Neuromuscular reflexes

Mass, quality, size and strength of the bones in the body Absorption by the body of the impact, this varies due to the amount of soft tissue between the blow and the bones Balance and neuromuscular reflexes to protect against the fall The presence of dizziness, sedatives, alcohol, acute and chronic diseases... 

Leg and foot cramps, hypertension, tachycardia, neuromuscular irritability, tremor, hyperactive deep tendon reflexes, confusion, disorientation, visual or auditory hallucinations, painful paresthesias, positive Trousseau s sign, positive Chvostek s sign, convulsions Hypermagnesemia... 

Neuromuscular Nicotinic Skeletal Excitation Fasciculations, cramps, followed by weakness, loss of reflexes, paralysis... 

FIGURE 6-1 Path of excitation in a simplified spinal reflex that mediates withdrawal of the leg from a painful stimulus. In each of the three neurons and in the muscle cell, excitation starts with a localized slow potential and is propagated via an action potential (a.p.). Slow potentials are generator potential (g.p.) at the skin receptor the excitatory postsynaptic potentials (e.p.s.p.) in the interneuron and the motoneuron and end-plate potential (e.p.p.) at the neuromuscular junction. Each neuron makes additional connections to other pathways that are not shown. 

Neuromuscular symptoms include altered mental status, abnormal behavior, seizures, stupor, and coma. Hypercapnia can mimic a stroke or CNS tumor by producing headache, papilledema, focal paresis, and abnormal reflexes. CNS symptoms are caused by increased cerebral blood flow and are variable, depending in part on the acuity of onset. 

With severe intoxication by all routes, an excess of acetylcholine at the neuromuscular junctions of skeletal muscle causes weakness aggravated by exertion, involuntary twitchings, fasciculations, and eventually paralysis. The most serious consequence is paralysis of the respiratory muscles. Effects on the central nervous system include giddiness, confusion, ataxia, slurred speech, Cheyne-Stokes respiration, convulsions, coma, and loss of reflexes. The blood pressure may fall to low levels, and cardiac irregularities, including complete heart block, may occur. ... 

Adults. 3 g PO q6h x 4 PRN Supl 1-2 g IM or IV repeat PRN Preeclampsia/pre-mature labor 4 g load then g/h IV inf Cardiac arrest 1-2 g IV push (2-4 mL 50% soln) in 10 mL DjW AMI Load 1-2 g in 50-100 mL D5W, over 5-60 min IV then 0.5-1.0 g/h IV up to 24 h (ECC 2005) Feds. 25-50 mg/kg/dose IM or IV q4-6h for 3-4 doses repeat PRN dose w/ low urine output or renal insuff Caution [B, +] Contra Heart block, renal failure Disp Inj 10, 20, 40, 80, 125, 500 mg/mL bulk powder SE CNS depression, D, flushing, heart block Interactions T CNS depression W/ antidepressants, antipsychotics, anxiolytics, barbiturates, hypnotics, narcotics EtOH T neuromuscular blockade Wf aminoglycosides, atracurium, gallamine, pancuronium, tubocurarine, vecuronium EMS Check for absent patellar reflexes this may indicate tox may cause hypokalemia (flattened T waves) and hypocalcemia OD May cause hypotension, resp arrest, T PR, QRS, and QT interval, AV block, and cardiac arrest calcium salts can be given to reverse resp depression... 

Baclofen appears to affect the neuromuscular axis by acting directly on sensory afferents, y-motor neurons, and collateral neurons in the spinal cord to inhibit both monosynaptic and polysynaptic reflexes. The principal effect is to reduce the release of excitatory neurotransmitters by activation of presynaptic GABAg receptors. This seems to involve a G protein and second-messenger link that either increases K+ conductance or decreases Ca conductance. 

Tizanidine is an a -adrenergic receptor agonist at supraspinal and spinal levels. This effect results in inhibition of spinal polysynaptic reflex activity. It presumably reduces spasticity by increasing presynaptic inhibition of motor neurons. Tizanidine has no direct effect on skeletal muscle, the neuromuscular junction or on monosynaptic reflex activity. 

Some sedative-hypnotics, particularly members of the carbamate (eg, meprobamate) and benzodiazepine groups, exert inhibitory effects on polysynaptic reflexes and internuncial transmission and at high doses may also depress transmission at the skeletal neuromuscular junction. Somewhat selective actions of this type that lead to muscle relaxation can be readily demonstrated in animals and have led to claims of usefulness for relaxing contracted voluntary muscle in muscle spasm (see Clinical Pharmacology). Muscle relaxation is not a characteristic action of zolpidem, zaleplon, and eszopiclone. 

Most signs which require a skeletal muscle reflex would not be apparent after treatment with a neuromuscular blocking drug or would be altered... 

Botulinum toxin induces weakness of striated muscles by inhibiting transmission of motor neurons at the neuromuscular junction. This has led to its use in conditions with muscular overactivity, such as dystonia. Transmission is also inhibited at y neurons in muscle spindles, which may alter reflex overactivity. 

No adverse effect on overall neurological optimality or suboptimality scores at 31 months of age. Some alterations in individual test scores which were indicative of enhanced neuromuscular maturation and higher reflexes (altered test scores were within normal range) high-exposure group median concentration of 67.7 ng TEQ low-exposure group median=13.7 ng TEQ llsen et al. 1996... 

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