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David Simmons FRCP, FRACP, MD

  • Consultant Diabetologist
  • Institute of Metabolic Science
  • Cambridge University Hospitals NHS Foundation Trust
  • Addenbrookes Hospital
  • Cambridge, UK

Introduction the inferior colliculi constitute the posterior portion of the roof of the midbrain or tectum herbals on demand shipping order 1pack slip inn free shipping. Nearly all auditory information ascending to the forebrain passes through the inferior colliculus herbals stock photos buy 1pack slip inn visa, making it a major station in the auditory pathway herbs landscaping buy slip inn without a prescription. Auditory information enters via a tract called the lateral lemniscus herbal salvation purchase slip inn 1pack without prescription, and leaves by way of the brachium of the inferior colliculus to ascend to the medial geniculate body of the thalamus herbals bestellen cheap slip inn amex. The inferior colliculus also participates in the descending auditory pathway herbals good for the heart order slip inn cheap, receiving input from the auditory cortex and sending output to the dorsal cochlear nucleus and part of the superior olivary complex. Two arteries supply the inferior colliculus, both of which arise indirectly from the basilar artery. One is the quadrigeminal artery, which branches from the posterior cerebral artery shortly after that artery arises as the terminal bifurcation of the basilar artery. The other artery supplying the colliculus is a branch of the superior cerebellar artery. Unilateral damage to the inferior colliculus does not produce a gross loss of hearing because of the bilaterality of pathways ascending to the midbrain. These involve an inability to accurately localize the source of a sound on the side opposite the damage. There is also evidence that the inferior colliculus is involved in the initiation and propagation of audiogenic seizures. The inferior colliculus is a complex structure, containing more than 10 times the number of neurons as there are axons in the auditory nerve. It is subdivided into a number of regions, which differ from each other in the kinds of neurons present, their afferent and efferent connections, and their internal organization. The central nucleus forms the core of the inferior colliculus and is covered by the cortex on its dorsal and caudal aspects. In addition to the central nucleus and cortex, there are a number of other paracentral nuclei. The subdivisions of the inferior colliculus are relatively constant across different species of mammals, including humans. For the most part, the subdivisions have similar types of neurons and are organized in the same way. However, little is known of either the ascending or descending connections of the inferior colliculus of primates. Central Nucleus the central nucleus is organized into layers of tightly packed neurons. The dendritic fields of most neurons are disk shaped and are oriented parallel to one another. Afferents to the central nucleus typically terminate in parallel with these layers. In addition, neurons within the central nucleus give off axonal collaterals that ramify within their layer of origin. In this way, the neurons, afferents, and axonal collaterals combine to form fibrodendritic laminae. A minority of neurons have dendritic fields that are not disk shaped, but are instead, oval or spherical. Insets show location and orientation of inferior colliculus in sections of the brainstem. The frequencies to which neurons are tuned vary perpendicular to the plane of the laminae. Neurons in the most dorsolateral laminae are tuned to low frequencies, and those in more ventromedial laminae are tuned to progressively higher frequencies. The frequencies to which neurons are tuned are not fixed, but can be modulated by cortical input. If a region of auditory cortex tuned to a particular frequency is stimulated, then neurons in the inferior colliculus that are tuned to nearby frequencies shift their preferred frequency to match that of the stimulated region. In this way, the inferior colliculus acts like a neural magnifying glass for the cortex. The neurons of the central nucleus can process incoming auditory information in a wide variety of ways. Although there are only two morphological types of neurons, these types consist of a number of subtypes. Subtypes have been defined on the basis of the size and organization of dendritic fields, neurotransmitter content (many neurons contain g-aminobutyric acid), and intrinsic electrophysiological properties. The different subtypes can process information from a larger or smaller region of the afferent innervation, either convey excitation or inhibition, and process just the onset portion of the incoming signal or the sustained portion as well. Adding to the intrinsic complexity of the central nucleus is the diversity of inputs it receives. For the most part, the ascending afferents convey auditory signals from the contralateral ear or, in the case of afferents from bilaterally innervated structures, auditory signals representing the contralateral sound field. Each neuron in the central nucleus receives input from only a subset of the ascending afferents, because the afferents from different nuclei that project with a banded pattern overlap in a complex way. The various combinations of afferents that individual neurons in the central nucleus can receive, combined with the diversity of functional types of neurons, indicate a complex level of neuronal processing. This processing may serve to generate topographical gradients of certain key acoustic features. Recall that frequency is already mapped in a dorsolateral to ventromedial direction, perpendicular to the plane of the fibrodendritic laminae. This leaves the two dimensions that lie in the plane of the laminae available for mapping other features. There are two acoustic features that are candidates for being mapped in the plane of the laminae: the location of a sound in the horizontal direction and the periodicity, or complex pitch, of a sound. Complex pitch appears to be mapped in a complicated pattern, with higher pitches in the center and lower pitches in surrounding concentric bands. The main efferent target of the central nucleus is the ventral division of the medial geniculate body. Many of the neurons that participate in the projection excite their targets, but others inhibit their targets. Like the central nucleus, the ventral division of the medial geniculate body is laminated and organized according to frequency. The central nucleus also participates in the descending connections of the inferior colliculus mentioned previously. As in the cerebral cortex, neurons with cell bodies in a particular layer often send dendrites into the other layers. This layer contains the most varied population of neurons and also the neurons with the largest dendritic fields. The cortex of the inferior colliculus receives both descending and ascending input, but the descending input predominates. The descending input arises in both primary and nonprimary auditory cortices and terminates in all layers of the cortex of the inferior colliculus. Input from primary auditory cortex is topographically organized, with small injections of tracers in cortex producing bands of label that run perpendicular to the layers. If a nucleus in the lower brainstem sends input to the cortex, its pattern of input in the cortex (banded or diffuse) is typically the same as that in the central nucleus. The cortex also receives a strong projection from the nucleus sagulum, which lies in the midbrain tegmentum lateral to the lateral lemniscus. The main targets of the cortex of the inferior colliculus are the dorsal and medial divisions of the medial geniculate body of both sides, with the geniculate of the same side receiving a larger projection. The lateral nucleus is also distinguished by afferents from somatosensory centers. These come from the spinal cord, dorsal column nuclei, and from nonprimary somatosensory cortex. The lateral nucleus sends outputs to the deep layers of the superior colliculus and medial geniculate body. The output to the superior colliculus is likely one of the substrates for the topographic representation of auditory space present in that structure. Suga N and Ma X (2003) Multiparametric corticofugal modulation and plasticity in the auditory system. Influenza A and B viruses are the major viruses that are highly contagious to humans and cause acute respiratory disease. However, both viruses periodically alter their nucleic acid sufficiently to be capable of starting new waves of infections by altering their outer coat proteins (hemagglutinin or neuraminidase). If the mutations affect outer coat proteins, sufficient antigenic drift (three-dimensional changes in the protein) may occur to allow the virus to infect hosts that have immunity against the parent virus. This mainly occurs in influenza A viruses that infect a wide variety of mammals and birds, enabling a coinfection with a virus circulating in another species. When major modifications of the virus coat proteins develop, influenza A viruses are capable of causing worldwide pandemics. Our current understanding of influenza is that the virus is coughed or sneezed into the air by an infected individual and then enters the upper respiratory tract of a susceptible individual. The virus replicates in cells lining the pharynx and trachea producing respiratory symptoms (cough and sore throat). Individuals with muscle aches often have an elevation of a muscle enzyme (serum creatine phosphokinase), suggesting that actual damage to muscle occurs. Although it is recognized that influenza commonly produces neurological symptoms, the cause is unclear. It is possible that the respiratory infection triggers release of chemicals called cytokines from inflammatory cells, attacking the infection. These cytokines, interleukins, and interferon may enter the blood stream to secondarily produce the nonrespiratory symptoms. Another possibility is that the respiratory infection releases influenza virus into blood, which then causes an incomplete or nonpermissive infection of cells in the brain, muscle, and liver, producing the nonrespiratory symptoms. Myositis or focal inflammation of skeletal muscle develops in occasional children with influenza. The children develop pain, swelling, and weakness in the calf muscles (gastrocnemius) of one or both legs. Biopsies of the involved muscles have generally shown patchy muscle fiber death (necrosis) with sparse inflammation. Cardiac muscle also can be damaged in influenza with patients developing a viral myocarditis that may be asymptomatic, cause sudden death, or progress to heart failure. Sudden loss of hearing in one ear or the development of severe dizziness and vertigo can develop in patients with influenza. Other patients may experience a sensation that the room is spinning (vertigo), with nausea and vomiting. Encephalopathy or postinfectious encephalitis develops in a few patients with influenza. These patients develop weakness, confusion, delirium, and may progress to even coma and death. Neuroimaging and autopsies of the brain may show lesions in the cerebral cortex and basal ganglia. This strain preferentially infected young adults, producing a severe illness that could kill within a few days. Patients were described as having daytime lethargy and somnolence with nocturnal restlessness. Visual blurriness on near vision (accommodation loss), headaches, dizziness, vertigo, and abnormal limb movements (choreoathetosis) were frequently present. Cerebrospinal fluid showed increased numbers of lymphocytes and elevated protein levels. Brains of patients who died Encyclopedia of the Neurological Sciences, Volume 2 doi:10. Worldwide, over 500 000 individuals died, and over half of those who survived were left with neurological sequelae. Subsequent influenza epidemics have not been associated with encephalitis lethargica. Patients experienced stiffness and rigidity in their bodies and characteristic arm tremors. The acute illness lasts approximately 1 month, and recovery takes months up to a year. Encephalopathy Associated with Influenza In the past 30 years, influenza A and B infections of different strains, including the 2009 influenza A (H1N1) pandemic strain, have occasionally been associated with a mild-to-severe encephalopathy. Neuroimaging demonstrates multiple abnormalities in the thalamus, brainstem, and cerebral white matter. Influenza virus was only rarely isolated from the brain or liver of patients, and the isolates did not differ from the current epidemic virus strain in the community. High proportions of children were also given aspirin (acetylsalicylic acid) during the prodromal illness. The children had elevated levels of serum liver enzymes (alanine aminotransferase) and arterial ammonia levels. Cerebrospinal fluid was under increased pressure, but the fluid contents were normal. At autopsy, the liver showed a fatty metamorphosis without inflammation, and the brain was swollen with massive cerebral edema and no inflammation. In survivors, the liver completely recovered, but varying degrees of permanent neuronal loss occurred in the brain, which could produce neurological sequelae. In the 1980s, warning labels were placed on aspirin bottles stating that infants and children should not take aspirin for flu-like illnesses. Human Influenza Due to Avian Influenza Virus H5N1 Since 2004, approximately 500 cases of influenza in humans have been due to a virulent strain of avian influenza called H5N1.

Diseases

  • Florid cystic endosalpingiosis of the uterus
  • Renal dysplasia limb defects
  • Aspergillosis
  • Follicular lymphoma
  • Congenital mitral malformation
  • Brachydactyly absence of distal phalanges
  • Sensory radicular neuropathy recessive form
  • Reynolds syndrome

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Often an infectious vasculitis herbals are us order slip inn on line amex, with large numbers of organisms in blood vessel walls herbalshopcompanynet order slip inn no prescription, results in pulmonary infarction herbs cooking buy genuine slip inn on line. Microscopically herbs philipson order discount slip inn line, alveoli are filled with fibrin-containing fluid vaadi herbals products order generic slip inn line, but neutrophils are few herbals on demand reviews slip inn 1pack with visa. Radiographically, a bronchopneumonia pattern is observed; lobar consolidation is not seen. Streptococcal pneumonia in the newborn is usually caused by group B streptococci (Streptococcus agalactiae), a normal resident of the female genital tract. The infants, however, are often full term, have severe toxemia and may die within a few hours. Pneumonias Caused by Anaerobic Organisms Many anaerobic organisms are normal commensals of the oral cavity, especially in people with poor dental hygiene. Swallowing disorders, as in stuporous alcoholics, anesthetized patients and people subject to seizures, predispose to aspirating anaerobic bacteria. Resulting pulmonary infections cause necrotizing pneumonias, which often lead to lung abscesses. The most dramatic complication is gangrene of the lung, a result of thrombosis of a branch of the pulmonary artery and consequent infarction. Psittacosis Psittacosis is a lung infection due to inhalation of Chlamydia psittaci in dust contaminated with excreta from birds, usually pets and often parrots. It is characterized by severe systemic symptoms, with fever, malaise and muscle aches, but Legionella Pneumonia In 1976, a mysterious respiratory disease with high mortality broke out at an American Legion convention in Philadelphia. The responsible organism, Legionella pneumophila, is a fastidious bacterium that is difficult to grow in culture. Serologic and histologic studies showed that several previously unrecognized epidemics of the same disease had occurred. Legionella organisms thrive in aquatic environments, and outbreaks of pneumonia have been traced to contaminated water in air-conditioning cooling towers, evaporative condensers and construction sites. Person-to-person spread does not occur, and there is no animal or human reservoir. Chest radiographs may be negative, and when abnormal, they show irregular consolidation and an interstitial pattern. The morphologic patterns in most cases are unknown, but the disease is likely to be an interstitial pneumonia. In fatal cases, varying degrees of diffuse alveolar damage are present, together with edema, intra-alveolar pneumonia and necrosis. Anthrax occurs in many species of domestic animals, but human infection occurs rarely, or in sporadic outbreaks. Transmission is via direct contact with the spores; person-to-person transmission is uncommon. When inhaled, they are transported to mediastinal lymph nodes where bacilli emerge and disseminate rapidly through the bloodstream to other organs, including the lungs. Hemorrhagic necrosis of infected organs ensues along with severe hemorrhagic mediastinitis related to local lymphadenopathy. In the lungs, the disease is manifested by hemorrhagic bronchitis and confluent areas of hemorrhagic pneumonia. In pneumonic plague, the organisms are inhaled directly without an intermediary arthropod vector, and disease may be spread from person to person. The lungs typically show extensive hemorrhagic bronchopneumonia, pleuritis and mediastinal lymph node enlargement. Inhaled organisms multiply in the alveoli because alveolar macrophages cannot readily kill them. When this lesion is associated with an enlarged mediastinal lymph node, a Ghon complex is formed. On gross examination, the healed, subpleural Ghon nodule is Mycoplasma Pneumoniae Causes "Atypical Pneumonia" Unlike lobar pneumonia, atypical pneumonia begins insidiously. Respiratory symptoms may be minimal or severe, and chest radiography shows patchy intra-alveolar pneumonia or interstitial infiltrates. Infection characteristically causes a bronchiolitis with a neutrophilic intraluminal exudate and intense lymphoplasmacytic infiltration in bronchiolar walls. Diagnosis is usually established by serologic detection of Mycoplasma pneumoniae antibodies or cold agglutinins. Tuberculosis Is the Classic Granulomatous Infection Known since ancient Egypt, tuberculosis was the scourge of the industrialized world in the 19th and early 20th centuries. It declined quickly as living and working conditions improved during the 20th century, and the introduction of antituberculosis drugs further decreased its impact. A healed Ghon complex is represented by a subpleural nodule (arrowhead) and involved hilar lymph nodes (arrow). Tuberculous cavities range from under 1 cm to large, cystic areas occupying almost the entire lung. The cavity wall is composed of an inner, thin, gray membrane encompassing soft necrotic nodules; a middle zone of granulation tissue; and an outer collagenous border. Cavities often communicate with a bronchus, and the release of infectious material into airways spreads infection within the lung. The walls of healed tuberculous cavities eventually become fibrotic and calcified. A small tuberculous granuloma with conspicuous central caseation is present in the pulmonary parenchyma. The microscopic features of draining hilar lymph nodes are similar to those of the peripheral parenchymal lesion. Most (>90%) primary tuberculous infections are asymptomatic; lesions remain localized and heal. Sometimes there is self-limited extension to the pleura, with secondary pleural effusion. Less often, primary tuberculosis is not limited but spreads to other parts of the lung (progressive primary tuberculosis). In this situation, the initial lesion enlarges, producing necrotic areas up to 6 cm. Central liquefaction results in cavities, which may expand to occupy most of the lower lobe. Erosion of a bronchus by the necrotizing process leads to further pulmonary dissemination of the disease. Miliary tuberculosis is the presence of multiple, small (size of millet seeds), tuberculous granulomas. The organisms disseminate from the lung or other sites via the blood, usually during secondary tuberculosis, but occasionally in primary disease. Hemoptysis is caused by erosion into small pulmonary arteries adjacent to the cavity wall. Bronchopleural fistula occurs when a subpleural cavity ruptures into the pleural space. Aspergilloma is a fungal mass arising by superinfection of a persistent open cavity with Aspergillus; the fungi may fill the entire cavity. A cellular immune response occurs after a latent interval and leads to formation of many granulomas and extensive tissue necrosis. Apical and posterior segments of the upper lobes are most commonly involved, but the superior segment of the lower lobe is also often affected, and no part of the lung can be excluded. A diffuse, fibrotic, poorly defined lesion develops, with focal areas of caseous necrosis. The apex of the left upper lobe shows tuberculous cavities surrounded by consolidated and fibrotic pulmonary parenchyma that contains small tubercles. Clubbed basophilic filaments, noted at the colony margins, are visible to the naked eye as small yellow particles ("sulfur granules"). The abscesses may extend to the pleura and produce bronchopulmonary fistulas and empyema. Nocardia Is Usually an Opportunistic Organism Nocardia is a gram-positive filamentous bacterium that causes an acute progressive or chronic bacterial pneumonia. Infection is mostly seen in immunocompromised patients, particularly those with lymphomas, neutropenia, chronic granulomatous disease of childhood and pulmonary alveolar proteinosis. The organisms are delicate, beaded, thin filaments, which branch mostly at right angles. Multiple millimeter-sized nodules (arrows) are scattered throughout the lung parenchyma. Fungal Infections May Be Geographic or Opportunistic Histoplasmosis Histoplasmosis is a disease of the midwestern and southeastern United States, particularly the Mississippi and Ohio river valleys. It is caused by inhalation of Histoplasma capsulatum in infected dust, commonly from bird droppings. Actinomycosis Features Multiple Lung Abscesses Actinomycosis is caused by infection with actinomycetes, and the usual pulmonary organism is Actinomyces israelii. Although actinomycetes resemble fungi in appearance, they are anaerobic, gram-positive, filamentous bacteria. They normally inhabit the mouth and nose and infect the lung by aspiration of oropharyngeal contents or by extension from an actinomycotic subdiaphragmatic abscess or liver abscess. Most infections are asymptomatic and result in lesions like Ghon complexes, including a parenchymal granuloma and similar lesions in the draining lymph nodes. The granulomas are particularly prone to calcify, often with a concentric laminar pattern. The organisms are thin, filamentous, branching bacteria (Gomori methenamine silver stain). The granulomas heal by fibrosis and calcification, but central necrotic areas may persist. In a few cases, pulmonary lesions progress or reactivate, leading to a progressive fibrotic and necrotic lesion that closely resembles that of reactivation tuberculosis. However, histoplasmosis lesions are more fibrotic than those of tuberculosis, and cavitation is less common. The reason for progression is not known, although large infective doses and poor host responses are usually considered to be responsible. Immunocompromised patients are at particular risk for the dissemination of Histoplasma within the lungs and spread to other organs. Most serious cases of pulmonary cryptococcosis occur in immunocompromised patients, in whom the organisms proliferate extensively within alveolar spaces, with little tissue reaction. North American Blastomycosis Blastomycosis is an uncommon condition caused by Blastomyces dermatitidis. It is concentrated in the Missouri, Mississippi and Ohio river basins in the United States, and in southern Manitoba and northwestern Ontario in Canada. Initial infection produces a lesion resembling a Ghon complex or progressive pneumonitis. Unlike tuberculous Ghon complexes, the focal lesions of blastomycosis show central necrosis with a purulent reaction, surrounded by granulomatous inflammation. Coccidioidomycosis Coccidioidomycosis, caused by inhalation of spores of Coccidioides immitis, was originally known as San Joaquin Valley fever, after the location where the disease has been endemic for many years. However, the infection is widespread throughout the southwestern part of the United States and shares many of the clinical and pathologic features of histoplasmosis and tuberculosis. Empty spherules or endospores that have been released into the tissue may also be visible. In immunocompromised hosts, the disease may progress rapidly, with release of endospores into the lung, in which case the tissue reaction may be purulent as well as granulomatous. Cryptococcosis Cryptococcosis results from the inhalation of spores of Cryptococcus neoformans, which are often found in pigeon droppings. Invasive aspergillosis is a fulminant pulmonary infection that is not amenable to therapy. Fungus balls are usually clinically silent and merely represent interesting radiologic findings. A branch of the pulmonary artery shows fungal hyphae in the wall and within the lumen (Gomori methenamine silver stain). Computed tomography shows thickened bronchial walls and mucous plugs in the bronchi. Patients receiving immunosuppressive drugs after organ transplantation or chemotherapy for malignant disease are particularly at risk. There are bronchial and bronchiolar mucous plugs, eosinophilic infiltrates and Charcot-Leyden crystals. A dilated bronchus is filled with a mucous plug that has dense layers of eosinophilic infiltrates. Higher magnification shows numerous eosinophils (arrowheads) and Charcot-Leyden crystals (arrows). The alveoli are filled with a foamy exudate, and the interstitium is thickened and contains a chronic inflammatory infiltrate. A centrifuged bronchoalveolar lavage specimen impregnated with silver shows a cluster of Pneumocystis cysts. Alveoli are filled with a characteristic foamy exudate, in which the organisms appear as small bubbles in a background of proteinaceous exudate. With silver impregnation, cysts appear as round or indented ("crescent moon") bodies, 5 m in diameter. After sporozoites develop within the cyst, it ruptures and assumes an indented shape. Sporozoites develop into trophozoites, which may be seen with stains such as Giemsa in cytology specimens but are very difficult to see in routine histologic sections.

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Entrapment of the median nerve proximal to the carpal tunnel can occur at different sites herbs mac and cheese buy slip inn amex. However herbals nature slip inn 1pack fast delivery, these two conditions can be confused because they can cause similar symptoms of arm and hand pain herbals and vitamins purchase 1pack slip inn visa, sensory disturbances godakanda herbals slip inn 1pack without prescription, and weakness vhca herbals order slip inn american express. Sensory Innervation the median nerve carries cutaneous sensation from the wrist and hand herbals for hair loss order slip inn with amex. The remaining fibers of the median nerve travel under the flexor retinaculum, through the carpal tunnel, and end in the hand. The nerve fibers are organized in clusters within the nerve according to how they branch off the main nerve trunk. This anatomical characteristic can explain why in a compressive injury certain branches of the nerve are affected while others are spared. It passes through the axilla and descends along the medial arm in proximity to the brachial artery. In the antecubital fossa, the median nerve is posterior to the bicipital aponeurosis and median vein and anterior to the brachialis muscle and elbow joint. The only branches of the median nerve above the elbow are articular branches that pass to the elbow joint. Entrapment Sites High median nerve entrapment is usually located in the regions around the shoulder or the elbow. The syndrome of high median nerve entrapment around the shoulder is usually due to trauma, such as humeral fracture, anterior shoulder dislocation, or crutch palsy. If the cause of the high median palsy is trauma, such as compression from crutches, the treatment is conservative and prognosis is good, especially if there is only partial functional loss or if recovery begins early. Clinically, patients complain of pain around the elbow and possibly sensory changes and paresthesias in the lateral palm, thenar eminence, and median-innervated digits. The symptoms may worsen with forceful extension of the wrist and Encyclopedia of the Neurological Sciences, Volume 2 doi:10. As the brachial artery also runs under the ligament with the median nerve, the blood vessel can be compressed during elbow extension causing a diminished radial pulse at the wrist. As the median nerve crosses the elbow to enter the forearm, it passes underneath the lacertus fibrosis, which is a fascial band extending from the biceps tendon to forearm fascia. Pain and paresthesias may be present in the median nerve distribution and tend to be intermittent and activity dependent. Weakness in the median nerve distribution is variable and depends on the severity of compression. On examination, the pronator compression test may help to evaluate proximal median nerve entrapments. The Tinel sign can also be elicited in the forearm, and when present it is helpful in the diagnosis. These tests are positive if they increase the pain and paresthesias in the median distribution. Patients may report that as pain began to improve, they noticed weakness and loss of motor dexterity. On physical examination, when weakness is present there is a decrease or loss of ability to flex the interphalangeal joint of the thumb and distal interphalangeal joint of the index finger. Owing to anatomical variations with possible innervation contributed by the ulnar nerve, the distal interphalangeal joint of the middle finger may or may not be affected. Compression can also be caused by forearm fractures, elbow dislocations, injection injuries, compartmental syndrome, or hemorrhage into nerve sheath. Trauma caused by bone fractures that leads to median nerve injury can do so from the direct force that caused the fracture, from nerve stretch or laceration from the displaced bone fragment, or from injury to blood vessels that supply the nerve. The median nerve is also susceptible to injury with a wrist fracture or dislocation, where the ulnar nerve can also be compromised. Differential Diagnosis Proximal median neuropathy can be difficult to diagnose because it rarely presents with all the expected features. Often, it presents as a partial syndrome because nerve fibers travel in fascicles and the compression or injury affects different fibers unevenly or selectively. However, in early cases the symptoms may be more nonspecific with sensory changes in the hand. Weakness of median-innervated forearm muscles also indicates a more proximal lesion. Cervical Radiculopathy Patients with C6 or C7 radiculopathy may present with symptoms similar to proximal median nerve compression. Both conditions can have prominent forearm pain, sensory changes in the hand, and arm weakness if severe. However, cervical radiculopathy usually also presents with neck or shoulder pain that radiates down the arm, and can be aggravated by neck movement. When weakness is present, muscles not innervated by the median nerve are affected in cervical radiculopathy, such as the biceps and triceps muscles. In addition, tendon reflexes may be diminished or absent, with biceps tendon reflex being affected in C6 lesions and triceps reflex with C7 lesions. Other causes of proximal median neuropathy include persistent median artery, a thrombosed artery of an epineural vessel, and pseudoaneurysms of the axillary or 1018 Median Nerve and Neuropathy Brachial Plexopathy Brachial plexopathy may present as proximal median neuropathy if only the median nerve fibers are involved. However, in many instances other nerves are also affected, and a careful sensory and motor examination will reveal weakness and sensory loss outside of median nerve distribution. Additional sensory or motor involvement suggests a more diffuse process rather than a focal compressive lesion of the median nerve. Diagnosis Electrophysiological testing in proximal median neuropathy is useful for localizing the lesion as well as for evaluating the severity of the neuropathy. The results may be normal when complaints are mainly of pain and dysesthesias without sensory loss or weakness. In this situation, nerve conduction studies and electromyography may be most useful in eliminating other causes, such as cervical radiculopathy or brachial plexopathy. The decrease in velocity and amplitude is seen because demyelination usually occurs before axonal loss in compressive lesions, and sensory fibers are more susceptible to injury than motor fibers. Distal latencies and F-wave latency studies are usually normal and do not aid in the diagnosis of proximal median nerve compression. The median-innervated muscles proximal to the lesion should be normal, whereas those distal to the lesion may show neurogenic changes, including signs of denervation (fibrillations, positive sharp waves, reduced recruitment patterns, and increased motor unit amplitude and duration). It is also prudent to study the contralateral median nerve because bilateral median neuropathies have been reported. In recent years, neuromuscular ultrasonography has advanced as a useful modality to complement electrodiagnostic studies for the diagnosis of nerve entrapment syndromes. It can detect structural nerve changes as well as provide information on nerve blood flow. The nerve enlargement is a result of entrapment, and the nerve becomes less echogenic on ultrasound, with increased intraneural vascularity proximal to the compression site, which can be seen on a Doppler ultrasound. As the size of the median nerve varies in individuals, it may limit the utility of the cross-sectional area. However, as the nerve size has correlation with wrist circumference, there are formulas proposed to account for individual variation. Among clinicians who regularly use ultrasound to aid in the diagnosis of median nerve entrapment at the wrist, the parameters used include focal nerve enlargement at the site of compression, decreased nerve echogenicity, increased intraneural vascularity, and decreased mobility of the median nerve. Treatment Treatment depends on the severity of the compression, as determined by clinical examination and electrodiagnostic testing. In patients whose symptoms are mild, intermittent, and use dependent, avoiding the provocative movement, such as elbow flexion and pronation, may be sufficient. Median Nerve and Neuropathy 1019 If symptoms persist despite conservative treatment, then surgery is needed to relieve compression. Surgery necessitates removal of the supracondylar process and resection of the ligament. Periosteum is also removed as the spur can regenerate, causing a recurrence of symptoms. In situations in which symptoms are exacerbated by specific movements, resting or immobilizing the arm in supination and a trial of antiinflammatory medication are indicated as part of conservative management. In a long-term follow-up, patients with only sensory symptoms appeared to have a complete recovery after surgery. The best results are reported in patients with definite anatomical constriction seen during the surgery. Seror P (1996) Anterior interosseous nerve lesion: Clinical and electrophysiological features. Surgical results depend on the cause and severity of the median nerve lesion as well as the duration of symptoms. Introduction the medulla oblongata, the lowermost portion of the brainstem, is composed of ascending and descending fiber pathways controlling motor (voluntary) functions of the body, and neuronal cell groups that are major sites of visceral sensory processing and the control of cardiovascular, respiratory, gastrointestinal, and other physiological functions. Many of the homeostatic functions of the nervous system are dependent on groups of medullary neurons, which are integral components of the central neuronal circuits controlling autonomic function. A comparison of the structure of the human medulla oblongata with that of the rat reveals a remarkable level of consistency, indicating that the medulla is one of the earlier evolved components of the central nervous system. In the embryo, neurons of the medulla arise from the lower part of the cranial portion of the neural tube. The primitive central canal widens to form a four-sided pyramid shape with a rhomboid floor, which becomes the fourth ventricle extending over the medulla and pons. Corticobulbar tract Corticobulbar pathway axons travel into the brainstem with those of the corticospinal tract. Motor neurons of the trigeminal, ambiguus nucleus, and facial nucleus, but not the hypoglossal nucleus, also receive input from the ipsilateral cerebral cortex. Medial forebrain bundle the medial forebrain bundle contains axons from neurons projecting from the hypothalamus, as well as axons projecting to the hypothalamus from other structures. Vestibulospinal tract Anatomical Features Descending Pathways A number of major axonal bundles traverse the rostrocaudal axis of the medulla. Although these pathways may not synapse within the confines of the medulla, their disruption by traumatic lesions may seriously impair the functions they subserve. Axons of the lateral vestibulospinal tract, emanating from the lateral vestibular nucleus, descend uncrossed through the medulla into the ventral white matter of the spinal cord. These vestibulospinal pathways facilitate rapid movements in response to changes in body position and provide control of antigravity muscles. These major conduits of the corticospinal tract convey motor impulses to the spinal cord and control voluntary movement. An important feature of the pyramidal tract is the decussation or crossing-over point of the majority of corticospinal tract fibers, which, apart from demarcating the boundary between the medulla oblongata and the spinal cord, allows the right side of the brain to send signals to the left side of the body, while the left cerebral hemisphere communicates with the right side. Axons terminating in the spinal dorsal gray matter modulate somatic sensory transmission, for example, pain, and originate in part from the ventral midline medullary raphe neurons, some of which produce the monoamine neurotransmitter serotonin. Neurons in the midline medullary raphe region also project to sympathetic preganglionic neurons of the thoracic spinal cord. Motor neuronal cell groups and fiber tracts are dark red and pale red, respectively. Sensory neuronal cell groups and fiber tracts are dark blue and pale blue, respectively. Located ventral to the motor neurons of the compact formation of the ambiguus nucleus and dorsal to the presympathetic vasomotor neurons of the rostral ventrolateral medulla are groups of respiratory premotor neurons, which send axons to phrenic nerve motor neurons and thoracic inspiratory motor neurons. These neurons are involved in head movements (turning) in response to visual and auditory stimuli. Ascending axons in the gracile and cuneate fasciculi convey information from the upper and lower halves of the body, respectively, to terminate in the gracile and cuneate nuclei of the dorsal medulla oblongata. In turn, the axons of neurons of the gracile and cuneate nuclei ascend, crossing in the midline at the lemniscal decussation of the medial lemniscus, relaying in the thalamus en route to the somatosensory cortex. Both pathways are involved in movement control, conveying sensory information from muscle spindles, tendon organs, and touch and pressure receptors. Cranial nerves and cranial nerve nuclei Apart from the major ascending and descending pathways traversing its length, somatic motor, somatic sensory, visceral motor, and visceral sensory neurons are major features of the medulla oblongata. It contains predominantly somatic motor axons supplying muscles of the face and scalp, ear, posterior belly of the digastric muscle, and stylohyoid muscle. In particular, motor neurons of the facial nucleus control the muscles of the forehead, lips, and cheeks, which together are called muscles of facial expression. Neurons of the superior salivatory nucleus give rise to parasympathetic preganglionic neurons that project in the facial nerve via the submandibular and sphenopalatine ganglia, to the submandibular and sublingual glands. Somatic motor fibers originate from neurons of the ambiguus nucleus to innervate the stylopharyngeus muscle. Parasympathetic neurons of the inferior salivatory nucleus exit the medulla in the glossopharyngeal nerve and, via the tympanic nerve, project to the otic ganglion to innervate the parotid gland. Visceral sensory afferent fibers arising from the carotid sinus baroreceptors and chemoreceptors travel in the glossopharyngeal nerve. The cell bodies of these afferents are found in the jugular and petrosal ganglia, and they terminate in the nucleus of the solitary tract onto second-order neurons of the baroreflex and chemoreflex. Vagus nerve (cranial nerve X): Three visceral motor cell groups consisting of parasympathetic preganglionic neurons are found in the medulla oblongata. Parasympathetic motor neurons coursing in the vagus nerve innervate parasympathetic ganglia located close to , or within, a diverse range of cervical, thoracic, and abdominal visceral structures. The most caudal group of parasympathetic neurons that contributes efferent fibers to the vagus, the dorsal motor nucleus of the vagus, lies ventral to , and at approximately the same level as, the hypoglossal nucleus. It supplies preganglionic parasympathetic vagal outflow to the smooth muscle and glands of the gastrointestinal tract as well as to the heart and respiratory tract via the vagus and glossopharyngeal nerves. Vagal stimulation activates gastrointestinal peristalsis and gastric, hepatic, and pancreatic secretory activity and reduces heart rate.

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Non-voltage-gated types of calcium channels respond to other types of stimuli jiva herbals order slip inn with a mastercard, for example herbals books discount slip inn online, mechanical stretch herbs de provence walmart buy slip inn 1pack amex. Their function is to couple electrical signals at the cell surface to intracellular events herbals detox purchase slip inn discount. The channels are named after the permeating ion (Ca) zenith herbals buy generic slip inn online, with the principal channel modulator herbals for liver purchase slip inn with paypal, i. Release of neurotransmitters leading to responses of effector organs innervated by the autonomic nervous system is mainly mediated by the Cav2. Calcium channels were initially grouped not according to amino acid homologies or molecular cloning of a subunit genes, but according to the tissue where they were first detected or according to their pharmacological properties. In accordance with this, patients usually improve by therapeutic plasma exchange or intravenous immunoglobulin treatment. Transmitter release from parasympathetic and sympathetic neurons is reduced due to antibody-mediated receptor downregulation. Novel and supplementary techniques for antibody detection represent a current research topic. In the autoimmune neurotransmission disorder myasthenia gravis, both these explanations have been confirmed. However, in the individual patient, there is a tendency for such correlation with a reduction in concentration during disease improvement. Such characteristics are typical for most autoimmune disorders, including early-onset myasthenia gravis. Determinants for the target organ variation for autoantibodies in patients with such a general autoimmune susceptibility are not known. The normal parallel arrays are disrupted, and the active zone particles tend to cluster and decrease in number. The functional and structural changes in the presynaptic nerve terminal can be fully explained by the autoantibody binding. T-lymphocyte activity in the tumor tissue as well as other local and systemic immunoregulatory factors may be determinants for the development of autoantibodies and disease. Myasthenia gravis and neuromyotonia represent the other autoimmune disorders at the neuromuscular junction. Such cofactors could be aspects of immune regulation, unspecific and nonimmune threshold factors, but also distinct external factors like infection. An atypical response to previous innocent and common viral infection has been hypothesized for decades, but never proven. Vincent A (2010) Autoimmune channelopathies: Well-established and emerging immunotherapy-responsive diseases of the peripheral and central nervous systems. He joined the Mayo Clinic Aeromedical Unit in the 1940s and helped the unit develop the G-suit and Mayo-1 maneuver to counteract the effect of high G forces in pilots. When this research was completed he began to investigate neuromuscular physiology and founded the electromyography laboratory at the Mayo Clinic in 1947. Lambert, Eaton, and Rooke provided the definitive delineation of the myasthenic syndrome from myasthenia gravis. The first patient diagnosed was a 73-year-old man with limb weakness and decreased reflexes on examination. Rooke examined strength with a repetitive pumping motion and thought the muscles became stronger. Lambert explained in 1961 that the discrepancy was related to whether the initial or the final phase of the contraction had been tested and showed that the action potential increased markedly in amplitude following exercise. Lambert went on to study the pathophysiology of the disorder in detail and was instrumental in developing many of the current concepts of neuromuscular disorders. He subsequently completed a neurology fellowship at the Mayo Clinic, and was appointed to the Mayo Clinic staff in 1936. He was director of the American Board of Psychiatry and Neurology from 1957 to 1958 and president of the Association of Research in Nervous and Mental Disease in 1958. Laminectomy is the removal of the posterior portion of the bony ring that surrounds the spinal cord or cauda equina. Laminectomies are performed to treat spinal stenosis or to create access for the treatment of herniated discs, spinal tumors, and other spinal lesions. Sometimes a laminectomy is performed in conjunction with a spinal fusion, but a laminectomy alone is not a fusion procedure. Laminectomies are most often performed in the lumbar spine, but they can also be performed in the sacral, thoracic, and cervical regions of the spine. The major anatomical structures of each spinal vertebra include the vertebral body, pedicles, laminae, transverse processes, and spinous process. Surgical laminectomy, however, was not practical until the late 1800s, when anesthetic, infection, and surgical improvements were established. The conventional open technique has been established as a well-tolerated and successful operation. The ring of the spinal canal is composed of the posterior aspect of the vertebral body, the pedicles, the lamina, and the spinous process. In 1967, Yasargil began using the operating microscope when performing a lumbar discectomy. This technology helped pioneer the way for smaller and less destructive surgical procedures. After anesthesia is induced, patients are typically placed in a prone position, although some surgeons prefer a lateral position. When a laminectomy of the cervical or thoracic spine is performed, the head is supported on a padded cushion or held in rigid three-point fixation. For a laminectomy of the lumbar spine, patients are placed on a frame such as a Wilson frame. This position induces flexion to increase the posterior intervertebral space and to decrease abdominal pressure. In cases of cervical or thoracic stenosis, somatosensory evoked potentials should be recorded both before and after positioning to ensure that no detrimental changes occur during positioning. The planned incision site is identified, often with the aid of plain X-rays, and the skin is prepared and draped in sterile towels. The skin incision varies with the type of procedure and with the number of levels treated. In an open laminectomy, retractors are placed as the midline dissection deepens from the fascia to the lamina on each side of the spinous process. Lateral exposure is limited to the medial aspect of the facet unless a fusion procedure is planned. Sequential dilation placed under fluoroscopic guidance is followed by a tubular retractor, which is aimed directly at the posterior elements of interest. With experience, multidirectional movement of the tubular retractor can allow Encyclopedia of the Neurological Sciences, Volume 2 doi:10. The lamina and spinous processes have been removed at two adjacent vertebral levels. Removal of the bone and ligament allows exposure of the dura, which contains the spinal cord and nerve roots. For intradural pathology, the dura is opened intentionally and then carefully closed when the intradural portion of the procedure is complete. The microscope provides magnification, coaxial illumination, and binocular vision through a small exposure. These advantages ensure the safest possible treatment and minimize the risk of complications. After the spinal pathology is treated, hemostasis is obtained and the wound is irrigated with antibiotic solution. Depending on the pathology being treated, a hemilaminectomy (one side), a partial laminectomy, or a full bilateral laminectomy may be performed. In an open bilateral laminectomy, the spinous process of the same level is removed. For lumbar stenosis, the bony decompression may proceed laterally to remove the remaining lamina and ligament and to undercut the facet to decompress the spinal canal and nerve root openings (foramina). Stenosis, Lumbar Further Reading Blazier C (1998) Operating room requirements for neurosurgical procedures. Later this was a focus of his Lettsomian Lectures before the Medical Society of London in 1887, which were published separately as the Mental Affections of Childhood and Youth (1887). The eyes are obliquely placed, and the internal canthi more than normally distant from one another. The forehead is wrinkled transversely y the lips are large and thick with transverse fissures. They are humorous, and a lively sense of the ridiculous often colours their mimicry. The coordinating faculty is abnormal, but not so defective that it cannot be greatly strengthened. Langdon Down studied medicine at the medical school of the London Hospital from 1853 to 1856, and in 1858 was appointed Medical Superintendent of the Earlswood Asylum for Idiots in Surrey. Although this position was considered one of limited prospects for a young man of his training, he accepted it and attempted to institute helpful reforms for the patients. These examples of the result of degeneracy among mankind, appear Encyclopedia of the Neurological Sciences, Volume 2 doi:10. He was elected Fellow of the Royal Society in 1883 and was its vice president in 1904. Langley initially studied glandular secretions and later focused on the vegetative nervous system. He investigated the effect of nicotine on synaptic transmission in autonomic ganglia and found that nicotine selectively blocked nervous conduction in these ganglia. Langley stimulated the nerve fibers running to and from a ganglion before and after applying nicotine to the ganglion. He was thus able to determine which fibers ended in the ganglion and which passed through. He proposed that there was a chemical combination between the drug and a constituent of the cell, which he called the receptive substance. He was a trim man who dressed well, with steely blue-gray eyes of an arresting quality. He enjoyed outdoor sports (especially iceskating), which may have been one of the reasons why his colleagues felt that he never grew old. Language matters for patients and for those engaged in understanding and measuring how individuals think, how thinking is altered across a variety of clinical conditions, and how it might be enhanced with therapeutics. The language used to convey ideas provides a vivid window into the higherorder cognitive potential of individuals in healthy aging, brain injury, and brain disease. Language is a way of communicating what one knows as reflected in breadth of vocabulary, fluency of expression, clarity and organization of ideas conveyed, selective attention to key points, depth of understanding, and ability to construct abstract meaning. Historically, much of our knowledge about the neurology of language has been gleaned from studies of aphasia. The language disturbances of the different forms of aphasia have been characterized using measures, with the most notable examples represented by naming objects, repeating sentences, defining words, generating a list of items within a category in a limited time period, identifying how two concepts are similar, and picture description tasks. These measures evaluate proficiency of lower-order language components such as phonology, semantics, and syntax. Although these measures are valuable for understanding classic aphasias, they are less informative as language metrics in elucidating the complex verbal expression deficits observed in other clinical populations where lower-order language disturbances are the exception rather than the rule. Indeed, clinicians recognize the relative insensitivity of lower-order language measures in characterizing early, residual, and worsening disease symptoms across many brain diseases and injuries. Over the years, higher-order language measures involving discourse have gained popularity among neurolinguists, neuropsychologists, and neurologists. Discourse refers to the use of language to express ideas in both spoken and written form, typically conveyed as a sequence of sentences that has coherent organization and meaning. There are a number of different discourse genres such as descriptive, conversational, narrative, procedural, and expository. Each genre has unique cognitive and linguistic requirements, with expository being the most complex and descriptive being the simplest. In the first approach, language content is described in terms of a detailed linguistic analysis of the vocabulary, accuracy of grammatical features, and complexity of syntax. In the second approach, discourse skills are analyzed for the ability to convey the gist or global meaning. Gist is defined as the capacity to comprehend and convey generalized meaning from complex information during everyday activities such as reading news stories, hearing medical information, learning how to use new devices, watching movies, making financial decisions, or writing job descriptions. The capacity to derive global meaning from large amounts of information is a skill critical for human functionality. This ability to bind details to form an abstracted gist meaning is strongly linked to academic success in younger ages, occupational achievements in adulthood, whether healthy or brain compromised, and cognitive vitality in later ages. People effortlessly use discourse to connect and communicate with their environment. The ability to understand and formulate discourse is modulated by a complex interplay of several different cognitive functions, with cognitive control serving as the core function. The ability to convey complex ideas through discourse is controlled by complex networks across multiple brain regions. In particular, greater activation for the gist is primarily observed in medial frontal, left inferior frontal, and left temporal regions. Greater activation for details is observed primarily in bilateral superior parietal regions. Studies that have examined discourse formulation have observed changes in volume of discourse output, number of details recalled, and number of indefinite words with normal aging. In contrast, the ability to abstract gist has been found to be relatively preserved in cognitively normal seniors well into their nineties. In a study, when young adults and seniors were asked to provide an interpretive gist meaning of a long text, no differences were observed in performance between the groups.

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