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1
D, Binder Marc, red. Peripheral and spinal mechanisms in the neural control of movement. Amsterdam: Elsevier, 1999.
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Magnetic stimulation of the human nervous system. Oxford: Oxford University Press, 1999.
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Cole, Jonathan. Pride and a daily marathon. Cambridge, Mass: MIT Press, 1995.
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Pride and a daily marathon. London: Duckworth, 1991.
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Takao, Kumazawa, Kruger Lawrence i Mizumura Kazue, red. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.
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Waldmann, Carl, Neil Soni i Andrew Rhodes. Death and dying. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0032.
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Confirming death using neurological criteria (brainstem death) 530Withdrawing and withholding treatment 532The potential heart-beating organ donor 534Non-heart-beating organ donation 538The brainstem provides the anatomical link between the spinal cord and cerebral hemispheres relaying sensory and motor impulses between the periphery and higher cortical centres. It also contains cranial nerve nuclei, the reticular activating system and cardiorespiratory control centres, the destruction of which underlies the process of confirming death according to neurological criteria (brainstem death)....
7
Donaghy, Michael. Focal peripheral neuropathy. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0487.
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Some causes of focal peripheral nerve damage are self-evident, such as involvement at sites of trauma, tissue necrosis, infiltration by tumour, or damage by radiotherapy. Focal compressive and entrapment neuropathies are particularly valuable to identify in civilian practice, since recovery may follow relief of the compression. Leprosy is a common global cause of focal neuropathy, which involves prominent loss of pain sensation with secondary acromutilation, and requires early antibiotic treatment. Mononeuritis multiplex due to vasculitis requires prompt diagnosis and immunosuppressive treatment to limit the severity and extent of peripheral nerve damage. Various other medical conditions, both inherited and acquired, can present with focal neuropathy rather than polyneuropathy, the most common of which are diabetes mellitus and hereditary liability to pressure palsies. A purely motor focal presentation should raise the question of multifocal motor neuropathy with conduction block, which usually responds well to high-dose intravenous immunoglobulin infusions.
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Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson i David Ledingham. Disorders of peripheral nerves and motor neuron disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0007.
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This chapter discusses the clinical features and evidence-based drug treatment regimens of polyneuropathies (Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy, paraproteinaemic neuropathies, and vasculitic neuropathies), mononeuropathies (Bell’s palsy), systemic conditions with peripheral nerve involvement (Sjögren’s and sarcoidosis), and motor neuron disease (MND).
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Mason, Peggy. Spinal Cord. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0004.
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The spinothalamic and lemniscal pathways carry somatosensory information from the periphery into the brain while the corticospinal pathway carries motor commands from the brain to motoneurons of the spinal cord. Following these pathways through the spinal cord allows the student to infer lesion location from symptoms. To exemplify the clinical importance of sympathetic outputs from thoracic segments, Horner syndrome is described. Similarly, the common problems caused by spinal cord injury on sacral parasympathetic functions are stressed. The contributions of specific spinal segments to breathing, hand and foot dexterity, and micturition are emphasized. Working through the logic of the symptoms caused by spinal hemisection (Brown-Séquard syndrome), pyramidal stroke, and syringomyelia provides the student with a clear framework for understanding spinal function in the clinical context.
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Guillery, Ray. The subcortical motor centres. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198806738.003.0004.
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This chapter looks more closely at some of the subcortical motor centres that play a peripheral or an auxiliary role in the standard view: primarily the basal ganglia, the cerebellum, and the superior colliculus; also several brainstem centres. These all play a significant role in motor control and between them receive inputs from the majority of cortical areas. The colliculus serves as an example of a centre that in mammals is often dominated by the cortex. The cortical action may be direct or may involve a strong inhibitory pathway through the basal ganglia. The standard view assigns even quite simple actions to the motor cortex, although comparable actions can be controlled in our vertebrate ancestors by the midbrain tectum which corresponds to the mammalian superior and inferior colliculi. The interactive view has information about movements going to most parts of the cortex, and has all cortical areas contributing to motor control through phylogenetically old centres. For most cortical areas, we must still learn how their motor outputs influence our actions.
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Katirji, Bashar. Routine Clinical Electromyography. Redaktor Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0002.
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Nerve conduction studies and needle EMG represent the two essential parts of the clinical EMG study. In almost all patients, both studies need to be completed before a final conclusion is made. This chapter outlines the basic concepts of nerve conduction studies including stimulations, recordings, variables and sources of errors. This is followed by detailed discussions of basic pathophysiological changes that accompany peripheral nerve disorders. The chapter then covers the normal needle EMG findings including normal insertional activity, motor unit action potential morphology and recruitment. This is followed by details on abnormal spontaneous activity findings and changes in motor unit action potential morphology and recruitment seen on needle EMG with peripheral nerve and muscle disorders.
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Lee, Stella Joonmyung. A Critical Period for Functional Motor Recovery After Peripheral Nerve Injury in the Mouse. 2014.
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Leung, Doris G. Other Proven and Putative Autoimmune Disorders of the Peripheral Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0098.
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Myasthenia gravis is in most cases an autoimmune disorder of the neuromuscular junction in which antibodies are directed at nicotinic acetylcholine receptors or other synaptic proteins, such as the MusK protein that is involved in the formation of the formation and maturation of the motor endplate. Less commonly, myasthenia gravis can result from antibodies directed to presynaptic calcium channels as a side effect of paraneoplastic antibodies (Lambert-Eaton syndrome) or from a developmental paucity of acetylcholine receptors in the neonatal form of the disease. Treatment is usually a combination of aceetylcoholinesterase inhibitors such as pyridostigmine to prolong the life of acetylcholine released at the neuromuscular junction and/or drugs such as corticosteroids aimed at reducing inflammation.
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Casha, Steve, i Philippe Mercier. Normal anatomy and physiology of the spinal cord and peripheral nerves. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0220.
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The spinal cord and peripheral nerves carry motor and autonomic efferents, as well as sensory afferents connecting the cerebrum with the body. Efferent and afferent fibres form predictable tracts within the spinal cord, forming spinal nerves as they exit the spinal canal. Peripheral nerves are often formed from complicated plexuses of spinal nerves in the cervical, lumbar, and sacral spine. Dermatomes are formed from spinal nerves that innervate specific areas of skin, while myotomes innervate a specific set of muscles. The detailed anatomy of these structures are discussed. Knowledge of the anatomy of these structures is relevant to many clinical situations encountered in the intensive care unit especially with caring for neurological, neurosurgical, orthopaedic, and trauma patients.
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Constantinescu, Cris S., i Su-Yin Lim. Weakness. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0044.
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Muscle weakness may reflect systemic disease (such as sepsis or severe hypokalaemia) or a neuromuscular disorder. The origin of neuromuscular weakness may be localized to upper motor neurons, lower motor neurons (including nerve roots, plexus, and peripheral nerves), anterior horn cells, neuromuscular junctions, or muscles. The mode of onset of weakness, its time course, and the findings on general and neurological examination will usually differentiate between the possible diagnoses. The approach to the patient with suspected neuromuscular weakness is described in this chapter.
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Belanger, James H. Aspects of insect motor control: central and peripheral mechanisms underlying oviposition digging in the locust. 1992.
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Sandbrink, Friedhelm. The MEP in clinical neurodiagnosis. Redaktorzy Charles M. Epstein, Eric M. Wassermann i Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0019.
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This article gives information on the clinical application of motor-evoked potential (MEP). Transcranial stimulation of the cerebral cortex to elicit MEPs is a noninvasive method for assessing the integrity of the central motor pathway function. Transcranial magnetic stimulation (TMS) is used in diagnosing and monitoring neurological disorders. This article highlights the neurophysiological differences between TMS and transcranial electric stimulation. All the different MEP parameters that can be measured by TMS, the latency of the MEP is generally regarded as the most reliable and useful. TMS studies have been described in many neurological disorders. The sensitivity of TMS in detecting subclinical upper motor neuron lesion varies in different disorders, depending on number of muscles and different parameters used. This article talks about the application of MEP in pathophysiology, multiple sclerosis, motor neuron diseases, meyloptahy, cerebral infarction, movement disorders, epilepsy, Lumbar spinal stenosis and radiculopathies, peripheral nerve disorders etc.
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Bowker, Lesley K., James D. Price, Ku Shah i Sarah C. Smith. Neurology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0007.
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This chapter provides information on the ageing brain and nervous system, tremor, neuropathic pain/neuralgia, presentation of Parkinson’s disease, management of Parkinson’s disease, diseases masquerading as Parkinson’s disease, epilepsy and its drug treatment, neuroleptic malignant syndrome, motor neuron disease, peripheral neuropathies, subdural haematoma, sleep and insomnia, and other sleep disorders.
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Elham, Bayat. Neurologic Manifestations of Hematological Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0193.
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A wide sprectum of hematologic disorders affect the central and peripheral nervous system. These disorders include porphyria, thrombotic thrombocytopenic purpura-hemolytic uremic syndromes, sickle cell disease, plasma cell dyscrasias, monoclonal gammopathy, primary systemic amyloidosis, primary systemic amyloidosis, Waldonstrom’s macroglobulinemia, myeloproliferative syndromes, cryoglobulinemia, and polycythemia vera. Some, like porphyria, cause both central and peripheral nervous system manifestations including sensory/motor peripheral neuropathy, dysautonomia, pain, seizures, and abdominal pain. Others such as sickle cell disease primarily affect the brain and cause both clinically apparent strokes associated with a vasculopathy of large intracranial blood vessels, as well as less obvious microstrokes that cause progressive cognitive decline if not treated.
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Jameson, Leslie. Acute Loss of Intraoperative Evoked Potential Signals. Redaktorzy Matthew D. McEvoy i Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0069.
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Monitoring of somatosensory and motor evoked potentials has become the standard of care for a large proportion of spine surgeons. Understanding how anesthetic management may affect these evoked potentials is critical to optimizing the ability to detect impending spinal cord or peripheral nerve injury. Similarly, once a nerve injury is detected, knowledge of the various anesthetic and surgical maneuvers possible to avoid permanent injury is essential for the best patient outcomes. This chapter discusses the effects of various anesthetic agents on somatosensory and motor evoked potentials and potential critical interventions that can be made when a nerve injury is identified by this monitoring.
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Rafferty, Gerrard, i John Moxham. Assessment of Peripheral and Respiratory Muscle Strength in ICU. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0047.
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Skeletal muscle weakness affecting the respiratory and peripheral muscles is common in critically ill patients and can lead to difficulties in weaning, prolonged ICU admission, and significant morbidity in survivors. A number of techniques can be used to assess muscle strength. In the peripheral muscles, volitional techniques employing scoring systems or portable hand dynamometers are relatively simple and quick to use, requiring little or no specialist equipment. Such techniques can, however, only be applied to conscious and cooperative patients, preventing assessment of muscle weakness in many ICU patients. The volitional requirement also limits the ability to distinguish poor motivation and impaired cognition from true loss of muscle function. Non-volitional techniques involving motor nerve stimulation provide measures of muscle force production in non-cooperative patients but require specialist equipment. Normative data for comparative purposes are limited. Also, it is not clear which peripheral muscle best reflects generalized muscle weakness. Measurements of maximal inspiratory and expiratory pressures are widely used to assess respiratory muscle strength in ICU patients and are applicable to patients who can make some respiratory effort. As with all tests requiring patient cooperation, reliability is limited. Phrenic nerve stimulation allows direct, non-volitional assessment of diaphragm and phrenic nerve function, and normative values for comparative purposes are available. Magnetic phrenic nerve stimulation is well tolerated, can be performed in the presence of vascular catheters, and is used to document respiratory muscle weakness and track progression in critically ill patients.
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Neuromuscular Function and Disease: Basic, Clinical, and Electrodiagnostic Aspects, 2-Volume Set. Saunders, 2002.
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Valls-Solé, Josep. Reflex studies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0010.
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Reflex studies are an important part of clinical neurophysiology assessment in health and disease. They are essential to get information on conduction in proximal segments of peripheral nerves, spinal and supraspinal integration of sensory inputs on the motor pathway, and excitability of motor structures. They do not require special equipment, except for a sweep-triggering hammer that is essential, for instance, to elicit monosynaptic reflexes, such as the jaw jerk. For consensual reflexes, it is also recommended to use two recording channels, which facilitate recognition of potential disturbances in the afferent or efferent path of the reflex. What follows is a review of some of the most relevant reflexes that can be studied for neurophysiology assessment in clinical practice.
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Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0020.
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Muscle stiffness is a nonspecific term meaning limited muscle mobility that is not due to weakness. It is opposite to flexibility. Muscle and joint pain may be described as stiffness. Painful sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy), while resting and nocturnal cramps are neurogenic (neuropathy, motor neuron disease, etc). Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome. Upper motor neuron lesions are associated with spasticity and stiffness (HSP, PLS, myelopathies, etc.). Painful cramps and fasciculations are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
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Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0020.
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Muscle stiffness as a nonspecific term means limited muscle mobility. Muscle and joint pain may be described as stiffness. Painful, sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy) while resting, and nocturnal cramps are neurogenic [neuropathy, motor neuron disease (MND), etc.]. Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome (SPS). Upper motor neuron (UMN) lesions are associated with spasticity and stiffness [hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), myelopathies, etc.]. Painful cramps and fasciculation are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
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Mason, Peggy. Cranial Nerves and Cranial Nerve Nuclei. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0005.
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The functions of cranial nerves, conduits for sensory information to enter and motor information to exit the brain, and the common complaints arising from cranial nerve injuries are described. The modified anatomical arrangement of sensory and motor territories in the brainstem provides a framework for understanding the organization of the cranial nerve nuclei. A thorough grounding in the anatomy of cranial nerves and cranial nerve nuclei allows the student to deduce whether a given set of symptoms arises from a central or peripheral lesion. The near triad, pupillary light reflex, and Bell’s palsy are particularly emphasized. The contributions of the six extraocular muscles to controlling eye position and to potential diplopia are described along with the consequences of oculomotor, trochlear, and abducens nerve dysfunction. The potential for lesions of facial, glossopharyngeal, vagus, and hypoglossal nerves to yield dysphagia and dysarthria are outlined.
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Burns, Ted, Michael J. Aminoff, Jones H. Royden Jr i Scott Pomeroy. Netter Collection of Medical Illustrations: Nervous System, Volume 7, Part II - Spinal Cord and Peripheral Motor and Sensory Systems. Elsevier - Health Sciences Division, 2013.
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Ratel, Sébastien, i Craig A. Williams. Neuromuscular fatigue. Redaktorzy Neil Armstrong i Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0009.
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Scientific evidence supports the proposition that prepubertal children fatigue less than adults when performing whole-body dynamic activities like maximal cycling, running bouts, and maximal voluntary isometric/isokinetic muscle contractions. Although the mechanisms underpinning differences in fatigue between children and adults are not all fully understood, there is a consensus that children experience less peripheral fatigue (i.e. muscular fatigue) than their older counterparts. Central factors may also account for the lower fatigability in children. Some studies report a higher reduction of muscle voluntary activation during fatiguing exercise in prepubertal children compared to adults. This could reflect a strategy of the central nervous system aimed at limiting the recruitment of motor units, in order to prevent any extensive peripheral fatigue. Further studies are required to clarify this proposition.
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Baumann, Nicole, i Jean-Claude Turpin. Metachromatic Leukodystrophy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0052.
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Metachromatic leukodystrophy can be observed in infantile, juvenile, and adult cases. It is due to deficiency of the enzyme sulfatide sulfatase arylsulfase A. The adult form includes two types—one characterized by predominantly central nervous system motor signs (mainly pyramidal and/or cerebellar) and a peripheral neuropathy, and the other presenting with behavioral abnormalities and progressive mental deterioration. Homozygosity for the P426L mutation is very frequent in motor forms of adult MLD and heterozygosity for the I179S is very frequently found in psychiatric forms. Hematopoietic stem cell transplantation or bone marrow transplantation is the only presently available therapy that attempts to treat the primary central nervous system manifestation of MLD, but substantial risk is involved and long-term effects are not clear. Potential therapeutic application of hematopoietic stem cell gene therapy and intracerebral gene transfer (brain gene therapy) are explored in infantile forms of patients with MLD.
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Lefaucheur, Jean-Pascal. TMS and pain. Redaktorzy Charles M. Epstein, Eric M. Wassermann i Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0046.
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Few clinical investigations show that repeated transcranial magnetic stimulation (rTMS) to the brain could produce analgesia. Apart from the relationship between TMS and pain with respect to the clinical observation of rTMS-induced analgesic effects, this article also reviews the effects of pain on motor cortex excitability assessed by single or paired-pulse TMS and the results obtained by applying peripheral magnetic stimulation to treat musculoskeletal pain. This article discusses the effects of acute phasic provoked pain, and prolonged tonic provoked pain on motor cortex excitability. The analgesic effects resulting from a single session of rTMS are too short-lived and thereby incompatible with a durable control of chronic pain. Repeated sessions of rTMS on consecutive days produce cumulative effects. However, repeated daily rTMS sessions can be applied to control pain syndromes for a limited period. Further work is needed to define the ultimate clinical role of TMS in the management of pain.
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Gupta, Pawan, i Anurag Vats. Regional anaesthesia of the lower limb. Redaktor Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0055.
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Lower limb nerve blocks gained popularity with the introduction of better nerve localization techniques such as peripheral nerve stimulation and ultrasound. A combination of lower limb peripheral nerve blocks can provide anaesthesia and analgesia of the entire lower limb. Lower limb blocks, as compared to central neuraxial blocks, do not affect blood pressure, can be used in sick patients, provide longer-lasting analgesia, avoid the risk of epidural haematoma or urinary retention, provide better patient satisfaction, and have acceptable success rates in experienced hands. Detailed knowledge of the relevant anatomy is essential before performing any nerve blocks in the lower limb as the nerve plexuses and the peripheral nerves are deep and obscured by bony structures and large muscles. The lumbosacral plexus provides sensory and motor innervation to the superficial tissues, muscles, and bones of the lower limb. This chapter covers different approaches and techniques for lower limb blocks, that is, the lumbar plexus, femoral nerve, fascia iliaca, saphenous nerve, sciatic nerve, popliteal nerve, ankle block, forefoot block, and the intra-articular infusion of local anaesthetics. Both peripheral nerve stimulator- and ultrasound-guided approaches are discussed. The use of ultrasound guidance is suggested as it helps in reducing the dose of local anaesthetic required and can ensure circumferential spread of local anaesthetic around peripheral nerves, which hastens the onset of block and improves success rate.
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Katirji, Bashar. Case 3. Redaktor Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0007.
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Sciatic nerve injury is a relatively uncommon lower extremity mononeuropathy. The various etiologies of sciatic neuropathies are highlighted in this case. The clinical manifestations and diagnosis include distinguishing foot drop due to sciatic neuropathy from peroneal (fibular) neuropathy across the fibular neck, L5 radiculopathy, and lumbosacral plexopathy. The electrodiagnostic features of sciatic nerve lesion are separated from those of foot drop due to other peripheral nerve causes. In contrast to sciatic nerve injury, the piriformis syndrome is mostly a painful syndrome with no or minimal sensory or motor deficits. The clinical manifestations of piriformis syndrome and controversies surrounding this syndrome completes the discussion in this case.
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Hanna, Amgad S., Lisa M. Block i A. Neil Salyapongse. Emergent Nerve Injury. Redaktorzy Meghan E. Lark, Nasa Fujihara i Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0027.
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Injuries to peripheral nerves must be assessed and treated in a thorough and timely manner to achieve optimal outcomes. Physical examination is the cornerstone in diagnosing acute nerve injuries and includes careful inspection as well as precise motor and sensory testing. Nerve conduction studies and electromyography are often more useful in the setting of delayed presentation. Microsurgical repair techniques differ for clean versus ragged lacerations, and resultant nerve gaps will require a conduit or graft to achieve the necessary tension-free closure. The surgeon and patient should be prepared for a lengthy postoperative course and possible complications as the nerve regenerates and function returns.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson i Nathaniel M. Robbins. A 44-Year-Old Man with Bilateral Facial Droop. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0017.
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Facial neuropathy is most commonly seen as an idiopathic unilateral palsy known as Bell’s palsy. Generally, acute onset of typical lower motor neuron facial weakness that is not associated with other atypical or suspicious features, remains unilateral, and recovers completely requires no further workup. A recurrent or bilateral peripheral facial palsy makes an idiopathic cause less likely and prompts a more in-depth workup. The appropriate work-up of unilateral or bilateral facial palsy guided by the presence or absence of associated clinical findings is discussed. The major differentials for bilateral facial paresis include brainstem (especially pontine and prepontine) tumors, Lyme disease (especially in endemic areas), basal menigitides, Guillain-Barre syndrome, and sarcoidosis.
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Shaibani, Aziz. Facial Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0005.
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Unilateral or bilateral facial weakness is an important manifestation of many neuromuscular disorders; some of them are as simple as Bell’s palsy, while others are as serious as Guillain-Barré syndrome (GBS). Facial weakness can be easily mimicked, and therefore, psychogenic etiology should always be kept in mind. Peripheral facial weakness affects all functions and parts, while central weakness may save the upper face and may affect emotional and voluntary functions differentially. Botulinum toxin injection has become a common cause of facial palsy, therefore detailed history is crucial. Examination of the sensory and motor systems is important to define the type and cause. Imaging and electrodiagnostic testing are often needed in the diagnostic process.
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Harrison, John Henry, i Magdalena Anitescu. Neuraxial Anesthesia in Coexisting Neurologic Conditions. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0041.
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Some patients who need surgery may have coexisting neurologic disorders like multiple sclerosis, amyotrophic lateral sclerosis, peripheral neuropathies (e.g., Charcot-Marie-Tooth disease or Guillain-Barré syndrome), or muscular dystrophies (e.g., Duchenne’s or myotonic dystrophy). When neuraxial analgesia and anesthesia are indicated, the anesthesiologist should be aware of the risks and benefits of the technique. Neuraxial anesthesia is not absolutely contraindicated in nervous system diseases and there are undeniable benefits to ruling out general anesthesia. In patients with coexisting neurologic disorders, prolonged sensory and motor block can be confused with epidural hematoma and abscess when present. Minor nerve injury from local anesthetic cytotoxicity or ischemia and mechanical trauma may cause permanent nerve injury through the double crush phenomenon. Lower concentrations of local anesthetics are generally recommended.
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Jolly, Elaine, Andrew Fry i Afzal Chaudhry, red. Neurology and neurosurgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0014.
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Chapter 14 covers the basic science and clinical topics relating to neurology and neurosurgery which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers the approach to the neurological Patient, neurological examination, neurological investigations, coma, acquired brain injury, encephalopathies, alcohol and the nervous system, brainstem disorders, common cranial nerve disorders, migraine, other primary headaches, secondary headache, neuro-ophthalmology, vertigo and hearing loss, seizures and epilepsy, intracranial pressure, stroke, central nervous system infections, neuro-oncology, multiple sclerosis, Parkinson disease, other movement disorders, spinal cord disorders (myelopathy), spinal nerve root disorders (radiculopathies), motor neurone disease, peripheral nerve disorders, mitochondrial disease and channelopathies, neuromuscular junction and muscle Disorders, sleep disorders, neurological disorders in pregnancy, the neurology of HIV infection, and functional neurology.
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Park, Susanna B., Cindy S.-Y. Lin i Matthew C. Kiernan. Axonal excitability: molecular basis and assessment in the clinic. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0009.
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Axonal excitability techniques were developed to assess axonal resting membrane potential and ion channel function in vivo, and thereby provide greater molecular understanding of the activity of voltage gated ion channels and ion pumps underlying nerve and membrane function. Axonal excitability studies provide complimentary information to conventional nerve conduction studies, using submaximal stimuli to examine the properties underlying the excitability of the axon. Such techniques have been developed both as a research technique to examine disease pathophysiology and as a clinical investigation technique. This chapter provides an overview of axonal excitability techniques, addressing the role of key ion channels and pumps in membrane function and highlighting examples of clinical case studies, where such techniques have been utilized, including motor neuronopathies, tracking progression of chemotherapy-induced peripheral neuropathy, and assessing treatment response in chronic inflammatory demyelinating polyneuropathy.
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Shaw, Pamela, i David Hilton-Jones. The lower cranial nerves and dysphagia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0429.
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Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.
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Daskalakis, Zafiris J., i Robert Chen. Evaluating the interaction between cortical inhibitory and excitatory circuits measured by TMS. Redaktorzy Charles M. Epstein, Eric M. Wassermann i Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0012.
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Transcranial magnetic stimulation was first introduced in the late 1980s. Numerous studies have used TMS as an investigational tool to elucidate cortical physiology and to probe cognitive processes. This article introduces TMS paradigms and presents information gathered on cortical neuronal connectivity. TMS paradigms that demonstrate intracortical inhibition include short-interval cortical inhibition (SICI), cortical silence period (cSP) and long interval cortical inhibition (LICI). There are two types of cortical inhibitions from the stimulation of other brain areas, interhemispheric inhibition and cerebellum inhibition. The inhibition of the motor cortex can also be induced through the stimulation of peripheral nerves. This article talks about studies that describe interaction between inhibitory and facilitatory paradigms, the results of which are discussed in terms of cortical physiology and connectivity. The study of the interactions among cortical inhibitory and excitatory circuits may help to elucidate pathophysiology of neurological and psychiatric diseases.
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Mauguière, François, i Luis Garcia-Larrea. Somatosensory and Pain Evoked Potentials. Redaktorzy Donald L. Schomer i Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0043.
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This chapter discusses the use of somatosensory evoked potentials (SEPs) and pain evoked potentials for diagnostic purposes. The generators of SEPs following upper limb stimulation have been identified through intracranial recordings, permitting the analysis of somatosensory disorders caused by neurological diseases. Laser activation of fibers involved in thermal and pain sensation has extended the applications of evoked potentials to neuropathic pain disorders. Knowledge of the effects of motor programming, paired stimulations, and simultaneous stimulation of adjacent somatic territories has broadened SEP use in movement disorders. The recording of high-frequency cortical oscillations evoked by peripheral nerve stimulation gives access to the functioning of SI area neuronal circuitry. SEPs complement electro-neuro-myography in patients with neuropathies and radiculopathies, spinal cord and hemispheric lesions, and coma. Neuroimaging has overtaken SEPs in detecting and localizing central nervous system lesions, but SEPs still permit assessment of somatosensory and pain disorders that remain unexplained by anatomical investigations.
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Hawkes, Christopher H., Kapil D. Sethi i Thomas R. Swift. Instant Neurological Diagnosis. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190930868.001.0001.
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Experienced neurologists work fast. They ask few questions, maybe perform a brief examination, and they come up with the right answer. Sometimes they do neither and their conclusions are accurate—but how do they do it? This book holds the answers. The book is divided into 14 chapters which, for the most part, focus on a particular neurologic condition, namely: demyelination, headache, epilepsy and sleep, myopathy and motor neuron disorders, movement disorders, stroke, peripheral neuropathy, cerebellar ataxia, and dementia. The remaining chapters are concerned with the clinician’s initial impressions (first encounters), cranial nerves, limbs and trunk, spinal lesions, and cerebrospinal fluid. At the end of each chapter is a summary of the salient points and a few key references. The final chapter relates to the fast neurological examination. Most diagnostic clues or “Handles” are illustrated by a table, figure, or video clip to reinforce a particular message, and the text is marked with Red Flags that the clinician must be alert for.
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Fuglsang-Frederiksen, Anders, Kirsten Pugdahl i Hatice Tankisi. Quantitative electromyography. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0008.
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Several quantitative electromyography (QEMG) methods are used for diagnosing and monitoring in patients with neuromuscular disorders. At weak effort of the muscle, motor unit potential (MUP) analyses as individual MUP, multi-MUP, and macro-EMG are diagnostically sensitive and well tested. At higher effort of the muscle, interference pattern analyses such as the turns amplitude analysis are also diagnostically sensitive. Other potential diagnostic methods are power spectrum analysis, muscle fibre conduction velocity analysis, and some surface EMG methods. In patients with myopathy, QEMG has an important role in the diagnosis as a supplement to blood tests, muscle biopsy, and genetic testing. In patients with neurogenic disorders such as anterior horn cell disorders, peripheral nerve lesions, or polyneuropathy, QEMG has important roles in characterizing the lesion and differential diagnosis. Furthermore, QEMG may be useful in the examination of patients with neuromuscular transmission failure, critical illness disorders, and in treatment of dystonic muscle with botulinum toxin.
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Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.
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The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.
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PRIDE AND A DAILY MARATHON. Duckworth, 1991.
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Hawkes, Christopher H., Kapil D. Sethi i Thomas R. Swift. Instant Neurological Diagnosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199361953.001.0001.
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Experienced neurologists work fast. They ask few questions, maybe perform a brief examination, and come up with the right answer. Sometimes they do neither and their conclusions are accurate—but how do they do it? Traditionally, the diagnostic process includes pattern recognition and probabilistic, causal, or deterministic methods. The aeronautical expert uses so-called demons—which are essentially memorized diagnostic shortcuts that help to solve problems rapidly. In this text they are called Handles. Another complementary diagnostic process is the use of caveats, or Red Flags, which are negative Handles in the sense that if one encounters a Red Flag, then the diagnosis should be reconsidered. This book provides diagnostic shortcuts, collected by the authors through their own observations, with many others identified at grand rounds and conferences. Thus a diagnosis may be reached rapidly by applying a mixture of Handles and Flags. The Handles and Flags are grouped into regions based on standard neurological history and examination, and others in relation to specific diseases. The book contains thirteen chapters, which for the most part focus on a particular neurological condition, namely demyelination, headache, epilepsy and sleep, myopathy and motor neuron disorders, movement disorders, stroke, peripheral neuropathy, cerebellar ataxia, and dementia. The remaining chapters are concerned with the clinician’s initial impressions (first encounters), cranial nerves, limbs and trunk, spinal lesions, and cerebrospinal fluid. At the end of each chapter is a summary of the salient points and a few key references. Most Handles, are illustrated by a table, figure, or video clip to reinforce a particular message.
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Donaghy, Michael. The clinical approach. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0030.
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This chapter describes the appropriate clinical approach to take when presented with a patient reporting a neurological symptom. Just under 10 per cent of the population consult their general practitioner about a neurological symptom each year in the United Kingdom. About 10 per cent of these are referred for a specialist opinion, usually to a neurologist. Nine conditions account for roughly 75 per cent of general neurological referrals and are diagnosed initially on purely clinical grounds, with the other 25 per cent representing the full range of other, potentially very rare, neurological disorders.This chapter underlines the importance of a thorough and informative history to achieve successful diagnosis. Crucial facets for a good history include information on the time course of symptom development, whether symptoms are negative or positive, previous neurological history (both personal and familial), as well as other potentially contributory general medical disorders. The general neurological examination is also described, as are specific examination manoeuvres that may be added to the general neurological examination in specific clinical circumstances.Reflexes play an important role in diagnostic neurology because they reflect the integrity of, or alterations in, the neural structures responsible for their arc. Loss of a reflex may be due to interruption of the afferent path by a lesion involving the first sensory neurone in the peripheral nerves, plexuses, spinal nerves, or dorsal roots, by damage to the central paths of the arc in the brainstem or spinal cord, by lesions of the lower motor neurone at any point between the anterior horn cells and the muscles, of the muscles themselves, or by the neural depression produced by neural shock. In clinical practice, the most useful and oft-elicited reflexes are the tendon reflexes of the limbs, the jaw jerk, the plantar response, the superficial abdominal reflexes, the pupil-light response, and in infants, the Moro reflex. The place of these particular reflexes in the routine neurological examination is outlined, and the elicitation and significance of these reflexes and of a wide variety of others which are used occasionally are described.Examinations that allow localization lesions that are responsible for muscle weaknesses and the assessment of somatosensory abnormalities are described, as are neurological disorders that result in identifiable gait disorders. The clinical signs and examinations relevant to autonomic disorders are also discussed.Intensive care may be required for patients critically ill either as a result of primary neurological disease, or in those in whom a neurological disorder is a component of, or secondary to, a general medical disorder. Indications for admission to neurological intensive care have been defined (Howard et al. 2003): impaired consciousness, bulbar muscle failure, severe ventilatory respiratory failure, uncontrolled seizures, severely raised intracranial pressure, some monitoring and interventional treatments, and unforeseen general medical complications. Naturally specific treatments indicated for the particular diagnosis should be instituted along with general intensive care measures.Finally, the discussion of diagnoses of chronic or terminal conditions with patients is discussed, with particular focus on the best way to present the diagnosis to the patient.
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(Editor), T. Kumazawa, L. Kruger (Editor) i K. Mizumura (Editor), red. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.
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