Muscle tension

Humans seek and want thermal comfort, even at work in industrial settings. Clothing, activities, posture, location, and shelter are chosen, adjusted, altered, and sought consciously and unconsciously to reduce discomforts and enable us to focus more on the other tasks of life. Discomfort can contribute to mistakes, productivity decreases, and industrial accidents. " Thermal discomfort results from the physiological strain of thermoregulation. The strain can be in the form of altered body temperatures, sweating and excessive skin moisture, muscle tension and stiffness, shivering, and loss of dexterity. A small... 

COLD Xblood flow to skin (vasocoiistriction, muscle tension and shivering t, body temperatures X, metabolism T... 

Anxiety. Mental apprehension frequently accompanied by somatic signs such as increased heart rate, palpations, and increased muscle tension. 

Muscle relaxant. A compound that, by either central or peripheral actions, decreases muscle tension. 

Tonic-clonic convulsions are abnormal motor behavior during a seizure characterized by slow movements with high muscle tension (tonic phase) and subsequent repetitive oscillating movements of limbs (clonic phase). 

Sahlin, K., Edstrom, L., Sjoholm, H., Hultman, E. (1981). Effects of lactic acid accumulation and ATP decrease on muscle tension and relaxation. Am. J. Physiol. 240, C121-C126. 

Cardiovascular (tachycardia, palpitations), sweating, respiration, GIT, muscle tension, tremor, muscle aches or soreness, nausea, exaggerated startle reflex, increased urinary frequency Hypervigilance, nail-biting, scratching... 

Muscle spasm. The pain induced by muscle spasm results partially from the direct effect of tissue distortion on mechanical nociceptors. Muscle spasm also causes tissue ischemia. The increased muscle tension compresses blood vessels and decreases blood flow. Furthermore, the increased rate of metabolism associated with the spasm exacerbates the ischemia. As discussed earlier, ischemia leads to stimulation of polymodal nociceptors. 

BZ dependence is defined by the appearance of a predictable withdrawal syndrome (i.e., anxiety, insomnia, agitation, muscle tension, irritability, nausea, malaise, diaphoresis, nightmares, depression, hyperreflexia, tinnitus, delusions, hallucinations, and seizures) upon abrupt discontinuation. 

MDMA stimulates the CNS, causes euphoria and relaxation, and produces a mild hallucinogenic effect. It can cause muscle tension, nausea, faintness, chills, sweating, panic, anxiety, depression, hallucinations, and paranoid thinking. It increases heart rate and blood pressure and destroys serotonin (5-HT)-producing neurons in animals. It is considered to be neurotoxic in humans. 

Physiologic effects are relatively few. Dilated pupils, hyperreflexia, increased muscle tension, incoordination, and ataxia are common physical signs. Effects on pulse rate, respiration, and blood pressure are so variable that they probably represent varying levels of anxiety of subjects rather than true physiologic effects. Changes in appetite and salivation are inconstant, being increased in some subjects and decreased in others. 

In 1985, 1 finally took the county public health psychiatrist s recommendation to try Desipramine, an ostensibly mild tricyclic antidepressant. I took tiny dot doses, and for a month or so I felt encouraged except for intense muscle tension and clenching. The psychiatrist said it was not remotely possible that this response was related to the medication. I took a low dose for four more months before throwing them out. The side effects had escalated horribly, and become what I later learned are called tardive dyskinesia and tardive dystonia. Subsequently, chemical and electromagnetic field exposures, feeling compromised or ashamed, or stress can trigger uncontrollable movement, hyperactivity, rigid posture and then, frequently, paralysis. 

In the same way that muscle spindles are responsible for the maintenance of muscle length, Golgi tendon organs are responsible for maintenance of muscle tension. 

Patients with depression usually do not present initially to mental health professionals. Most visit their primary care physicians, complaining not of depressed mood but of other symptoms of depression. Fatigue, insomnia, loss of appetite, loss of interest in sex, muscle tension, body aches, and poor concentration are all commonly reported. These so-called masked presentations of depression may in part explain the documented failure of primary care physicians to diagnose depression reliably. This underscores the importance of considering depression in the differential diagnosis of physical complaints that appear vague or exaggerated. 

Gastrointestinal Nausea, vomiting, diarrhea, dry mouth, lump in throat, butterflies Musculoskeletal Restlessness, muscle tension, pacing, muscle pain Neurological Dizziness, lightheadedness, fainting, headache, tremulousness, tingling... 

Congestive heart failure In myocardial insufficiency, the heart depends on a tonic sympathetic drive to maintain adequate cardiac output. Sympathetic activation gives rise to an increase in heart rate and systolic muscle tension, enabling cardiac output to be restored to a level comparable to that in a healthy subject. When sympathetic drive is eliminated during p-receptor blockade, stroke volume and cardiac rate decline, a latent myocardial insufficiency is unmasked, and overt insufficiency is exacerbated (A). 

Benzodiazepines are effective as monotherapy (Rickels et al. 1993) but are rarely used as first-line in this context because of their side-effect profile. They have a useful short-term role for the rapid control of anxiety symptoms or for the control of somatic symptoms such as muscle tension and insomnia, particularly in the early stages of antidepressant therapy. Hydroxyzine has a limited role but can be considered if other treatments are unsuitable (Lader and Scotto 1998). 

GAD differs from other types of anxiety disorders because, although the anxiety is present most of the time, GAD patients do not fear specific events such as social situations or having a panic attack (as in social anxiety or panic disorder). GAD is distinguished from normal worry or anxiety because of its long-term duration. GAD is frequently the underlying cause of many symptoms, including irritability, insomnia, headache, and muscle tension. This can often make it very hard to diagnose. A person with GAD will often go to his or her family physician and complain of nerves. ... 

Several studies [cited in N. Sussman 1994) suggest a preferential effect of buspirone on psychological symptoms of anxiety. Buspirone promotes a greater decrease in symptoms [e.g., anger, hostility, worry, difficulty in concentration) indicative of cognitive and interpersonal problems, whereas diazepam and clorazepate favor somatic symptoms of anxiety [e.g., muscle tension, insomnia). 

Some patients may experience jitteriness, restlessness, muscle tension, and disturbed sleep. These side effects typically occur early in treatment, before the antidepressant effect. All patients should be informed of the possibility of these side effects and be reassured that if they develop, they tend to be transient. In patients with preexisting anxiety, therapy should be started at low doses, with subsequent titration as tolerated. If overstimulation occurs with this approach, it will be less likely to be severe enough to result in nonadherence with therapy. The short-term use of a benzodiazepine also may help the patient cope with overstimulation in the early stages of treatment until tolerance to this side effect occurs. Despite these common transient stimulating effects, SSRIs are clearly effective in patients with anxiety or agitated depression. Similarly, insomnia that commonly occurs early in treatment may be tolerable if the patient is reassured that the side effect will be transient. Symptomatic, short-term treatment with a hypnotic at bedtime is reasonable. 

Increased muscle tension (rigor), trembling (tremor)... 

Arteriolar and venous tone (smooth muscle tension) both play a role in determining myocardial wall stress (Table 12-1). Arteriolar tone directly controls peripheral vascular resistance and thus arterial blood pressure. In systole, intraventricular pressure must exceed aortic pressure to eject blood arterial blood pressure thus determines the systolic wall stress in an important way. Venous tone determines the capacity of the venous circulation and controls the amount of blood sequestered in the venous system versus the amount returned to the heart. Venous tone thereby determines the diastolic wall stress. 

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