67 Sentences With "incoordination" | Random Sentence Generator

Ketamine hangovers can also include "dizziness, incoordination, [and] impaired attention and memory," Masand adds.

PEOPLE Pet Vet Dr. Evan Antin says that overheating in dogs generally starts with excessive panting, followed by lethargy and then mental and physical incoordination.

In 1885, Georges Gilles de la Tourette, a young French neurologist, published an article entitled "Study on a Nervous Affliction Characterized by Motor Incoordination and Echolalia and Coprolalia," in the French journal Archives de Neurologie.

Infected animals develop tremors and incoordination that progress to decumbency and death.

Motor symptoms vary more from patient to patient, but can include incoordination and tremors, nystagmus, loss of conjugate eye movements, rigidity and hemiparesis.

Other side effects include increase in drinking or urination, jaundice, bloody or black stools, pale gums, hot spots, increased respiration (fast or heavy breathing), incoordination, and behavior changes.

Intoxication symptoms included confusion, poor judgment, hostility, and motor incoordination. Upon abrupt withdrawal of barbiturates, initial symptoms included tremor, anxiety, weakness, and vomiting, followed by convulsion, delirium, and hallucinations.

Other reported side effects are hyperactivity, panting, lethargy, vomiting, fever, decreased appetite, nervousness, diarrhea, difficulty breathing, salivation, incoordination, seizures, pupil dilation, increased heart rate, trembling and nervousness. In other studies no adverse effects were observed.

It can cause swallowing incoordination, high-peaked esophageal peristalsis, bronchospasm, delayed cricopharyngeal relaxation, and severe respiratory distress necessitating ventilatory support in children. Nitrazepam may promote the development of parasympathetic overactivity or vagotonia, leading to potentially fatal respiratory distress in children.

An extensive study of the toxicology of tetraethylammonium chloride in mice, rats and dogs was published by Gruhzit and co-workers in 1948. These workers reported the following symptoms in mice and rats receiving toxic parenteral doses: tremors, incoordination, flaccid prostration, and death from respiratory failure within 10–30 minutes; dogs exhibited similar symptoms, including incoordination, flaccid prostration, respiratory and cardiac depression, ptosis, mydriasis, erythema, and death from respiratory paralysis and circulatory collapse. After non-lethal doses, symptoms abated within 15–60 minutes. There was little evidence of toxicity from chronic administration of non-lethal doses.

The third is the paralytic stage and is caused by damage to motor neurons. Incoordination is seen, owing to rear limb paralysis, and drooling and difficulty swallowing is caused by paralysis of facial and throat muscles. Death is usually caused by respiratory arrest.

Tick paralysis is included in avian spirochetosis and appears in the same fashion. The flaccid paralysis ascends throughout the body. Incoordination first occurs followed by paralysis of the hind limbs, forelimbs, and then leads to respiratory distress and failure. Death then follows.

CNS depression including slight drowsiness to deep sleep, lassitude, dizziness, incoordination. Headache, psychomotor impairment and antimuscarinic effects. Rarely, rashes and hypersensitivity reactions, blood disorders, convulsions, sweating, myalgia, paraesthesias, extrapyramidal effects, tremor, confusion, sleep and GI disturbances, tinnitus, hypotension, hair loss. Photosensitivity, jaundice.

Cypermethrin is moderately toxic through skin contact or ingestion. It may cause irritation to the skin and eyes. Symptoms of dermal exposure include numbness, tingling, itching, burning sensation, loss of bladder control, incoordination, seizures and possible death. Pyrethroids may adversely affect the central nervous system.

Phenibut is generally well-tolerated. Possible side effects may include sedation, somnolence, nausea, irritability, agitation, anxiety, dizziness, headache, and allergic reactions such as skin rash and itching. At high doses, motor incoordination, loss of balance, and hangovers may occur. Tolerance develops to phenibut with repeated use.

Signs include weight loss, weakness, sleepiness, yawning, incoordination, yellowish discoloration to mucous membranes (icterus), neurologic problems secondary to liver failure (aimless walking, chewing motions, head pressing). Animals may appear to be normal at first, then become suddenly affected; the syndrome progresses rapidly over a few days to a week.

Dogs that have been infected with distemper tend to suffer a progressive deterioration of mental abilities and motor skills. With time, the dog can develop more severe seizures, paralysis, reduction in sight, and incoordination. These dogs are usually humanely euthanized because of the immense pain and suffering they face.

The side effects for Levonantradol include ptosis, sedation, and ataxia in non-human primates. In rodents, the symptoms include dysphoria, memory impairment, motor incoordination, reduced concentration, and disorientation. Levonantradol also decreases startle response. In humans, side effects include dry mouth, drowsiness, dizziness, altered perception, mild sedation, and lack of concentration.

Type 3, familial dysautonomia (FD) or Riley-Day syndrome, is an autosomal recessive disorder seen predominantly in Jews of eastern European descent. Patients present with sensory and autonomic disturbances. Newborns have absent or weak suck reflex, hypotonia and hypothermia. Delayed physical development, poor temperature and motor incoordination are seen in early childhood.

It is usually well tolerated, but in some individuals it may cause mild headache, itching, nausea, vomiting or blurred vision. Rarely incoordination, convulsions, peripheral neuritis and bleaching of hair can occur. Diminution of T waves has been noticed on routine electrocardiographic recordings. Retinopathy does not occur with the usual dosage for amoebic liver abscess.

Sleeping pills, including zopiclone, have been associated with an increased risk of death. The British National Formulary states adverse reactions as follows: "taste disturbance (some report a metallic like taste); less commonly nausea, vomiting, dizziness, drowsiness, dry mouth, headache; rarely amnesia, confusion, depression, hallucinations, nightmares; very rarely light headedness, incoordination, paradoxical effects [...] and sleep-walking also reported".

Usually, within minutes of ingestion of the poisoned shellfish, paranesthesia of the oral region and fingertips are noticed. This gradually proceeds to the neck, arms, legs and toes, together with general muscular incoordination. Patients can start feeling numb, due to which it is hard to make voluntary movements. Also symptoms as dizziness, weakness and incoherence can occur.

A lethal dose of NRB to rats causes behavioural changes which look a lot like the signs associated to cyanide toxicity. The first indications of the NRB toxicity present themselves about ten minutes after administration. At first the rats start showing signs of increased motor activity and incoordination. Subsequently, the rats' hind extremities weaken and become ashen.

Early symptoms of cicutoxin poisoning include excessive salivation, frothing at the mouth, nervousness, and incoordination. These symptoms can progress to tremors, muscular weakness, seizures and respiratory failure. Ingestion of green materials of western water hemlock in amounts equivalent to about 0.1% of a person's body weight can even lead to death. In addition to being extremely hazardous to humans, this plant has an enormous impact on animals.

Following the sub-acute phase, the patients experience a few mild symptoms including some behavioral changes, incoordination, and difficulty in speech. Eventually the disease developed fully and those infected were stricken with the characteristic symptoms of rigidity, slurred speech, and deterioration of cognitive functions. Ultimately, brain function depreciates rapidly resulting in death. Many patients who undergo the chronic form claim never to have had an acute attack.

In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness, and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur. Phosphorus- deficient cattle, especially in southern Africa, are inclined to ingest bones and carrion containing clostridial toxins and consequently suffer lame sickness or lamsiekte.

Rabies can be contracted in horses if they interact with rabid animals in their pasture, usually through being bitten (e.g. by vampire bats) on the muzzle or lower limbs. Signs include aggression, incoordination, head-pressing, circling, lameness, muscle tremors, convulsions, colic and fever. Horses that experience the paralytic form of rabies have difficulty swallowing, and drooping of the lower jaw due to paralysis of the throat and jaw muscles.

Around 30 to 50% of them will also have developmental delay/learning difficulties, psychotic-like features, incoordination of movements or behavioral abnormalities. Most patients are born with normal hearing; however, the onset of hearing loss is very common in early adolescence. About 15% of patients are estimated to develop all the features of the disease. Due to the X-linked recessive pattern of inheritance, Norrie disease affects almost entirely males.

Typically patients fail to reach motor milestones and show a qualitative difference in motor development. During the neonatal period (first 28 days of life), children are noted to be lethargic, relatively immobile, and floppy. Moreover, hypotonia is greatest during this period, even though muscle tone increases with age, it never reaches normal levels. The limbs show weakness, incoordination in voluntary movement, dysdiadochokinesis (in inability to perform rapidly alternating movements), and titubation.

There is evidence that auto mechanics had disproportionate levels of mesothelioma. Those who do maintenance work on brakes can also be exposed to the solvents 1,1,1-trichloroethane and 2-butoxyethanol (a main ingredient in Greasoff No. 19). Exposure to these solvents can cause irritation, including to the eyes and mucous membranes. Exposure to 1-1-1-trichloroethane vapors can cause central nervous system damage, dizziness, incoordination, drowsiness, and increased reaction time.

However, effects such as incoordination, cognitive impairment, and vision and hearing loss may become permanent with repeated exposure, especially at high levels associated with intentional solvent abuse. High levels of toluene exposure during pregnancy, such as those associated with solvent abuse, may lead to developmental effects, such as retardation of mental abilities and growth in children. Other health effects of potential concern may include immune, kidney, liver, and reproductive effects.

An uncommon, less understood result of stroke is a condition called apraxia. This condition was initially recognized as: 'Disorders of the execution of learned movements which cannot be accounted for by either weakness, incoordination, or sensory loss, nor by incomprehension of, or inattention to commands.' Several forms of apraxia are recognized. Limb-kinetic apraxia is the inability to make precise or exact movements with a finger, an arm or a leg.

When exposed to polar narcotics, rainbow trout first exhibited increased muscular activity followed by incoordination and unresponsiveness to external stimuli. In general, narcosis II is characterized by greater toxicity than narcosis I. Thus, Baseline-narcosis models should be used for predicting the toxicity of nonpolar narcotics. In addition, narcosis I is the generalized depression of biological activity. In contrast, narcosis II symptoms include stimulation of respiratory-cardiovascular responses followed by generalized depression of activity.

A male with gluten ataxia: previous situation and evolution after 3 months of gluten-free diet. Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten. With gluten ataxia, damage takes place in the cerebellum, the balance center of the brain that controls coordination and complex movements like walking, speaking and swallowing, with loss of Purkinje cells. People with gluten ataxia usually present gait abnormality or incoordination and tremor of the upper limbs.

Pseudoparalysis (pseudo- meaning "false, not genuine", from Greek ψεῦδος) is voluntary restriction or inhibition of motion because of pain, incoordination, orgasm, or other cause, and is not due to actual muscular paralysis.TheFreeDictionary > pseudoparalysis, in turn citing The American Heritage Medical Dictionary 2007, 2004 In an infant, it may be a symptom of congenital syphilis. Pseudoparalysis can be caused by extreme mental stresses, and is a common feature of mental disorders such as panic anxiety disorder.

Those inflicted with the disease survive for a period of only a few months to several years. VE follows three main courses of infection: an acute form, a sub-acute form subsiding into a progressive form, and a chronic form. Initially, the infected patients experience symptoms such as: severe headaches, delirium, lethargy, meningism, bradykinesia, and incoordination. A small percentage of patients die during the acute phase as result of a severe coma.

Lesions in cerebrocerebellum, which receives input exclusively from the cerebral cortex and projects its output to premotor and motor cortices, result in impairments in highly skilled sequences of learned movements, for instance, playing a musical instrument. Lesions may also result in problems with planning movements and ipsilateral incoordination, especially of the upper limb and to faulty phonation and articulation. Pathological interaction between cerebellothalamic tract and basal ganglia may be the explanation for the resting tremor in Parkinson's disease.

Ethanol binding to GABAA receptor Many of the effects of activating GABAA receptors have the same effects as that of ethanol consumption. Some of these effects include anxiolytic, anticonvulsant, sedative, and hypnotic effects, cognitive impairment, and motor incoordination. This correlation between activating GABAA receptors and the effects of ethanol consumption has led to the study of ethanol and its effects on GABAA receptors. It has been shown that ethanol does in fact exhibit positive allosteric binding properties to GABAA receptors.

P0- mice developed behavioral deficits around 2 weeks of age when mice began to show signs of slight trembling. Gross incoordination also arose as the animals developed, while trembling became more severe and some older mice developed convulsing behaviors. Despite the array of impaired motor behavior, no paralysis was observed in these animals. P0 is also an important gene expressed early within the Schwann cell lineage, expressed in Schwann cell precursors after differentiating from migrating neural crest cells within the developing embryo.

Samuel Alexander Kinnier Wilson, the neurologist most known for his description of what came to be known as Wilson's disease. Wilson's disease (WD) is a rare inherited disorder in which patients have a problem metabolizing copper. In patients with WD, copper accumulates in the liver and other parts of the body, particularly the brain, eyes and kidneys. Upon accumulation in the brain, patients may experience speech problems, incoordination, swallowing problems, and prominent hyperkinetic symptoms including tremor, dystonia, and gait difficulties.

Several reactions have been noted in manufacturer guidelines—deep sleep, incoordination, sedation, calmness, and dizziness have been reported in children and adults, as well as others such as hypotension, tinnitus, and headaches.UCB South-Africa, et al., (2004) Gastro-intestinal effects have also been observed, as well as less serious effects such as dryness of the mouth and constipation caused by the mild antimuscarinic properties of hydroxyzine. Central nervous system problems such as hallucinations or confusion have been observed in rare cases, attributed mostly to overdosage.

Many mutations in the SLC2A1 gene, including LYS456TER, TYR449TER, LYS256VAL, ARG126HIS, ARG126LEU and GLY91ASP, have been shown to cause GLUT1 deficiency syndrome 1 (GLUT1DS1), a neurologic disorder showing wide phenotypic variability. This disease can be inherited in either an autosomal recessive or autosomal dominant manner. The most severe 'classic' phenotype comprises infantile-onset epileptic encephalopathy associated with delayed development, acquired microcephaly, motor incoordination, and spasticity. Onset of seizures, usually characterized by apneic episodes, staring spells, and episodic eye movements, occurs within the first 4 months of life.

A male with gluten ataxia: previous situation and evolution after three months of gluten-free diet Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten. With gluten ataxia, damage takes place in the cerebellum, the balance center of the brain that controls coordination and complex movements like walking, speaking and swallowing, with loss of Purkinje cells. People with gluten ataxia usually present gait abnormality or incoordination and tremor of the upper limbs. Gaze-evoked nystagmus and other ocular signs of cerebellar dysfunction are common.

Newer agents such as the melatonin receptor agonists may be more suitable and effective for the management of chronic insomnia in elderly people. Long-term use of sedative-hypnotics for insomnia lacks an evidence base and is discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls. In addition, the effectiveness and safety of long-term use of nonbenzodiazepine hypnotic drugs remains to be determined.

Research showed that spinocerebellar ataxia 2 (SCA2) patients with a mild stage of the disease gained significant improvement in static balance and neurological indices after six months of a physical therapy exercise training program. Occupational therapists may assist patients with incoordination or ataxia issues through the use of adaptive devices. Such devices may include a cane, crutches, walker, or wheelchair for those with impaired gait. Other devices are available to assist with writing, feeding, and self care if hand and arm coordination are impaired.

Chronic use of sedative-hypnotic drugs for the management of insomnia does not have an evidence base and has been discouraged due to concerns including potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls. In addition, the effectiveness and safety of long-term use of sedative hypnotics has been determined to be no better than placebo after 3 months of therapy and worse than placebo after 6 months of therapy.NEJM, 1983, 1994, et seq.

Central nervous system signs include a localized involuntary twitching of muscles or groups of muscles, seizures with salivation and jaw movements commonly described as "chewing-gum fits", or more appropriately as "distemper myoclonus". As the condition progresses, the seizures worsen and advance to grand mal convulsions followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly, they may lead to blindness and paralysis.

The diagnosis of pufferfish poisoning is based on the observed symptomatology and recent dietary history. Symptoms typically develop within 30 minutes of ingestion, but may be delayed by up to four hours; however, if the dose is fatal, symptoms are usually present within 17 minutes of ingestion. Paresthesia of the lips and tongue is followed by developing paresthesia in the extremities, hypersalivation, sweating, headache, weakness, lethargy, incoordination, tremor, paralysis, cyanosis, aphonia, dysphagia, and seizures. The gastrointestinal symptoms are often severe and include nausea, vomiting, diarrhea, and abdominal pain; death is usually secondary to respiratory failure.

Alcohol causes generalized central nervous system depression and associated cognitive, memory, motor, and sensory impairment. It slows and impairs cognition and reaction time, impairs judgement, interferes with motor function resulting in motor incoordination, loss of balance, and slurred speech, impairs memory formation, and causes sensory impairment. At high concentrations, amnesia, analgesia, spins, stupor, and unconsciousness result. At very high concentrations, anterograde amnesia, markedly decreased heart rate, pulmonary aspiration, positional alcohol nystagmus (PAN), respiratory depression, and death can result due to profound suppression of central nervous system function and consequent dysautonomia.

Louping-ill is an acute viral disease primarily of sheep that is characterized by a biphasic fever, depression, ataxia, muscular incoordination, tremors, posterior paralysis, coma, and death. Louping-ill is a tick-transmitted disease whose occurrence is closely related to the distribution of the primary vector, the sheep tick Ixodes ricinus. It also causes disease in red grouse, and can affect humans. The name 'louping-ill' is derived from an old Scottish word describing the effect of the disease in sheep whereby they 'loup' or spring into the air.

It is very similar to the other subspecies, the Andean crested duck, differing in being slightly smaller, with more distinctively mottled underparts, and a lighter purple speculum with green or bronze reflections.Blake (1977). Although, some crested ducks can also have rather fat bodies that may lead to varying degrees of motor incoordination Young ducks have smaller crests than the adults, or lack crests entirely. The faces of the young birds are browner than those of the adults; the abdomen is also much whiter and the mandible a pinkish colour.

Adverse drug reactions are most commonly associated with the first-generation H1-antihistamines. This is due to their relative lack of selectivity for the H1-receptor and their ability to cross the blood-brain barrier. The most common adverse effect is sedation; this "side-effect" is utilized in many OTC sleeping-aid preparations. Other common adverse effects in first-generation H1-antihistamines include dizziness, tinnitus, blurred vision, euphoria, incoordination, anxiety, increased appetite leading to weight gain, insomnia, tremor, nausea and vomiting, constipation, diarrhea, dry mouth, and dry cough.

Mountain laurel is poisonous to several animals, including horses, goats, cattle, deer, monkeys, and humans, due to grayanotoxin and arbutin. The green parts of the plant, flowers, twigs, and pollen are all toxic, including food products made from them, such as toxic honey that may produce neurotoxic and gastrointestinal symptoms in humans eating more than a modest amount. Symptoms of toxicity begin to appear about 6 hours following ingestion. Symptoms include irregular or difficulty breathing, anorexia, repeated swallowing, profuse salivation, watering of the eyes and nose, cardiac distress, incoordination, depression, vomiting, frequent defecation, weakness, convulsions, paralysis, coma, and eventually death.

The predominant symptom is peripheral sensory neuropathy that is experienced as numbness, pins-and-needles and burning sensations (paresthesia) in a patient's limbs on both sides of their body. Patients may experience unsteadiness of gait, incoordination (ataxia), involuntary muscle movements (choreoathetosis) the sensation of an electric zap in their bodies (Lhermitte's sign), a heightened sensitivity to sense stimuli including photosensitivity (hyperesthesia), impaired skin sensation (hypoesthesia), numbness around the mouth, and gastrointestinal symptoms such as nausea and heartburn. The ability to sense vibrations and to sense one's position are diminished to a greater degree than pain or temperature. Skin lesions have also been reported.

One of the most common side effects of spironolactone is frequent urination. Other general side effects include dehydration, hyponatremia (low sodium levels), mild hypotension (low blood pressure), ataxia (muscle incoordination), drowsiness, dizziness, dry skin, and rashes. Because of its antiandrogenic activity, spironolactone can, in men, cause breast tenderness, gynecomastia (breast development), feminization in general, and demasculinization, as well as sexual dysfunction including loss of libido and erectile dysfunction, although these side effects are usually confined to high doses of spironolactone. At very high doses (400 mg/day), spironolactone has also been associated with testicular atrophy and reversibly reduced fertility, including semen abnormalities such as decreased sperm count and motility in men.

Some symptoms of an overdose typically include sluggishness, incoordination, difficulty in thinking, slowness of speech, faulty judgement, drowsiness, shallow breathing, staggering, and, in severe cases, coma or death. The lethal dosage of barbiturates varies greatly with tolerance and from one individual to another. The lethal dose is highly variable among different members of the class with superpotent barbiturates such as pentobarbital being potentially fatal in considerably lower doses than the low-potency barbiturates such as butalbital. Even in inpatient settings the development of tolerance is still a problem, as dangerous and unpleasant withdrawal symptoms can result when the drug is stopped after dependence has developed.

Long-term use of sedative-hypnotics for insomnia lacks an evidence base and has traditionally been discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment, anterograde amnesia, daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls. One study found no evidence of sustained hypnotic efficacy throughout the 9 weeks of treatment for triazolam. In addition, the effectiveness and safety of long- term use of these agents remain to be determined. More research is needed to evaluate the long-term effects of treatment and the most appropriate management strategy for elderly persons with chronic insomnia.

Spinocerebellar ataxia (SCA) is one of a group of genetic disorders characterized by slowly progressive incoordination of gait and is often associated with poor coordination of hands, speech, and eye movements. A review of different clinical features among SCA subtypes was recently published describing the frequency of non-cerebellar features, like parkinsonism, chorea, pyramidalism, cognitive impairment, peripheral neuropathy, seizures, among others. As with other forms of ataxia, SCA frequently results in atrophy of the cerebellum, — Gives a concise description of SCA, along with a picture of shrunken degenerated cerebellum. loss of fine coordination of muscle movements leading to unsteady and clumsy motion, and other symptoms.

CNS involvement (primary or secondary) can lead to seizures, incoordination and paralysis. Regenerative and non-regenerative anemia have been consistently documented in hemophagocytic HS. Lameness is often observed in periarticular HS. Treatment of HS complex Localized HS affecting skin and subcutis have been cured by early surgical excision. In the case of periarticular HS which occurs in the subsynovial tissues of the extremities, amputation of the affected limb is enforced by the inoperable nature of the primary lesion which ensnares structures vital to limb function. Disseminated HS (including MH) is not readily treated surgically, since even in the splenic form, early metastasis to the liver has often occurred.

EVT-201 is a benzodiazepine derivative drug and partial positive allosteric modulator of the benzodiazepine site of the GABAA receptor. It has 2–4-fold higher functional affinity for the α1 subunit relative to the α2, α3, and α5 subunits and significantly less intrinsic activity in comparison to currently- marketed benzodiazepines and the Z-drugs. Despite the lower efficacy, EVT-201 still shows effectiveness in the treatment of insomnia, and it is thought that the lower efficacy may result in fewer side effects, such as motor incoordination. The drug was originally developed by Roche, based on preclinical data, as a non-sedating anxiolytic, but was found to produce sedation in humans in phase I clinical trials.

It was found that newer agents with novel mechanisms of action and improved safety profiles, such as the melatonin receptor agonists, hold promise for the management of chronic insomnia in elderly people. Long-term use of sedative-hypnotics for insomnia lacks an evidence base and has traditionally been discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls. In addition, the effectiveness and safety of long-term use of these agents remain to be determined. It was concluded that more research is needed to evaluate the long-term effects of treatment and the most appropriate management strategy for elderly persons with chronic insomnia.

It cannot be accepted, surely, that a people were ever held together by the mere unity of physical origin, or, if it were, could maintain that unity for ten generations. It cannot be too often reiterated that this physiological provenance has no existence except for science—never for folk- consciousness—and that no people was ever stirred to enthusiasm by this ideal of blood purity. In race (Rasse haben) there is nothing material but something cosmic and directional, the felt harmony of a Destiny, the single cadence of the march of historical Being. It is the incoordination of this (wholly metaphysical) beat which produces race hatred... and it is resonance on this beat that makes the true love—so akin to hate—between man and wife.

An extensive review of the medical literature regarding the management of insomnia and the elderly found that there is considerable evidence of the effectiveness and lasting benefits of non-drug treatments for insomnia in adults of all age groups and that these interventions are underused. Compared with the benzodiazepines, the nonbenzodiazepine sedative-hypnotics offer little if any advantages in efficacy or tolerability in elderly persons. It was found that newer agents such as the melatonin agonists may be more suitable and effective for the management of chronic insomnia in elderly people. Long-term use of sedative- hypnotics for insomnia lacks an evidence base and is discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls.

An extensive review of the medical literature regarding the management of insomnia and the elderly found that there is considerable evidence of the effectiveness and durability of non-drug treatments for insomnia in adults of all ages and that these interventions are underutilized. Compared with the benzodiazepines including quazepam, the nonbenzodiazepine sedative/hypnotics appeared to offer few, if any, significant clinical advantages in efficacy or tolerability in elderly persons. It was found that newer agents with novel mechanisms of action and improved safety profiles, such as the melatonin agonists, hold promise for the management of chronic insomnia in elderly people. Long-term use of sedative/hypnotics for insomnia lacks an evidence base and has traditionally been discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls.

An extensive review of the medical literature regarding the management of insomnia and the elderly found that there is considerable evidence of the effectiveness and durability of non-drug treatments for insomnia in adults of all ages and that these interventions are underutilized. Compared with the benzodiazepines including estazolam, the nonbenzodiazepine sedative-hypnotics appeared to offer few, if any, significant clinical advantages in efficacy or tolerability in elderly persons. It was found that newer agents with novel mechanisms of action and improved safety profiles, such as the melatonin agonists, hold promise for the management of chronic insomnia in elderly people. Long-term use of sedative- hypnotics for insomnia lacks an evidence base and has traditionally been discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls.

A dog with degenerative myelopathy often stands with its legs close together and may not correct an unusual foot position due to a lack of conscious proprioception Canine degenerative myelopathy, also known as chronic degenerative radiculomyelopathy, is an incurable, progressive disease of the canine spinal cord that is similar in many ways to amyotrophic lateral sclerosis (ALS). Onset is typically after the age of 7 years and it is seen most frequently in the German shepherd dog, Pembroke Welsh corgi, and boxer dog, though the disorder is strongly associated with a gene mutation in SOD1 that has been found in 43 breeds as of 2008, including the wire fox terrier, Chesapeake Bay retriever, Rhodesian ridgeback, and Cardigan Welsh corgi. Progressive weakness and incoordination of the rear limbs are often the first signs seen in affected dogs, with progression over time to complete paralysis. Myelin is an insulating sheath around neurons in the spinal cord.