to reduced blood flow to the nerve, often due to atherosclerosis (narrowing of the blood vessels) or other conditions that affect blood flow.
3. Neuritis: This type of injury occurs due to inflammation of the nerve, often due to viral infections such as herpes zoster (shingles).
4. Tumors: Benign or malignant tumors in the neck or throat can compress or damage the recurrent laryngeal nerve.
5. Surgical injury: Recurrent laryngeal nerve injuries can occur during surgical procedures such as thyroid or parathyroid surgery, or laryngotomy (surgery on the voice box).

Symptoms of Recurrent Laryngeal Nerve Injuries:

The symptoms of recurrent laryngeal nerve injuries can vary depending on the severity and location of the injury. Common symptoms include:

1. Hoarseness or weakness of the voice
2. Difficulty swallowing (dysphagia)
3. Pain in the neck, throat, or ear
4. Numbness or tingling sensations in the neck or face
5. Weakness or paralysis of the vocal cords
6. Inability to speak or vocalize
7. Breathing difficulties

Diagnosis and Treatment of Recurrent Laryngeal Nerve Injuries:

To diagnose a recurrent laryngeal nerve injury, a thorough medical history and physical examination are essential. Imaging studies such as MRI or CT scans may also be ordered to confirm the presence and extent of the injury. Electromyography (EMG) and nerve conduction studies (NCS) may also be performed to assess the function of the nerve.

Treatment of recurrent laryngeal nerve injuries depends on the underlying cause and severity of the injury. Some common treatment options include:

1. Supportive care: Patients with mild symptoms may require only supportive care, such as voice therapy or speech therapy to improve communication.
2. Medications: Anti-inflammatory medications or steroids may be prescribed to reduce swelling and inflammation.
3. Surgery: In some cases, surgical intervention may be necessary to repair the damaged nerve or remove any compressive lesions.
4. Botulinum toxin injections: Botulinum toxin injections can be used to relax the vocal cord muscles and improve voice quality.
5. Thyroid hormone replacement: Patients with hypothyroidism may require thyroid hormone replacement therapy to improve vocal cord function.
6. Laryngeal framework surgery: This type of surgery is used to correct any structural abnormalities in the larynx that may be contributing to the nerve injury.
7. Vocal fold injection: Injecting material into the vocal folds can help to improve voice quality and reduce symptoms.
8. Speech therapy: Patients with persistent symptoms may require speech therapy to improve communication and address any swallowing difficulties.

Conclusion:

Recurrent laryngeal nerve injuries can have a significant impact on an individual's quality of life, causing a range of symptoms that affect communication, breathing, and swallowing. Prompt diagnosis and appropriate treatment are essential to prevent long-term damage and improve outcomes. While treatment options vary depending on the underlying cause and severity of the injury, surgical interventions, botulinum toxin injections, and speech therapy may be effective in managing symptoms and improving voice quality.

The symptoms of GBS can range from mild to severe and may include:

* Weakness or tingling sensations in the legs, arms, or face
* Muscle weakness that progresses to paralysis
* Loss of reflexes
* Difficulty swallowing or speaking
* Numbness or pain in the hands and feet
* Fatigue and fever

The diagnosis of GBS is based on a combination of symptoms, physical examination findings, and laboratory tests. There is no cure for GBS, but treatment can help manage symptoms and prevent complications. Plasmapheresis, immunoglobulin therapy, and corticosteroids are common treatments used to reduce inflammation and slow the progression of the disease.

GBS is a rare condition that affects about one in 100,000 people per year in the United States. It can affect anyone, but it is more common in children and young adults. The prognosis for GBS varies depending on the severity of the disease, but most people recover fully within a few weeks or months with proper treatment.

In conclusion, Guillain-Barré Syndrome is a rare autoimmune disorder that can cause muscle weakness and paralysis. While there is no cure for GBS, early diagnosis and treatment can help manage symptoms and prevent complications. With proper care, most people with GBS can recover fully within a few weeks or months.

There are several different types of spinal cord injuries that can occur, depending on the location and severity of the damage. These include:

1. Complete spinal cord injuries: In these cases, the spinal cord is completely severed, resulting in a loss of all sensation and function below the level of the injury.
2. Incomplete spinal cord injuries: In these cases, the spinal cord is only partially damaged, resulting in some remaining sensation and function below the level of the injury.
3. Brown-Sequard syndrome: This is a specific type of incomplete spinal cord injury that affects one side of the spinal cord, resulting in weakness or paralysis on one side of the body.
4. Conus medullaris syndrome: This is a type of incomplete spinal cord injury that affects the lower part of the spinal cord, resulting in weakness or paralysis in the legs and bladder dysfunction.

The symptoms of spinal cord injuries can vary depending on the location and severity of the injury. They may include:

* Loss of sensation in the arms, legs, or other parts of the body
* Weakness or paralysis in the arms, legs, or other parts of the body
* Difficulty walking or standing
* Difficulty with bowel and bladder function
* Numbness or tingling sensations
* Pain or pressure in the neck or back

Treatment for spinal cord injuries typically involves a combination of medical and rehabilitative therapies. Medical treatments may include:

* Immobilization of the spine to prevent further injury
* Medications to manage pain and inflammation
* Surgery to relieve compression or stabilize the spine

Rehabilitative therapies may include:

* Physical therapy to improve strength and mobility
* Occupational therapy to learn new ways of performing daily activities
* Speech therapy to improve communication skills
* Psychological counseling to cope with the emotional effects of the injury.

Overall, the prognosis for spinal cord injuries depends on the severity and location of the injury, as well as the age and overall health of the individual. While some individuals may experience significant recovery, others may experience long-term or permanent impairment. It is important to seek medical attention immediately if symptoms of a spinal cord injury are present.

There are several types of channelopathies, including:

1. Long QT syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
2. Short QT syndrome: This is a rare condition that has the opposite effect of long QT syndrome, causing the heart to beat too quickly.
3. Catecholaminergic polymorphic ventricular tachycardia (CPVT): This is a rare disorder that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
4. Brugada syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
5. Wolff-Parkinson-White (WPW) syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
6. Neuromuscular disorders: These are disorders that affect the nerve-muscle junction, leading to muscle weakness and wasting. Examples include muscular dystrophy and myasthenia gravis.
7. Dystrophinopathies: These are a group of disorders that affect the structure of muscle cells, leading to muscle weakness and wasting. Examples include Duchenne muscular dystrophy and Becker muscular dystrophy.
8. Myotonia: This is a condition that affects the muscles, causing them to become stiff and rigid.
9. Hyperkalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to abnormal potassium levels in the body.
10. Hypokalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to low potassium levels in the body.
11. Thyrotoxic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to an overactive thyroid gland.
12. Hyperthyroidism: This is a condition where the thyroid gland becomes overactive, leading to increased heart rate, weight loss, and muscle weakness.
13. Hypothyroidism: This is a condition where the thyroid gland becomes underactive, leading to fatigue, weight gain, and muscle weakness.
14. Pituitary tumors: These are tumors that affect the pituitary gland, which regulates hormone production in the body.
15. Adrenal tumors: These are tumors that affect the adrenal glands, which produce hormones such as cortisol and aldosterone.
16. Carcinoid syndrome: This is a condition where cancer cells in the digestive system produce hormones that can cause muscle weakness and wasting.
17. Multiple endocrine neoplasia (MEN): This is a genetic disorder that affects the endocrine system and can cause tumors to grow in the thyroid, adrenal, and parathyroid glands.

These are just some of the many potential causes of muscle weakness. It's important to see a healthcare professional for an accurate diagnosis and appropriate treatment.

1. Muscular dystrophy: A group of genetic disorders characterized by progressive muscle weakness and degeneration.
2. Myopathy: A condition where the muscles become damaged or diseased, leading to muscle weakness and wasting.
3. Fibromyalgia: A chronic condition characterized by widespread pain, fatigue, and muscle stiffness.
4. Rhabdomyolysis: A condition where the muscle tissue is damaged, leading to the release of myoglobin into the bloodstream and potentially causing kidney damage.
5. Polymyositis/dermatomyositis: Inflammatory conditions that affect the muscles and skin.
6. Muscle strain: A common injury caused by overstretching or tearing of muscle fibers.
7. Cervical dystonia: A movement disorder characterized by involuntary contractions of the neck muscles.
8. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, leading to muscle weakness and fatigue.
9. Oculopharyngeal myopathy: A condition characterized by weakness of the muscles used for swallowing and eye movements.
10. Inclusion body myositis: An inflammatory condition that affects the muscles, leading to progressive muscle weakness and wasting.

These are just a few examples of the many different types of muscular diseases that can affect individuals. Each condition has its unique set of symptoms, causes, and treatment options. It's important for individuals experiencing muscle weakness or wasting to seek medical attention to receive an accurate diagnosis and appropriate care.

There are several causes of muscle weakness, including:

1. Neuromuscular diseases: These are disorders that affect the nerves that control voluntary muscle movement, such as amyotrophic lateral sclerosis (ALS) and polio.
2. Musculoskeletal disorders: These are conditions that affect the muscles, bones, and joints, such as arthritis and fibromyalgia.
3. Metabolic disorders: These are conditions that affect the body's ability to produce energy, such as hypoglycemia and hypothyroidism.
4. Injuries: Muscle weakness can occur due to injuries such as muscle strains and tears.
5. Infections: Certain infections such as botulism and Lyme disease can cause muscle weakness.
6. Nutritional deficiencies: Deficiencies in vitamins and minerals such as vitamin D and B12 can cause muscle weakness.
7. Medications: Certain medications such as steroids and anticonvulsants can cause muscle weakness as a side effect.

The symptoms of muscle weakness can vary depending on the underlying cause, but may include:

1. Fatigue: Feeling tired or weak after performing simple tasks.
2. Lack of strength: Difficulty lifting objects or performing physical activities.
3. Muscle cramps: Spasms or twitches in the muscles.
4. Muscle wasting: Loss of muscle mass and tone.
5. Difficulty speaking or swallowing: In cases where the muscle weakness affects the face, tongue, or throat.
6. Difficulty walking or standing: In cases where the muscle weakness affects the legs or lower back.
7. Droopy facial features: In cases where the muscle weakness affects the facial muscles.

If you are experiencing muscle weakness, it is important to seek medical attention to determine the underlying cause and receive proper treatment. A healthcare professional will perform a physical examination and may order diagnostic tests such as blood tests or imaging studies to help diagnose the cause of the muscle weakness. Treatment will depend on the underlying cause, but may include medication, physical therapy, or lifestyle changes. In some cases, muscle weakness may be a sign of a serious underlying condition that requires prompt medical attention.

1. Raspy or strained voice
2. Breathy voice
3. Scratchy or rough voice
4. Weak or falsetto voice
5. Loss of vocal range
6. Difficulty speaking for long periods of time
7. Fatigue or exhaustion of the vocal cords
8. Pain in the throat or larynx (voice box)
9. Difficulty articulating certain sounds or words

Hoarseness can be caused by a variety of factors, including:

1. Overuse or strain of the vocal cords, such as from screaming, shouting, or singing
2. Acid reflux or gastroesophageal reflux disease (GERD), which can irritate the throat and vocal cords
3. Viral infections, such as laryngitis or common cold
4. Bacterial infections, such as strep throat
5. Injury to the vocal cords or larynx
6. Neurological conditions, such as Parkinson's disease or multiple sclerosis
7. Hormonal changes, such as those experienced during pregnancy or menopause
8. Anxiety or stress, which can lead to tension in the throat and vocal cords
9. Smoking or exposure to secondhand smoke, which can irritate the throat and vocal cords
10. Aging, which can cause wear and tear on the vocal cords over time.

Hoarseness can be diagnosed through a series of tests, including:

1. Physical examination of the throat and larynx
2. Laryngoscopy, which involves inserting a scope into the throat to examine the vocal cords
3. Acoustic analysis, which measures the quality and characteristics of the voice
4. Imaging tests, such as X-rays or CT scans, to rule out other potential causes of hoarseness
5. Voice assessment, which involves evaluating the quality and functionality of the voice.

Treatment for hoarseness depends on the underlying cause and may include:

1. Resting the voice and avoiding heavy talking or singing
2. Drinking plenty of fluids to keep the throat moist
3. Using a humidifier to add moisture to the air
4. Avoiding irritants such as smoke and pollution
5. Taking over-the-counter pain relievers, such as acetaminophen or ibuprofen, to reduce inflammation and pain
6. Antibiotics if the hoarseness is caused by a bacterial infection
7. Steroids to reduce inflammation
8. Vocal therapy to improve vocal technique and reduce strain on the voice
9. Surgery, such as laser surgery or cordotomy, to remove lesions or improve vocal cord function.

There are several types of myotonic disorders, including:

1. Myotonia congenita: This is the most common form of myotonia and affects about 1 in 250,000 people worldwide. It is caused by mutations in the DMPK gene and typically affects the muscles of the face, neck, and limbs.
2. Myotonic dystrophy: This is a more severe form of myotonia that affects about 1 in 8,000 people worldwide. It is caused by mutations in the CNBP or PTPN1 genes and can lead to progressive muscle weakness and wasting.
3. Myotonic syndrome: This is a rare condition that affects about 1 in 100,000 people worldwide. It is caused by mutations in the SCN5A or CAV3 genes and can lead to muscle stiffness, spasms, and weakness, as well as other symptoms such as heart problems and vision loss.

Myotonic disorders can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and genetic testing. Treatment for myotonic disorders is focused on managing symptoms and improving quality of life. This may include physical therapy, muscle relaxants, and other medications to help manage muscle stiffness and spasms. In some cases, surgery may be necessary to relieve compression on nerves or to correct deformities.

Overall, myotonic disorders are a group of rare genetic conditions that can have a significant impact on quality of life. While there is currently no cure for these disorders, advances in medical research and technology are helping to improve diagnosis and treatment options for those affected.

There are several types of facial nerve injuries, including:

1. Bell's palsy: This is a condition that affects the facial nerve and causes weakness or paralysis of the muscles on one side of the face. It is often temporary and resolves on its own within a few weeks.
2. Facial paralysis: This is a condition in which the facial nerve is damaged, leading to weakness or paralysis of the muscles of facial expression. It can be caused by trauma, tumors, or viral infections.
3. Ramsay Hunt syndrome: This is a rare condition that occurs when the facial nerve is affected by a virus, leading to symptoms such as facial paralysis and pain in the ear.
4. Traumatic facial nerve injury: This can occur as a result of trauma to the head or face, such as a car accident or a fall.
5. Tumor-related facial nerve injury: In some cases, tumors can grow on the facial nerve and cause damage.
6. Ischemic facial nerve injury: This occurs when there is a reduction in blood flow to the facial nerve, leading to damage to the nerve fibers.
7. Neurofibromatosis type 2: This is a rare genetic disorder that can cause tumors to grow on the facial nerve, leading to damage and weakness of the facial muscles.

Treatment for facial nerve injuries depends on the underlying cause and severity of the injury. In some cases, physical therapy may be recommended to help regain strength and control of the facial muscles. Surgery may also be necessary in some cases to repair damaged nerve fibers or remove tumors.

The hypoglossal nerve is a cranial nerve that controls the movement of the tongue and other muscles in the throat. Hypoglossal nerve diseases refer to conditions that affect the functioning of this nerve, leading to symptoms such as difficulty swallowing, weakness or paralysis of the tongue, and speech difficulties.

Some examples of hypoglossal nerve diseases include:

1. Hypoglossal neuritis: This is an inflammation of the hypoglossal nerve, which can be caused by viral infections, head injuries, or other conditions.
2. Hypoglossal nerve palsy: This is a condition where the hypoglossal nerve is damaged or compressed, leading to weakness or paralysis of the tongue and other muscles in the throat.
3. Congenital hypoglossal nerve defects: These are birth defects that affect the development of the hypoglossal nerve, leading to a range of symptoms including difficulty swallowing and speech difficulties.
4. Trauma to the hypoglossal nerve: This can occur due to injury or trauma to the neck or head, leading to weakness or paralysis of the tongue and other muscles in the throat.
5. Tumors or cysts affecting the hypoglossal nerve: These can cause compression or damage to the nerve, leading to symptoms such as difficulty swallowing, speech difficulties, and weakness or paralysis of the tongue.

Hypoglossal nerve diseases can be diagnosed through a range of tests, including electromyography (EMG), nerve conduction studies (NCS), and imaging studies such as MRI or CT scans. Treatment depends on the underlying cause of the condition and may include physical therapy, medication, or surgery.

Cataplexy is often associated with narcolepsy, a neurological disorder that affects the brain's ability to regulate sleep-wake cycles. However, it can also occur in people without narcolepsy. In these cases, cataplexy may be a symptom of another condition or a side effect of certain medications.

The exact cause of cataplexy is not fully understood, but it is thought to be related to an imbalance in the brain chemicals that regulate muscle tone and emotion. Treatment for cataplexy typically involves addressing any underlying conditions or adjusting medications that may be contributing to the condition. In some cases, botulinum toxin injections may be recommended to reduce muscle stiffness and spasms.

Examples of 'Cataplexy' in a sentence:

1. The patient experienced cataplexy during laughing attacks, causing temporary paralysis of their limbs.
2. The doctor diagnosed the patient with cataplexy, a symptom of their narcolepsy.
3. The medication side effect was causing cataplexy, leading to muscle weakness and paralysis.

The symptoms of myotonia congenita can vary in severity and may include:

* Muscle stiffness and rigidity, especially in the legs, arms, and neck
* Difficulty relaxing muscles after contraction, leading to prolonged muscle tensing
* Muscle cramps and spasms
* Weakness and fatigue of the muscles
* Delayed or absent deep tendon reflexes
* Abnormal posture or gait
* Difficulty with speech and swallowing in severe cases

Myotonia congenita can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and genetic testing. Treatment for the condition typically involves physical therapy, massage, and relaxation techniques to help manage muscle stiffness and improve mobility. In severe cases, medications such as sodium channel blockers or chloride channel activators may be prescribed to help regulate muscle contraction and relaxation.

Myotonia congenita is a rare condition, and its prevalence is not well established. However, it is estimated to affect approximately 1 in 100,000 to 1 in 200,000 individuals worldwide. The condition can be inherited in an autosomal dominant manner, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be sporadic, meaning they are not inherited from either parent.

Overall, myotonia congenita is a rare and complex genetic disorder that affects the muscles and can significantly impact an individual's quality of life. With proper diagnosis and management, individuals with myotonia congenita can lead fulfilling lives despite the challenges posed by the condition.

There are several types of narcolepsy, including:

* Type 1 narcolepsy: This is the most common form of the disorder, and it is characterized by the presence of cataplexy and low levels of hypocretin-1, a neurotransmitter that helps regulate sleep and wakefulness.
* Type 2 narcolepsy: This form of narcolepsy is similar to type 1, but it does not involve cataplexy. Instead, people with type 2 narcolepsy may experience other symptoms such as memory loss, anxiety, and depression.
* Narcolepsy with cataplexy: This is a subtype of type 1 narcolepsy that is characterized by the presence of both cataplexy and low levels of hypocretin-1.
* Narcolepsy without cataplexy: This is a subtype of type 2 narcolepsy that is characterized by the absence of cataplexy and low levels of hypocretin-1.

There is no cure for narcolepsy, but medications such as stimulants, modafinil, and sodium oxybate can help manage symptoms. Behavioral interventions such as scheduled napping and exercise can also be helpful in managing the disorder.

Some common examples of cranial nerve diseases include:

1. Bell's palsy: A condition that affects the facial nerve, causing weakness or paralysis of one side of the face.
2. Multiple sclerosis: An autoimmune disease that damages the protective covering of nerve fibers, leading to communication problems between the brain and the rest of the body.
3. Trigeminal neuralgia: A condition that affects the trigeminal nerve, causing facial pain and numbness.
4. Meningitis: An inflammation of the meninges, the protective covering of the brain and spinal cord, which can damage the cranial nerves.
5. Acoustic neuroma: A type of non-cancerous tumor that grows on the nerve that connects the inner ear to the brain.
6. Cranial polyneuropathy: A condition where multiple cranial nerves are damaged, leading to a range of symptoms including muscle weakness, numbness, and pain.
7. Tumors: Both benign and malignant tumors can affect the cranial nerves, causing a variety of symptoms depending on their location and size.
8. Trauma: Head injuries or trauma can damage the cranial nerves, leading to a range of symptoms.
9. Infections: Bacterial or viral infections such as meningitis or encephalitis can damage the cranial nerves, leading to a range of symptoms.
10. Genetic disorders: Certain genetic disorders such as Charcot-Marie-Tooth disease can affect the cranial nerves, leading to a range of symptoms.

It's important to note that this is not an exhaustive list and there may be other causes of cranial nerve damage. If you are experiencing any symptoms that you think may be related to cranial nerve damage, it's important to seek medical attention as soon as possible for proper diagnosis and treatment.

Dysphonia can manifest in different ways, including:

1. Hoarseness: A raspy, strained, or rough quality to the voice.
2. Breathy voice: A weak, airy, or faint voice.
3. Harsh voice: A loud, screeching, or grating voice.
4. Rough voice: A scratchy, raw, or bumpy voice.
5. Stuttering: Repetition or prolongation of sounds, syllables, or words.
6. Slurred speech: Difficulty articulating words or speaking clearly.
7. Monotone speech: Speaking in a flat, emotionless tone.

Dysphonia can be acute or chronic, and it can affect individuals of all ages and backgrounds. In some cases, dysphonia may be a symptom of an underlying medical condition, such as a viral infection, allergies, or a neurological disorder. In other cases, it may be caused by overuse or misuse of the voice, such as shouting, singing, or speaking loudly for extended periods.

Treatment options for dysphonia depend on the underlying cause and severity of the condition. Some common treatments include:

1. Voice therapy: Techniques to improve breath support, vocal technique, and speech clarity.
2. Medications: To reduce inflammation, allergies, or other underlying conditions that may be contributing to dysphonia.
3. Surgery: In some cases, surgery may be necessary to correct structural problems in the vocal cords or other areas of the voice box.
4. Laryngeal electromyography (LEMG): A test used to evaluate the function of the vocal cords and surrounding muscles.
5. Speech therapy: To improve communication skills and address any language or cognitive impairments that may be contributing to dysphonia.
6. Botulinum toxin injections (Botox): Injected into the vocal cords to reduce spasms and improve voice quality.
7. Vocal cord paralysis: In some cases, injection of a local anesthetic or botulinum toxin may be used to paralyze one or both vocal cords, allowing for rest and healing.

It's important to seek medical attention if you experience any persistent or severe changes in your voice, as early diagnosis and treatment can improve outcomes and reduce the risk of long-term vocal cord damage. A healthcare professional will be able to assess your symptoms and recommend appropriate treatment options based on the underlying cause of your dysphonia.

There are several types of polyradiculoneuropathy, each with its own set of causes and characteristics:

1. Polyneuropathy: This is the most common type of polyradiculoneuropathy and affects multiple nerves throughout the body. It can be caused by a variety of factors, such as diabetes, vitamin deficiencies, alcoholism, and certain medications.
2. Mononeuritis multiplex: This is a condition in which there is damage to multiple nerves that innervate a specific area of the body, such as the legs or arms. It can be caused by various factors, including diabetes, autoimmune disorders, and certain medications.
3. Radiculoneuropathy: This type of polyradiculoneuropathy affects the nerves that originate from the spinal cord and extend to other parts of the body. It can be caused by compression or inflammation of the nerve roots, such as in the case of herniated discs or spinal stenosis.
4. Autonomic neuropathy: This type of polyradiculoneuropathy affects the nerves that control involuntary functions, such as heart rate, blood pressure, and digestion. It can be caused by a variety of factors, including diabetes, vitamin deficiencies, and certain medications.

The symptoms of polyradiculoneuropathy can vary depending on the specific type and severity of the condition. Common symptoms include:

* Weakness or numbness in the affected areas
* Pain or discomfort in the affected areas
* Difficulty walking or maintaining balance
* Difficulty with fine motor skills, such as buttoning a shirt or tying shoelaces
* Digestive problems, such as constipation or diarrhea
* Urinary incontinence or retention

The diagnosis of polyradiculoneuropathy is typically made based on a combination of physical examination findings, medical history, and results of diagnostic tests such as nerve conduction studies or electromyography. Treatment options for polyradiculoneuropathy depend on the underlying cause of the condition, but may include:

* Medications to manage pain or inflammation
* Physical therapy to improve strength and coordination
* Lifestyle modifications, such as quitting smoking or losing weight, to reduce pressure on the nerves
* Surgery to relieve compression or repair damaged nerves

In some cases, polyradiculoneuropathy may be a symptom of an underlying condition that can be treated or managed with medication or other therapies. It is important to seek medical attention if you experience any symptoms of polyradiculoneuropathy to receive an accurate diagnosis and appropriate treatment.

There are several types of nerve compression syndromes, including:

1. Carpal tunnel syndrome: Compression of the median nerve in the wrist, commonly caused by repetitive motion or injury.
2. Tarsal tunnel syndrome: Compression of the posterior tibial nerve in the ankle, similar to carpal tunnel syndrome but affecting the lower leg.
3. Cubital tunnel syndrome: Compression of the ulnar nerve at the elbow, often caused by repetitive leaning or bending.
4. Thoracic outlet syndrome: Compression of the nerves and blood vessels that pass through the thoracic outlet (the space between the neck and shoulder), often caused by poor posture or injury.
5. Peripheral neuropathy: A broader term for damage to the peripheral nerves, often caused by diabetes, vitamin deficiencies, or other systemic conditions.
6. Meralgia paresthetica: Compression of the lateral femoral cutaneous nerve in the thigh, commonly caused by direct trauma or compression from a tight waistband or clothing.
7. Morton's neuroma: Compression of the plantar digital nerves between the toes, often caused by poorly fitting shoes or repetitive stress on the feet.
8. Neuralgia: A general term for pain or numbness caused by damage or irritation to a nerve, often associated with chronic conditions such as shingles or postherpetic neuralgia.
9. Trigeminal neuralgia: A condition characterized by recurring episodes of sudden, extreme pain in the face, often caused by compression or irritation of the trigeminal nerve.
10. Neuropathic pain: Pain that occurs as a result of damage or dysfunction of the nervous system, often accompanied by other symptoms such as numbness, tingling, or weakness.

Brachial plexus neuropathies refer to a group of disorders that affect the brachial plexus, a network of nerves that run from the neck and shoulder down to the hand and fingers. These disorders can cause a range of symptoms including weakness, numbness, and pain in the arm and hand.

The brachial plexus is a complex network of nerves that originates in the spinal cord and branches off into several nerves that supply the shoulder, arm, and hand. Brachial plexus neuropathies can occur due to a variety of causes such as injury, trauma, tumors, cysts, infections, autoimmune disorders, and genetic mutations.

There are several types of brachial plexus neuropathies, including:

1. Erb's palsy: A condition that affects the upper roots of the brachial plexus and can cause weakness or paralysis of the arm and hand.
2. Klumpke's palsy: A condition that affects the lower roots of the brachial plexus and can cause weakness or paralysis of the hand and wrist.
3. Brachial neuritis: An inflammatory condition that causes sudden weakness and pain in the arm and hand.
4. Thoracic outlet syndrome: A condition where the nerves and blood vessels between the neck and shoulder become compressed, leading to pain and weakness in the arm and hand.
5. Neurodegenerative conditions such as amyotrophic lateral sclerosis (ALS) and peripheral neuropathy.

The symptoms of brachial plexus neuropathies can vary depending on the type and severity of the condition, but may include:

* Weakness or paralysis of the arm and hand
* Numbness or loss of sensation in the arm and hand
* Pain or aching in the arm and hand
* Muscle wasting or atrophy
* Limited range of motion in the shoulder, elbow, and wrist joints
* Decreased grip strength
* Difficulty with fine motor skills such as buttoning a shirt or tying shoelaces.

Brachial plexus neuropathies can be diagnosed through a combination of physical examination, imaging studies such as MRI or EMG, and nerve conduction studies. Treatment options vary depending on the specific condition and severity of the symptoms, but may include:

* Physical therapy to improve strength and range of motion
* Occupational therapy to improve fine motor skills and daily living activities
* Medications such as pain relievers or anti-inflammatory drugs
* Injections of corticosteroids to reduce inflammation
* Surgery to release compressed nerves or repair damaged nerve tissue.

The symptoms of encephalomyelitis can vary depending on the cause and severity of the condition. Common symptoms include fever, headache, neck stiffness, muscle weakness, confusion, seizures, and loss of sensation or paralysis in parts of the body. In severe cases, encephalomyelitis can lead to life-threatening complications such as brain damage, stroke, and respiratory failure.

The diagnosis of encephalomyelitis is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include blood tests to detect the presence of inflammatory markers or antibodies against specific infectious agents. Imaging studies such as CT or MRI scans can help to identify inflammation in the brain and spinal cord.

Treatment of encephalomyelitis depends on the underlying cause of the condition. In some cases, antiviral medications may be used to treat infections such as herpes simplex or West Nile virus. In other cases, corticosteroids may be prescribed to reduce inflammation and prevent further damage. Supportive care such as intravenous fluids, oxygen therapy, and physical therapy may also be necessary to manage symptoms and promote recovery.

In conclusion, encephalomyelitis is a serious condition that can cause significant morbidity and mortality. Early diagnosis and prompt treatment are essential to prevent complications and improve outcomes for patients with this condition.

ALS is caused by a breakdown of the nerve cells responsible for controlling voluntary muscle movement, leading to muscle atrophy and loss of motor function. The disease can affect anyone, regardless of age or gender, but it is most common in people between the ages of 55 and 75.

The symptoms of ALS can vary from person to person, but they typically include:

* Muscle weakness or twitching
* Muscle wasting or atrophy
* Loss of motor function, such as difficulty walking, speaking, or swallowing
* Slurred speech or difficulty with language processing
* Weakness or paralysis of the limbs
* Difficulty with balance and coordination
* Fatigue and weakness
* Cognitive changes, such as memory loss and decision-making difficulties

There is currently no cure for ALS, but there are several treatments available to help manage the symptoms and slow the progression of the disease. These include:

* Riluzole, a medication that reduces the amount of glutamate in the brain, which can slow down the progression of ALS
* Physical therapy, to maintain muscle strength and function as long as possible
* Occupational therapy, to help with daily activities and assistive devices
* Speech therapy, to improve communication and swallowing difficulties
* Respiratory therapy, to manage breathing problems
* Nutritional support, to ensure adequate nutrition and hydration

The progression of ALS can vary greatly from person to person, but on average, people with the disease live for 2-5 years after diagnosis. However, some people may live for up to 10 years or more with the disease. The disease is usually diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electromyography (EMG) and magnetic resonance imaging (MRI).

There is ongoing research into the causes of ALS and potential treatments for the disease. Some promising areas of research include:

* Gene therapy, to repair or replace the faulty genes that cause ALS
* Stem cell therapy, to promote the growth of healthy cells in the body
* Electrical stimulation, to improve muscle function and strength
* New medications, such as antioxidants and anti-inflammatory drugs, to slow down the progression of ALS

Overall, while there is currently no cure for ALS, there are several treatments available to help manage the symptoms and slow the progression of the disease. Ongoing research offers hope for new and more effective treatments in the future.

The main symptoms of Melkersson-Rosenthal Syndrome include:

1. Recurrent attacks of swelling on one side of the face, particularly the cheek and lips. These attacks can be triggered by various factors, such as stress, fatigue, or certain foods.
2. Pain and twitching in the affected facial muscles during these attacks.
3. Weakness or paralysis of the facial muscles on one side of the face.
4. Difficulty speaking or eating due to weakened facial muscles.
5. In some cases, MRS can also cause other symptoms such as headaches, fever, and vision problems.

The exact cause of Melkersson-Rosenthal Syndrome is not known, but it is believed to be related to abnormalities in the nerves that control facial muscles. The condition is thought to be rare, affecting approximately 1 in 100,000 people worldwide. There is no cure for MRS, but various treatments can help manage the symptoms and prevent attacks. These treatments may include medications such as anticonvulsants or steroids, as well as lifestyle changes such as avoiding triggers and getting regular exercise. In some cases, surgery may be necessary to relieve pressure on the nerves or to repair damaged facial muscles.

Anatomy16

Organisms7

Diseases49

Chemicals and Drugs13

Analytical, Diagnostic and Therapeutic Techniques and Equipment6

Psychiatry and Psychology3

Phenomena and Processes2

Antitumor and immunotherapeutic effects of activated invasive T lymphoma cells that display short-term interleukin 1alpha expression. (1/1176)

Common peroneal nerve palsy: a clinical and electrophysiological review. (2/1176)

Incidence of deep vein thrombosis and leg oedema in patients with strokes. (3/1176)

Hypoglossal nerve injury as a complication of anterior surgery to the upper cervical spine. (5/1176)

Isolated dysarthria due to extracerebellar lacunar stroke: a central monoparesis of the tongue. (6/1176)

Awareness during anesthesia: a closed claims analysis. (7/1176)

Golli-induced paralysis: a study in anergy and disease. (8/1176)

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Paralysis

Respiratory Paralysis

Vocal Cord Paralysis

Paralyses, Familial Periodic

Facial Paralysis

Sleep Paralysis

Tick Paralysis

Paralysis, Hyperkalemic Periodic

Muscle Hypotonia

Hypokalemia

Poliomyelitis

Thyrotoxicosis

NAV1.4 Voltage-Gated Sodium Channel

Dicistroviridae

Paraplegia

Hyperkalemia

Bell Palsy

Facial Nerve Diseases

Neuromuscular Blocking Agents

Quadriplegia

Recurrent Laryngeal Nerve

Paralysis, Obstetric

Poliovirus

Poliovirus Vaccine, Oral

Phrenic Nerve

Botulinum Toxins, Type A

Pancuronium

Laryngoplasty

Diaphragm

Botulinum Toxins

Enterovirus Infections

Andersen Syndrome

Myotonia

Laryngoscopy

Neuromuscular Nondepolarizing Agents

Spinal Cord

Ophthalmoplegia

Acidosis, Renal Tubular

Neuromuscular Blockade

Vocal Cords

Facial Nerve

Botulism

Colony Collapse

Neuromuscular Junction

Insect Viruses

Motor Neurons

Succinylcholine

Spinal Cord Diseases

Brachial Plexus Neuritis

Electromyography

Recurrent Laryngeal Nerve Injuries

Guillain-Barre Syndrome

Myelitis

Muscle, Skeletal

Spinal Cord Injuries

Channelopathies

Muscular Diseases

Muscle Weakness

Hoarseness

Thyroid Cartilage

Poliovirus Vaccines

Myotonic Disorders

Facial Nerve Injuries

Hypoglossal Nerve Diseases

Larynx

Cataplexy

Bungarus

Myotonia Congenita

Narcolepsy

Sodium Channels

Doxapram

Cranial Nerve Diseases

Dysphonia

Laryngeal Nerve Injuries

Bees

Muscle Denervation

Facial Muscles

Polyradiculoneuropathy

Nerve Compression Syndromes

Brachial Plexus Neuropathies