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Argon laser trabeculoplasty (ALT) has been increasingly used instead of surgery for treating open-angle glaucoma that is unresponsive to drugs. The treatment consists of tiny laser burns evenly spaced around the trabecular meshwork; it can also be used as a preventive measure, while pharmacological treatment continues.

ALT is being increasingly replaced by diode laser with continuous wave, and in recent years by "Q-Switched Nd:YAG laser," second harmonic 532 nm (106). This laser allows for selective photoablation of pigmented cells in trabeculum without a thermal effect. These new lasers enable safer, quicker, more effective antiglaucoma operations, increase efficacy of laser surgery, and allow for bypassing hospitalization, with less treatment cost.

peripheral auditory components, the central neural aspects, or both. Here, too, more is known about the aging of the ear than the central auditory system (Table 3).

■ Age-Related Hearing Loss (Presbycusis)

Age-related hearing loss (ARHL) is called presbycusis. Numerous studies have reported loss of hearing with age, particularly for sounds in the high-frequency range (28,122,123). Presbycusis occurs in both ears but not necessarily at the same time. To assess auditory loss with age, pure-tone audiograms of subjects in different age groups are determined. That is, the hearing threshold in decibels (dB) (unit of sound intensity) for sounds of increasing frequency is determined, and the results are presented as relative loss of decibels at different frequencies.

Progressive Hearing Loss with Aging in the High-Frequency Range

In the low-frequency range (0.125-1 kHz), young subjects have essentially no hearing deficits, while old subjects show deficits of about 10 to 15 dB. In the high-frequency range, hearing loss for the young group is mild, while in the old group, it becomes progressively worse with increasing sound frequency (Fig. 7) (28,123). Typical magnitudes of hearing loss are 30 dB at 2 kHz, increasing by about 10 dB for each additional kHz. In octogenarian men living in urban areas, the hearing loss may be as much as 80 dB. Another way of determining ARHL is by measuring the maximum frequency of sound capable of being heard. This frequency is 20 kHz for children (10 years), which decreases to only 4 kHz for the elderly (80 years); the decline is steady and linear, occurring at the rate of about 2.3 kHz per decade (Fig. 7).

Pure-Tone Audiograms and Effects of Age, Sex, and Environment

Typical pure-tone audiograms for normal men and women at different age groups are shown in Figure 7. Hearing loss is higher in men than women; this sex difference, which begins after the age of 35 years, possibly reflects the effects of higher exposure of men to work-related and environmental noise.

BOX 3 Risk Factors for and Treatment of Aging-Related Macular Degeneration

The higher incidence of age-related macular degeneration (ARMD) in monozygotic, compared to dizygotic, twins suggests the importance of genetic factors (114). Alcohol consumption does not increase the risk of ARMD (115), but cigarette smoking poses a significant risk (116). Treatment of macular degeneration is not nearly as successful as that of cataract and glaucoma (108). Although a protective role for antioxidants and trace minerals against ARMD development is widely believed, the use of antioxidants for ARMD treatment remains controversial (117).

Laser therapy in ARMD. The only realistic goal of treatment for ARMD is to prevent subretinal detachment and hemorrhage, disorders that lead to an acute loss of vision. To accomplish this, the sites of subretinal neovascular formation are located using fluorescin angiography followed by laser photocoagulation. According to Ciulla et al. (118), laser photocoagulation of choroidal neovascular membranes (CNVMs) is currently the only well-studied and widely accepted treatment. New treatments may be divided into four major categories: (i) photodynamic therapy, (ii) pharmacologic inhibition of CNVM formation with antiangiogenic agents, (iii) surgical intervention, and (iv) radiation therapy.

Rosen et al. (125) have also shown that the elderly people from noise-free rural areas of Sudan show lesser hearing loss compared to those in the urban environment, suggesting that urban environmental noise is one of the determinants of presbycusis [see, however, an Italian population study by Megighian et al. (126) discussed below]. In a recent study, Lee et al. (127) found an average increase of 1 dB per year for subjects 60 years and over. Male and female subjects showed faster rates of change at different specific frequencies than younger, gender-matched controls. Also, older males and females showed increased rates of change in pure-tone threshold at different frequencies (males had a faster rate of change at 1 kHz, and a slower rate of change at 6 and 12 kHz, compared to age-matched females). Noise history did not play a role in these parameters.

Atherosclerosis and Role of Blood Lipids in Presbycusis

Another cause of presbycusis may be vascular, such as atherosclerosis and similar disorders related to elevated blood lipids (hyperlipoproteinemia) (Chapter 16). Incidence of hearing loss and inner-ear diseases may be high in patients with elevated cholesterol levels (128). With regard to the role of lipids in presbycusis, recent animal studies suggest that statin drugs that are commonly used to treat coronary artery disease and hypercholesterolemia may slow down presbycusis in humans, possibly by reducing vascular endothelial inflammation. In a mouse strain with accelerated aging (C57BL/6J mice), which is a model for presbycusis in humans, Syka et al. (129) found that atorvastatin (a statin drug) slows down the deterioration of inner-ear function with age. It was found that more outer hair cells survived in mice treated over a two-month period with atorvastatin versus control mice of the same strain, as measured by distortion-product otoacoustic emissions (DPOAE) amplitude (greater in treated mice).

Presbycusis Related to Ear Structure

The major structures of the ear include the following: (i) The external ear (pinna, external auditory canal, and tympanic membrane); (ii) the middle ear (the ossicular chain); and (iii) the

BOX 4 Visual Dysfunctions in Alzheimer's Disease

The Alzheimer's disease (AD) patients perform significantly worse than subjects without AD on tests measuring static spatial contrast sensitivity, visual attention, shape-form-motion, color, visuospatial construction, and visual memory (119-122). Correlation analyses showed strong relationships between visual and cognitive scores. Thus, effects of AD on multiple visual neural pathways and regions are compatible with the hypothesis that visual dysfunction in AD may contribute to performance decrements in other cognitive domains.

A better understanding of vision-related deficits can lead to better diagnosis and interventions that may, in turn, help improve functional capacity in patients with dementia and AD. Decreased attention may severely limit cognitive performance in the elderly. Deficits in sustained, divided, and selective attention, and in visual processing speed, occur early in AD, and can be significantly correlated with diminished overall cognitive function (120). These findings indicate that assessment of visual attentional ability may prove useful for AD diagnosis and lead to more precise measures of useful perception in AD patients with normal visual fields and acuity.

In mild to moderate cases of AD, a significant effect on perception of structure from motion occurs with relative sparing of motion direction discrimination. This problem is likely to have a cerebral basis and can potentially affect navigation and the recognition of objects in relative motion, as encountered during walking or automobile driving (119,120).

Certain atypical AD patients show characteristic visual abnormalities. Visual association pathways are usually not as disrupted in the more common form of AD (121). These visual symptoms were the most identifiable signs of this particular form of AD. In these patients, visual association areas in the occipito-temporo-parietal junction and posterior cingulate cortex as well as primary visual cortical areas demonstrated high concentrations of lesions, while the prefrontal cortical regions had fewer lesions than found typically in AD patients (121).

TABLE 3 Summary of the Normal Aging Changes in the Human Ear

Structural changes

Hair cell degeneration Basal cochlea

Apical cochlea Nerve cell degeneration Observed in spiral ganglia often with basal cochlear hair cell loss but not with apical cases (involved in neural presbycusis); is accompanied by loss of myelinated auditory nerve fibers Atrophic changes Generally occur in nonneural components (vascular and connective tissue) of cochlea and lead to strial or conductive types of presbycusis In stria vascularis

In spiral ligaments

In Reissner's membrane

Central neural changes

Little neuronal loss in lower auditory centers; heavy loss in conical auditory centers; dendritic degeneration of cortical pyramidal neurons Increased latency and decreased amplitude of auditory-evoked potentials; effects more marked in elderly males than in females Functional changes Pure-tone hearing

Speech perception

Sound localization

Frequent, especially in the first quadrant; diffuse and patchy; main cause of sensory presbycusis Infrequent

Frequent in the middle and apical turns of cochlea Accompanied with devascularization in inner and outer spiral vessels Due to vacuolization in basilar membrane, leading to mechanical damage

Loss of hearing in the high-frequency range (presbycusis): loss progressively worsens with age; effects more pronounced in males; noise exposure enhances loss Decline in maximum sound frequency capable of being heard, from 20 kHz at 10 yrs to 4 kHz at 80 yrs Diminished ability to hear consonants; speech is heard but unintelligible Diminished ability to localize sound source, particularly at high frequencies inner ear (cochlea and the organ of Corti). The organ of Corti contains the hair cells that are the auditory receptors and the mechanoelectrical transducing organs (Fig. 8A). The cell bodies of the primary auditory neurons are in the cochlea's spiral ganglia, and the axons comprising the auditory nerve enter the medulla to synapse with central auditory neurons.

Auditory pathways in the brain include the medullary and midbrain centers for signal transmission and auditory reflexes, the inferior colliculi, and the auditory cortex in the temporal lobe of the cerebral cortex. The selective nature of presbycusis indicates that it is probably not associated with aging changes in the outer or middle ear (tympanic membrane and ossicles) but is more likely due to changes in the inner ear (cochlea) or the central auditory system (122,123,130).

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