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Books on the topic 'TMJ syndrome'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Goldman, A. Richard. TMJ syndrome: The overlooked diagnosis. New York: Congdon & Weed, 1987.

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2

Virginia, McCullough, ed. TMJ syndrome: The overlooked diagnosis. New York: Simon & Schuster, 1989.

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3

Levitt, S. R. TMJ scale manual. Durham, N.C. (P.O. Box 2836, Durham 27705): Pain Resource Center, 1987.

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4

1933-, Schrader Constance, and Dillon James 1946-, eds. TMJ, the self-help program. [La Jolla, Calif.]: Surrey Park Press, 1990.

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5

Moles, Randall C. Ending head and neck pain: The TMJ connection. Racine, Wis: CGM Publications, 1989.

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6

TMJ, the jaw connection: The overlooked diagnosis : a self-care guide to diagnosing and managing this hidden ailment. Santa Fe, NM: Aurora Press, 1991.

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7

Marie, Lois. Does your marriage suffer from TMS? (traveling mate syndrome). Dallas, TX: Beginnings, 1992.

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8

Horowitz, Leonard. Freedom from Tmj Pain Syndrome/Bk. and Audio Cassette. Tetrahedron, 1988.

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9

Relief of Pain from Headaches and TMJ. Solomon Books, Incorporated, 1989.

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10

Fish. Myofascial Pain Syndromes of Head, Neck and Tmj. Jones & Bartlett Learning, LLC, 2020.

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11

Coomes, Annie. Trigger point therapy routine for TMJ: Massage techniques to unlock your TMJ. 2017.

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12

Lipskis, Dr Lynn, and Dr Edmund Lipskis. Breathe, Sleep, Live, Smile: Integrative Treatments For TMJ, Sleep Apnea, And Orthodontics. Advantage Media Group, 2019.

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13

Berardelli, Alfredo, and Mark Hallett. TMS in movement disorders. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0021.

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Transcranial magnetic stimulation (TMS) is applied to study patients with movement disorders. This article reviews the findings of such applications in patients with Parkinson's disease, dystonia, Huntington's disease, Tourette's syndrome, and essential tremor. The findings related to Parkinson's disease are characterized by a shortening of the cortical silence period (cSP), a reduction of short intracortical inhibition, an increase in the long-lasting intracortical inhibition, and a reduction of the normal motor evoked potential facilitation after single and repetitive TMS stimuli. Studies with paired-pulse TMS have provided controversial information on cortical motor excitability in Huntington's disease. The findings in dystonia include: a reduction of the short intracortical inhibition and a shortening of the cSP. In Tourette's syndrome patients, the cSP is short and intracortical inhibition is decreased. Patients with essential tremor have normal corticospinal conduction, normal duration of the cSP, and normal intracortical inhibition. Such application of TMS has produced enormous data and continues to do so.

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14

Stewart, Jessica Ann, L. Mark Russakoff, and Jonathan W. Stewart. Pharmacotherapy, ECT, and TMS. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199326075.003.0016.

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Physicians’ attention to patients’ concerns and attitudes about taking medication will engender adherence, as will close monitoring of potentially disconcerting side effects. The primary indication for antipsychotic medications is the treatment of psychotic disorders and mania, even in the absence of psychosis. The more troublesome side effects of antipsychotic medications include increased appetite and weight gain; extrapyramidal side effects, tardive dyskinesia, and neuroleptic malignant syndrome. Antidepressants are effective for treating depressive illness, including major depression, persistent depressive disorder (dysthymia) and premenstrual dysphoric disorder. They are also often used effectively in the treatment of anxiety disorders, obsessive-compulsive disorder, bulimia nervosa, and somatic symptom disorders. Selective serotonin reuptake inhibitors (SSRIs) are generally well tolerated. Other important categories of medications include mood stabilizers and anxiolytics.

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15

Lefaucheur, Jean-Pascal. TMS and pain. Edited by Charles M. Epstein, Eric M. Wassermann, and 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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16

Lachmann, Robin H., and Nigel Manning. Trimethylaminuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0064.

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Trimethylaminuria (TMAU) or “Fish Odor Syndrome” is a disorder caused by increased concentrations of the volatile amine trimethylamine (TMA) in body fluids resulting in an unpleasant odor. The excess TMA may occur either due to deficient hepatic oxidation (primary) or increased bacterial generation (secondary). Testing urine for TMA concentration is the first line of investigation, preferably following a dietary load of a TMA precursor such as choline. Measurement of TMA and TMA-oxide are used as a guide to determine a primary or secondary cause, which can be confirmed by DNA analysis. FMO3 deficiency may have further clinical consequences due to the wide range of substrates oxidized by the enzyme including many drugs. Treatment of both primary and secondary TMAU relies on restriction of dietary precursors of TMA, antibiotic-based reduction of gut flora, and odor chelators. Riboflavin may also benefit some patients.

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17

Hallett, Mark, and Alfredo Berardelli. Movement Disorders. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0044.

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This article focuses on the potential therapeutic uses of transcranial magnetic stimulation (TMS) in movement disorders. The brain can be stimulated with low levels of direct electrical current, called direct current polarization (tDCS). High-frequency repetitive TMS might increase brain excitability and be used for therapy in Parkinson's disease. Single sessions with TMS, however, have not proven to be very effective. Treatment with tDCS has been performed in some open studies with some success, but these results need confirmation. Physiological findings in dystonia reveal a decrease in intracortical inhibition. There have been a few studies of patients with Tourette's syndrome with mixed results. To date, clinical results with TMS in movement disorders have been mixed, and more work will be needed to clarify the potential clinical role of TMS.

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18

O’Connor, Daniel W., and Chris Plakiotis. Brain stimulation therapies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0014.

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Electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS) and deep brain stimulation (DBS) all entail the delivery of electrical impulses to the brain with the aim of relieving mental disorders. ECT is an effective treatment of depression, mania and catatonia and, to a lesser extent, of schizophrenia. Its side effects, principally cognitive impairment, are mitigated through the use of individually tailored, unilateral delivery. TMS is more convenient but of lesser effectiveness. DBS, while reversible and thus safer than lesional surgery, is a major undertaking that is reserved at present for profoundly disabling depression, obsessive-compulsive disorder and Tourette’s syndrome.

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19

Brennfleck, Shannon Joyce, ed. Pain sourcebook: Basic consumer health information about acute and chronic pain, including nerve pain, bone pain, muscle pain, cancer pain, and disorders characterized by pain, such as arthritis, temporomandibular muscle and joint (tmj) disorder, carpal tunnel syndrome, headaches, heartburn, sciatica, and shingles, and facts about diagnostic tests and treatment options for pain, including over-the-counter and prescription drugs, physical rehabilitation, injection and infusion therapies, implantable technologies, and complementary medicine; along with tips for living with pain, a glossary of related terms, and a directory of additional resources. 3rd ed. Detroit: Omnigraphics, 2008.

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20

Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.

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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.

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