Sensory impairments

Diseases selectively targeting spinal cord and brainstem motor neurons (e.g. amyotrophic lateral sclerosis and the familial spinal muscular atrophies) or the presynaptic component of neuromuscular junctions (e.g. Lambert-Eaton syndrome, botulism and Ixodes tick paralysis) cause weakness without sensory impairment. Disorders involving the enteric nervous system (e.g. Chagas disease and Hirschsprung s disease) impair bowel motility. 

Pain in response to a stimulus despite sensory impairment. 

Severe headaches occurred in an individual exposed to diesel fuel vapor for 10 days (Reidenberg et al. 1964). Anorexia occurred in a man following dermal and/or inhalation exposure to diesel fuel over several weeks (Crisp et al. 1979). Other neurological effects were reported following inhalation of JP-5 vapor in two individuals who had fatigue and coordination and concentration difficulties other effects included headache, apparent intoxication, and anorexia. Effects subsided within 24 hours for one individual and within 4 days for the other (Porter 1990). Sensory impairment did not occur in these individuals. However, experimental data indicate that olfactory fatigue and taste sensation may occur in some individuals after a 15-minute inhalation exposure to 140 mg/m deodorized kerosene vapor (Carpenter et al. 1976). These data suggest that the different types of fuel oils may behave differently under inhalation exposure conditions. The effect of deodorized kerosene may also occur at lower doses, but this cannot be determined from these data. 

Some information is available to identify neurological effects in humans from inhalation exposures. The available data indicate that coordination and concentration difficulties, headache, intoxication, and/or anorexia may be induced by inhalation of JP-5 vapor (Porter 1990), headaches may be induced by diesel fuel vapor (Reidenberg et al. 1964), and sensory impairment may be induced by deodorized kerosene vapor (Carpenter et al. 1976). In animals, a few studies were found that document neurological effects from inhalation of fuel oils. Acute inhalation of diesel fuel no. 2 vapor produced behavioral changes, tremors, ataxia, reduced coordination, and increased sensitivity to heat in mice (Kainz and White 1984). 

Cancer-associated Guillain Barre syndrome is generally infrequent. However, some case reports describe acute onset of paraneoplastic neuropathy with bulbar and respiratory affection quite similar to the common features of Guillain Barre syndrome. There is a male preponderance in cancer-associated Guillain Barre syndrome, sensory impairment is often minor, and the acute mortality is reported to be much higher than in Guillain Barre syndrome patients in general [122]. 

More than 140 cases of toxic polyneuropathy have been reported. The frequency depends on dose, tissue concentration, and renal function in up to 90% of cases polyneuropathy occurred in patients with renal insufficiency (32). Symptoms usually start 9-45 days (at the earliest 3 days) after beginning nitrofurantoin. The neuropathy starts peripherally, predominantly affects the limbs, and remains more severe distaUy. Initially, there is sensory loss with paresthesia. Later, motor loss develops, often with severe muscle atrophy. As a rule, no further deterioration occurs after withdrawal of nitrofurantoin, and there may be total regression (34% of cases) or partial regression (45% of cases) (32). In some severe cases there is residual disability. The motor loss resolves more slowly and less completely than the sensory impairment. Single cases of retrobulbar optic neuritis, lateral rectus muscle palsy, and facial nerve palsy have been reported (33). 

Operant training of an animal allows a very detailed evaluation of sensory function. Such techniques are time-consuming and sometimes expensive, but they are useful for careful characterization of toxicant effects for which there is good evidence of sensory impairment. The species chosen for testing must have sensory function as similar to humans as possible. For visual system testing, for example, the rodent is usually not an appropriate model because its visual system differs in fundamental ways from that of humans. 

Numerous risk factors for nonadherence have been identified. Clearly, nonadherence is a multifactorial problem, and a host of contributing social, economic, medical, and behavioral factors have been identified.As shown in Table 1, some risk factors for nonadherence relate to the disease (e.g., a chronic or asymptomatic illness), others relate to the patient (forgetfulness, sensory impairment, and economic problems), and still others relate to the drug regimen (concerns about cost, real or perceived adverse effects, or dosing schedule). 

Use of thyrotropin-releasing hormone (TRH) as an adjunct to antenatal corticosteroids was thought to further accelerate fetal lung maturation. However, the Australian Collaborative Trial of Antenatal Thyrotropin-Releasing Hormone (ACTOBAT) study failed to show additional benefits from TRH 200 meg every 12 hours. The frequencies of RDS (relative risk [RR] 1.17, 95% Cl 1.00-1.36) and need for ventilation (RR 1.15, 95% Cl 1.01-1.31) were not reduced, and treatment was associated with maternal nausea, vomiting, and light-headedness. Of more concern was the 12-month follow-up report in which TRH treatment was associated with motor delays (OR 1.51, 95% Cl 1.11-2.05), sensory impairment (OR 2.00, 95% Cl 1.06-3.74), social delays (OR 1.41, 95% Cl 1.01-1.95), and severe neurodevelopmental impairment (OR 1.75, 95% Cl 1.07-2.87). At this point, antenatal TRH treatment cannot be advised. 

Dizziness, nystagmus, sensory impairment, seizures Cardiovascular... 

Mercury has also been implicated in the etiology of acrodynia (pink disease) in children when mercury-containing teething powder was used. The methyl mercury contained in fungicides has been responsible for toxicity in children in Iraq. This toxicity is characterized by phalangeal erythema, muscular weakness, ataxia, hyperirritability, sensory impairment, visual disturbances, involuntary movement, and sometimes unconsciousness. 

Hunter and Russell 1954) - subsequently became known as Minamata disease " (see below), and is normally characterized by an extreme latent period of several months, or even years. These conditions start with nonspecific symptoms such as intention tremor, parenthesis, nausea, blurred vision, malaise, sensorial impairments and auditory disturbances, followed by ataxia and massive damage of the CNS. Characteristic is a concentric narrowing of the visual field (Harada 1995). At autopsy, the most conspicuous destructive lesion in the cerebrum was found in the anterior portions of the calcarine cortex. Less severe but similar lesions may be found in the post-central, pre-central and temporal transverse cortices. Secondary degeneration from primary lesions may be seen in cases with long-term survival. In the cerebellum, pathological changes occur deep in the... 

B. After a latency period which may be prolonged (up to several weeks or more), chloracne, porphyria cutanea tarda, hirsutism, or hyperpigmentation may occur. Elevated levels of hepatic transaminases and blood lipids may be found. Polyneuropathies with sensory impairment and lower-extremity motor weakness have been reported. 

By 1982, there were 1800 verified human victims of mercury poisoning in a total regional population of 200,000. Symptoms evidenced by human victims included sensory impairment, constriction of visual fields, hearing loss, ataxia, and speech disturbances. Congenital cases were accompanied by disturbance of physical and mental development about 6.0% of babies bom in Minamata had cerebral palsy (vs. 0.5% elsewhere). Some recovery was evident in 1986 as judged by the finding that mercury concentrations in erythrocytes... 

In this section of the handbook, we focus only on applications of rehabilitation engineering. The concepts of rehabflitation engineering, rehabilitation science, and rehabilitation technology are outHned in Chapter 67. Chapter 69 discusses the importance of personal mobility and various wheeled modes of transportation (wheelchairs, scooters, cars, vans, and public conveyances). Chapter 70 looks at other non-wheeled ways to enhance mobility and physical performance. Chapter 71 covers techniques available to augment sensory impairments or to provide a substitute to input sensory information. Conversely, Chapter 72 looks at the output side. 

The Trace Research and Development Center, Madison, Wise., pubHshes a comprehensive resource book on commercially available assistive devices, organizations, etc. for communication, control, and computer access for individuals with physical and sensory impairments. 

Electronic Devices for Rehabilitation, edited by J.G. Webster [Whey, 1985], summarizes the technologic principles of electronic assistive devices for people with physical and sensory impairments. 

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