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Books on the topic 'Upper motor neuron syndrome'

Author: Grafiati
Published: 4 June 2021
Last updated: 24 April 2022

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1

Barnes, Michael P., and Garth R. Johnson, eds. Upper Motor Neurone Syndrome and Spasticity. Cambridge: Cambridge University Press, 2008. http://dx.doi.org/10.1017/cbo9780511544866.

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2

(Editor), Michael P. Barnes, and Garth R. Johnson (Editor), eds. Upper Motor Neurone Syndrome and Spasticity: Clinical Management and Neurophysiology. Cambridge University Press, 2001.

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3

1952-, Barnes Michael P., and Johnson Garth R. 1945-, eds. Upper motor neurone syndrome and spasticity: Clinical management and neurophysiology. New York, NY: Cambridge University Press, 2001.

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4

Thakore, Nimish, and Erik P. Pioro. Types of Motor Neuron Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0022.

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Disorders of lower motor neurons (LMNs, or anterior horn cells) and upper motor neurons (UMNs), jointly termed motor neuron disorders (MNDs), are diverse and numerous. The prototypical MND, namely amyotrophic lateral sclerosis (ALS), a relentlessly progressive lethal disorder of adults, is the subject of another section and will not be discussed further here. Other MNDs include spinal muscular atrophy (SMA), of which there are four types: Kennedy’s disease, Brown-Violetto-Van Laere, and Fazio-Londe syndromes, lower motor neuron disorders as part of neurodegenerations and secondary motor neuron disease as part of malignancy, radiation and infection.
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5

Upper Motor Neurone Syndrome and Spasticity: Clinical Management and Neurophysiology. 2nd ed. Cambridge University Press, 2008.

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6

1952-, Barnes Michael P., and Johnson Garth R. 1945-, eds. Upper motor neurone syndrome and spasticity: Clinical management and neurophysiology. 2nd ed. Cambridge: Cambridge University Press, 2008.

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7

Paganoni, Sabrina, and Nazem Atassi. Upper Motor Neuron Disorders Hereditary Spastic Paraplegia and Primary Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0032.

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Upper motor neuron (UMN) syndromes are a group of rare, degenerative neurological disorders that are classified as either hereditary spastic paraplegia (HSP) or primary lateral sclerosis (PLS). Our understanding of their underlying pathophysiology is unfortunately very limited and has been a significant barrier to the development of disease-modifying treatments. Recent advances in genetics and in vitro and in vivo disease modeling have provided new insights into disease mechanisms and hold the promise to lead to the future development of mechanism-based therapies.
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8

Miller, Aaron E., and Teresa M. DeAngelis. Bickerstaff’s Brain Stem Encephalitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0026.

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Bickerstaff’s brain stem encephalitis is an idiopathic autoimmune condition considered part of the spectrum of GQ1b mediated diseases such as Miller Fisher variant of Guillain-Barré syndrome. In this chapter, we review the upper and lower motor neuron features and typical laboratory findings, and discuss the most common clinical course, prognosis, and important treatment considerations.
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9

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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10

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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11

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 54-Year-Old Male with Right-Hand Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0002.

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Early in its course, amyotrophic lateral sclerosis (ALS) is mistaken for a number of other neuromuscular problems, including spinal disease, multifocal motor neuropathy, and even carpal tunnel syndrome (CTS) when the weakness is distal and focal. In our patient CTS or cervical spine disease was considered. MRI scan of the appropriate spinal level is important to rule out spinal disease. Nerve conduction studies (NCS) and electromyography (EMG) help to exclude other possibilities and point to the diagnosis of ALS. Later in the clinical course, the clinical picture is pathognomonic with upper and lower motor neuron signs. The differential diagnosis of focal weakness is discussed, as is recognition of the more typical ALS clinical syndrome and familial ALS. NCS and EMG findings in ALS are discussed.
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12

Fink, John K. Upper Motor Neuron Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0031.

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Symptomatic disturbance of corticospinal and corticobulbar tracts (collectively, the upper motor neuron UMN) occurs in innumerable acquired central nervous system disorders including the consequences of trauma, hypoxia-ischemia, inflammation (e.g. multiple sclerosis), toxins (e.g. thiocyanate1 and specific organophosphorus compound toxicity2) and deficiencies (e.g. hypocupremia3 and vitamin B12 deficiency). Variable degrees of UMN disturbance frequently accompany degenerative disorders in which disturbance of another neurologic system results in the primary clinical. Neuropathologic studies have shown prominent axon degeneration involving corticospinal tracts (HSP and PLS) and corticobulbar tracts (PLS); and mildly affecting dorsal columns (HSP and PLS to some degree). Myelin loss is considered secondary to axon degeneration. Loss of cortical motor neurons is observed in PLS. Anterior horn cells are typically spared in both HSP and PLS. Presently, treatment for HSP and PLS is symptomatic and includes physical therapy and spasticity reducing medications.
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13

R, Dimitrijevic Milan, and Eccles, John C. Sir, 1903-, eds. Upper motor neuron functions and dysfunctions. Basel: Karger, 1985.

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14

(Editor), John Eccles, and Milan R. Dimitrijevic (Editor), eds. Upper Motor Neuron Functions and Dysfunctions. S. Karger AG (Switzerland), 1985.

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15

Turner, Martin R. Motor neuron disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0232.

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Motor neuron disease (MND) is characterized by progressive muscular weakness due to simultaneous degeneration of lower and upper motor neurons (L/UMNs). Involvement of LMNs, arising from the anterior horns of the spinal cord and brainstem, leads to secondary wasting as a result of muscle denervation. Involvement of the UMNs of the motor cortex and corticospinal tract results in spasticity. In ~85% of cases, there is clear clinical involvement of both, and the condition is termed ‘amyotrophic lateral sclerosis’ (ALS; a term often used synonymously with MND). In ~13% of cases, there may be only LMN signs apparent, in which case the condition is termed ‘progressive muscular atrophy’, although such cases have a natural history that is to largely identical to that of ALS. In a very small group of patients (~2%), there are only UMN signs for at least the first 4 years, in which case the condition is termed ‘primary lateral sclerosis’; such cases have a uniformly slower progression. There is clinical, neuropathological, and genetic overlap between MND and some forms of frontotemporal dementia.
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16

Shaw, Pamela. The motor neurone disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0524.

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The motor neurone diseases are a group of disorders in which there is selective loss of function of upper and/or lower motor neurones in the motor cortex, brainstem, and spinal cord resulting in impairment in the nervous system control of voluntary movement. The term ‘motor neurone disease’, often abbreviated to ‘MND’, is used differently in different countries. In the United Kingdom it is used as an umbrella term to cover the related group of neurodegenerative disorders including amyotrophic lateral sclerosis, the commonest variant, as well as progressive muscular atrophy, primary lateral sclerosis, and progressive bulbar palsy. However, in many other countries amyotrophic lateral sclerosis, referred to as ALS, has been adopted as the umbrella term for this group of clinical variants of motor system degeneration. There is a tendency now internationally to use the ALS/MND abbreviation to cover this group of conditions. Careful diagnosis within the motor neurone diseases is essential for advising about prognosis, potential genetic implications, and for identifying those with acquired lower motor neurone syndromes who may benefit for the administration of immunomodulatory therapy.
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17

Kaplan, Tamara, and Tracey Milligan. Motor Neuron Disease (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0018.

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The video in this chapter explores motor neuron disease, including amytrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). It discusses the signs of upper motor neuron (UMN) and lower motor neuron (LMN) pathology, as well as Kennedy disease.
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18

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and 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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19

Shaw, Pamela, and 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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20

Katirji, Bashar. Case 19. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0023.

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Amyotrophic lateral sclerosis is a fatal neurological disorder, classically presenting with signs of upper motor neuron and lower motor neuron degeneration. Several motor neuron disease variants with purely upper or lower motor neuron degeneration exist. These includes primary lateral sclerosis, progressive muscular atrophy and progressive bulbar palsy. The diagnostic criteria, including El-Escorial criteria and its most recent Awaji revision, are not used in clinical practice and for research purposes. This case highlights the clinical features and electrodiagnostic characteristics of amyotrophic lateral sclerosis. The findings on nerve conduction studies and needle electromyography are emphasized in detail. The role of electrodiagnostic studies in the diagnosis of amyotrophic lateral sclerosis is to establish evidence of lower motor neuron degeneration, confirm its diffuse nature, and exclude treatable causes (such as multifocal motor neuropathy and mimickers of motor neuron disease such as chronic myopathies).
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21

Katumbay, Desire Tshala. On the Site of the Lesion in Konzo: Clinical and Neurophysiological Studies on a Non-Progressive Upper Motor Neuron Disorder (Comprehensive Summaries of ... from the Faculty of Medicine, 1092). Uppsala Universitet, 2001.

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22

Thakore, Nimish J., and Erik P. Pioro. Clinical Presentations, Diagnostic Criteria, and Lab Testing. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0023.

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Amyotrophic lateral sclerosis (ALS) is the protypical motor neuron disease, which is characterized by the simultaneous presence of upper motor neuron (UMN) and lower motor neuron (LMN) signs in the same extremity or in the cranial-bulbar region. UMN signs at spinal levels include spasticity, slowness of motor activation, hyperactive deep tendon reflexes and extensor plantar responses, whereas UMN signs at the cranial level include spastic dysarthia (slow, labored, nasal); slowness of tongue movements, and hyperactive jaw, gag, and facial reflexes. LMN signs at the spinal level include muscle atrophy, fasciculations, and weakness and LMN signs at the cranial level include tongue atrophy and weakness, facial weakness, tongue and facial fasciculations, palatal weakness, weak cough, and dysphonia. ALA is fatal in 2 to 4 years, and the only medication known to prolong tracheostomy-free survival
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23

Bowker, Lesley K., James D. Price, Ku Shah, and 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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24

Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0018.

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Hyperactive deep tendon reflexes area sign of upper motor neuron lesion. They are also commonly seen in normal but tense people. Proper technique of reflexes examination and experience play a major role in eliciting and categorizing deep tendon reflexes. Clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is ALS due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, PLS, HSP, and other causes of myelopathies should be entertained. Jaw clonus often indicates a lesion above the midpontine level. When hyperreflexia is found, it is wise to look for other features of upper motor neuron dysfunction such as positive Babiniski signs and hypertonia.
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25

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 72-Year-Old Female with Facial Weakness and Droopy Eyelids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0030.

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Fatigable weakness is the hallmark of myasthenia gravis (MG). It may present with false localizing signs leading to an itinal incorrect diagnosis of a brainstem stroke. MRI scanning of the brain with specific sequences can rule out the diagnosis of stroke. Differential diagnosis of MG may also include also motor neuron disease. Electromyography is very helpful in confirming the diagnosis of motor neuron disease. The two major diseases of the neuromuscular junction are MG and Lambert-Eaton syndrome (LEMS). A table presents the differing characteristics of each. LEMS can be associated with malignancy and MG with thyoma. Laboratory examinations have greatly assisted in differentiating these two conditions. There is specific antibody testing for each condition. Repetitive stimulation and single fiber electromyography also improve diagnostic acumen.
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26

Katirji, Bashar. Case 25. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0029.

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Multifocal motor neuropathy (MMN) is a relatively rare chronic immune-mediated neuropathy. Distinguishing MMN from motor neuron disease is essential since the disorder is amenable to treatment. This case presents a patient with MMN and multiple conduction blocks of motor nerves. It highlights the total sparing of sensory nerve conduction studies. Criteria for the diagnosis of MMN are emphasized. The importance and relevance of serum anti-glycolipid antibodies and conduction blocks in the diagnosis of MMN remains a controversial issue. The differential diagnosis often includes chronic inflammatory demyelinating polyradiculoneuropathy and Lewis-Sumner syndrome (multifocal acquired demyelinating sensory and motor neuropathy).
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27

Sandbrink, Friedhelm. The MEP in clinical neurodiagnosis. Edited by Charles M. Epstein, Eric M. Wassermann, and 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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28

Teasdale, Andrew, and Jane Halsall. Neurological and muscular disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198719410.003.0011.

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This chapter describes the anaesthetic management of the patient with those neurological or muscular disorders which are relevant to anaesthetic practice, including malignant hyperthermia. Other topics covered include epilepsy, cerebrovascular disease, Parkinson’s disease, spinal cord lesions, myasthenia gravis, multiple sclerosis, Guillain-Barré syndrome, motor neuron disease, dystrophia myotonica, and the muscular dystrophies. For each topic, preoperative investigation and optimization, treatment, and anaesthetic management are described. For malignant hyperthermia, trigger-free anaesthetic techniques are described, as well as the management of an acute episode.
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29

Teasdale, Andrew, and Jane Halsall. Neurological and muscular disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198719410.003.0011_update_001.

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This chapter describes the anaesthetic management of the patient with those neurological or muscular disorders which are relevant to anaesthetic practice, including malignant hyperthermia. Other topics covered include epilepsy, cerebrovascular disease, Parkinson’s disease, spinal cord lesions, myasthenia gravis, multiple sclerosis, Guillain-Barré syndrome, motor neuron disease, dystrophia myotonica, and the muscular dystrophies. For each topic, preoperative investigation and optimization, treatment, and anaesthetic management are described. For malignant hyperthermia, trigger-free anaesthetic techniques are described, as well as the management of an acute episode.
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30

Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0018.

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Hyperactive deep tendon reflexes (DTRs) is a sign of upper motor neuron (UMN) lesions. It is also commonly seen in normal but anxious people. The proper technique of deep tendon reflex examination and experience play a major role in eliciting and categorizing DTRs. Sustained clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is amyotrophic lateral sclerosis (ALS) due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), and other causes of myelopathies should be entertained. Compressive myelopathies are easily excludable by neuroimaging.
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31

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and 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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32

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 30-Year-Old Male with Severe Cramps. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0029.

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Muscle cramps are a common complaint. When not associated with weakness, the course is usually benign but can still be frustrating to patients. Diffuse cramping may be indicative of a neuromuscular disorder. Cramps can be associated with a metabolic or endocrine disorder or medications. Normal nerve conduction studies and electromyography are reassuring for a benign cause of cramps. In motor neuron disease cramps are common. There are rare spontaneous activity syndromes associated with cramping. Stiff person syndrome is rare and usually has severe axial rigidity. It can be treated with immune modulating medications. McArdles disease has a prominent symptom of diffuse muscle cramping associated with activity. Unfortunately not always will a specific cause for cramps be discovered. Various treatment modalities are presented.
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33

Shaibani, Aziz. Tongue Signs. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0006.

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The tongue is heavily innervated and plays a central role in articulation, swallowing, and tasting. Unilateral weakness is usually well tolerated. Intermittent weakness of the tongue is highly suspicious of myasthenia gravis, while progressive weakness and atrophy are typical for amyotrophic lateral sclerosis(ALS). Tongue weakness without atrophy or fasciculations is a sign of upper motor neuron or cerebellar involvement. Lingual dysarthria should be differentiated from other types of dysarthria. Tongue tremor is common and may be confused with fasciculations. Inspection of the tongue is often diagnostically useful in neuromuscular patients. Fasciculations, myokymia, grooving with pressure, and trigrooved tongue are examples.
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34

Wise, Matt, and Paul Frost. ICU treatment of respiratory failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0149.

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Respiratory failure is a syndrome characterized by defective gas exchange due to inadequate function of the respiratory system. There is a failure to oxygenate blood (hypoxaemia) and/or eliminate carbon dioxide (hypercapnoea). Respiratory failure can develop over years when it is due to conditions such as kyphoscoliosis or motor neuron disease, or minutes in the case of an acute asthma attack or pneumothorax. In this context, respiratory failure is often called acute (e.g. asthma), chronic (e.g. kyphoscoliosis), or acute on chronic (kyphoscoliosis complicated by pneumonia). Chronic respiratory failure is characterized by compensatory mechanisms which aim to adjust the pH of the blood back to the normal physiological range and involve the retention of bicarbonate by the kidney. This topic covers the etiology of respiratory failure as well as signs, symptoms, diagnosis, investigations, prognosis, and treatment.
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35

Shaibani, Aziz. Clinical Signs. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0026.

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In clinical neuromuscular medicine, clinical signs are very important for elucidation of the right diagnosis. There is nothing better than videos to demonstrate these signs and their elicitation and significance. We selected several clinical signs from our video archives for this purpose. Babinski sign is an important clue to upper motor neuron dysfunction. Bell’s phenomenon is a normal response. Facilitation of reflexes is a strong indication of a presynaptic neuromuscular transmission disorder. By definition a sign is a clinical finding as opposed to a symptoms which is what the patient report. Some signs are transient and not captured during clinical examination. The advent of video recording ability to general public facilitate capturing of physical signs in videos.
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36

Shaibani, Aziz. Tongue Signs. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0006.

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The tongue is heavily innervated and plays a central role in articulation, swallowing, and tasting. Unilateral weakness is usually well tolerated. Intermittent weakness of the tongue is highly indicative of myasthenia gravis (MG), while progressive weakness and atrophy is typical for amyotrophic lateral sclerosis (ALS). Tongue weakness without atrophy or fasciculations is a sign of upper motor neuron (UMN) or cerebellar involvement. Lingual dysarthria should be differentiated from other types of dysarthria. Tongue tremor is common and may be confused with fasciculation. Inspection of the tongue while resting in the mouth is more telling than a contracted and protruded tongue for the presence of fsciculations. Direct needle examination of the tongue is painful and is rarely needed.
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37

Katirji, Bashar. Case 16. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0020.

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Neuralgic amyotrophy is a relatively uncommon disorder but important to recognize since it may be confused with brachial plexopathy, cervical radiculopathy and entrapment/compressive mononeuropathies of the upper extremity. Neuralgic amyotrophy is also known as acute brachial neuritis, acute brachial plexitis, and Parsonage-Turner syndrome. This case highlights the variable clinical and electrodiagnostic findings encountered in patients with neuralgic amyotrophy, with special attention to the most common mononeuropathies affected in this disorder. This include the long thoracic nerve, axillary nerve, phrenic nerve and anterior interosseous nerve. The peculiar needle electromyography findings associated with neuralgic amyotrophy, including selective motor branch involvement, are also discussed.
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38

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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39

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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40

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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