Paresis

Anhalonine produces increased reflex excitability in the frog after a phase of paresis (Heffter, 1898). The symptoms in the rabbit are analogous, but the transitory paresis is less marked. The lethal dose of the hydrochloride for rabbits is 0-16-0-2 gm. per kilo, body weight. 

Anhalonidine is not so active and resembles pellotine in action. In frogs it produces a type of narcosis or paresis, followed by a phase of increased excitability. Larger doses have a curare action. On mammals the action is slight. 

Lophophorine is the most toxic of the group. No preliminary paresis is observed in either the frog or rabbit 15-20 mg. per kilo, body weight is fatal in rabbits. 

Amylin analogue Gastro paresis Hypoglycaemia, nausea b... 

Seizure with postictal Todd s paresis Migraine with aura H3 poglycemia or h3fperglycemia H3fponatremia... 

With regard to neurosyphilis, a reduction in neurologic manifestations is desired, which may include seizures, paresis, hyperreflexia, visual disturbances, hearing loss, neuropathy, or... 

College of Veterinary Medicine. "Enterovirus Encephalomyelitis Teschen Disease, Talfan Disease, Poliomyelitis Suum, Benign Enzootic Paresis." Iowa State University, August 5, 2005. 

No effect on growth or survival Lower bone density in females at day 60 Tremors and paresis beginning at day 14 71% dead by day 60. Survivors weighed less at day 28 than did birds fed other diets. Lower bone density evident at day 30. Livers and kidneys of survivors had <1.0 mg Ni/kg FW dead birds had as much as 22.7 mg Ni/kg FW liver and 74.4 mg Ni/kg FW kidney... 

Tertiary Cardiovascular syphilis (aortitis or aortic insufficiency), neurosyphilis (meningitis, general paresis, dementia, tabes dorsalis, eighth cranial nerve deafness, blindness), gummatous lesions involving any organ or tissue... 

A pressure sore is also called a decubitus ulcer and bed sore. A classification system for pressure sores is presented in Table 47-5. Many factors are thought to predispose patients to the formation of pressure ulcers paralysis, paresis, immobilization, malnutrition, anemia, infection, and advanced age. Four factors thought to be most critical to their formation are pressure, shearing forces, friction, and moisture however, there is still debate as to the exact pathophysiology of pressure sore formation. The areas of highest pressure are generated over the bony prominences. 

Impairment in visual accommodation results from paresis of ciliary muscles. Photophobia may also result. If severe, pilocarpine ophthalmic solution may be necessary. 

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. 

A number of OPC are capable of rendering a delayed neurotoxic effect (DNE). This effect becomes apparent gradually, after a certain latent period (usually 14 to 21 days, sometimes 1 to 5 years after the acute poisoning survived) and is characterized clinically by the development of ataxia, muscular weakness, paresis and paralysis of the extremities. Morphologically, it is characterized by fiber demyelinization of spinal pathways and peripheral nerves. Till present time, near 40,000 cases have been described, when paresis and paralysis developed in human beings as a result of their exposure to OPC (TOCP, mipaphox, chloropyrophos, trichlorfon, etc.) [1],... 

The usage of specific therapeutic means (quaternary ChE reactivators, cholinolytics) with this purpose prevents only the development of cholinergic symptoms of intoxication, but does not exert influence on the development of paresis and paralysis in the remote period. 

Ingestion of hallucinogenic plant alkaloids and allied compounds does not always result in death. Many grazing animals display paresis, ataxia, dullness, and a tendency to isolate themselves from the herd. Some animals appear to act bizarre. Observations of such animal-plant interactions could have provided man with much information about hallucinogens. 

Exposure of humans to dichloroacetylene in a variety of settings has caused headache, dizziness, nausea, vomiting, eye irritation, mucous membrane irritation, and neurological disorders, manifested as paresis and neuralgia in several cranial and cervical nerves. " In some cases the cranial nerve involvement persisted for several days to years. Extreme nausea occurred among individuals exposed to levels as low as 0.5-1.0ppm. In an early report two deaths occurred several days after dichloroacetylene exposure autopsy revealed cerebral edema. 

Repeated exposure of rats to 650 ppm 6 hours/day, 5 days/week for 14 weeks caused hypoactivity, incoordination, ataxia, paresis, and slowed righting reflexes death occurred in all females and 10 of 30 males between the... 

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