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PubMed1997

Lumbar facet joint tropism does not accelerate degeneration of the facet joints.

PURPOSE: To study the relationship of lumbar facet joint tropism to degeneration of the cartilage and subcortical bone in the facet joints and the effect of tropism in intervertebral disk degeneration. METHODS: The orientation of 104 cadaveric lumbar facet joints with respect to sagittal plane was measured on CT scans, and the joints were classified as having no tropism, mild tropism, or severe tropism. On MR images, the severity of cartilage degeneration and bony sclerosis was measured. The correlation between tropism and degeneration was calculated, as was the relationship among age, spinal level, and degeneration. RESULTS: We identified four spinal levels with severe tropism, six with moderate tropism, and 94 without tropism. Cartilage degeneration was not significantly more severe in the joints with tropism than in the joints without. Sclerosis was slightly greater in the joints with tropism than in the joints without it. Sclerosis and cartilage degeneration were significantly related to age and spinal level. CONCLUSION: Age, spinal level, and overall facet joint angle are more important factors in facet joint degeneration than is tropism.

Adult↗
PubMed1998

Muscle degeneration following remote nerve injury.

Muscle depends upon innervation and contraction to maintain a differentiated state. Denervation can therefore induce muscle atrophy. In grasshoppers, muscle degeneration can also be triggered by the severing of a leg during autotomy. In this case, the muscles that degenerate are neither damaged nor denervated. This phenomenon suggests the existence of transneuronal mechanisms that influence muscle survival. To characterize this autotomy-induced process, we studied the degeneration of a thoracic tergotrochanteral depressor muscle (M#133b,c) subsequent to the shedding of a hindlimb in the grasshoppers Barytettix psolus and Barytettix humphreysii. Both histochemical and electrophysiological methods were used to follow muscle degeneration 1, 3, 5, 10, and 15 days postautotomy. Muscle fibers began to show denervation-like electrophysiological changes (i.e., depolarized resting membrane potentials and postinhibitory rebound) as soon as 3 days postautotomy. By 10 days, significant muscle degeneration was evident and electrophysiological changes were found in all animals tested. Muscle anatomical degeneration was not induced by synaptic transmission failure, because neuromuscular transmission was maintained in most fibers. The rate of muscle degeneration was not constant. Between 1 and 10 days, mean fiber cross-sectional area did not change on the autotomized side, although this is normally a time of muscle growth. However after 10 days, cross-sectional area became drastically reduced and the number of muscle fibers within M#133b,c was decreased. The variability in rate of fiber degeneration was not dependent upon fiber type, since M#133b,c only contains fast-type fibers.

Animals↗
PubMed1981

Wallerian degeneration of the optic nerve in light of histological and biochemical studies.

Wallerian degeneration of the rabbit optic nerve was produced by enucleation. The ultrastructure, enzyme histochemistry, myelin output as well as the lipid composition of degenerated nerve were studied. The obtained results lead to following conclusions: 1. Esterified cholesterol appeared in the lipid spectrum of myelin membranes undergoing Wallerian degeneration preceding a significant drop of myelin mass, without an involvement of lipomacrophages and without notable changes in the structure of myelin. 2. Esterification of cholesterol could function as a primary factor injuring the myelin membrane in central Wallerian degeneration, similarly as in other demyelinating processes. 3. Lipomacrophages occurring in the later stage of Wallerian degeneration of the optic nerve are of astroglial origin. 4. The slow progress of phagocytosis in the degenerating optic nerve might explain the almost unaffected pattern of myelin lipids in the course of Wallerian degeneration of this structure. 5. Lysocompounds play an important role in the pathomechanism of demyelination in the central nervous system including the optic nerve during further steps of myelin decay.

Animals↗
PubMed1989

Perineurial permeability and endoneurial edema during Wallerian degeneration of the frog peripheral nerve.

Perineurial permeabilities to [3H]sucrose and [14C]dextran (MW = 70,000), and water content, conduction velocity (CV) and maximum amplitude (MAP) of the compound action potential, were determined in Wallerian degenerated nerves (sciatic or tibial) of the frog and compared with values in the contralateral uncut nerves. Three days after transection of the lumbosacral plexuses, about 2 cm proximal to the sciatic nerve, mean water content of the sciatic nerve was significantly higher than in the contralateral uncut nerve. After 10 days, the degenerating sciatic nerve showed significant increases in the mean perineurial permeabilities to [3H]sucrose and [14C]dextran when compared to values in the contralateral nerve. Means MAP's and CV's were significantly decreased. At 21 days and after, no compound action potential was detected and perineurial permeability and nerve water content had increased further. Decreases in mean MAP's and CV's and permeability increases of the perineurium were less in degenerating tibial nerves than in degenerating sciatic nerves. It is concluded that following transection, (1) Wallerian degeneration produces an irreversible increase in perineurial permeability, (2) the increase of perineurial permeability follows a proximodistal gradient, and (3) the frog peripheral nerve develops endoneurial edema during Wallerian degeneration as do degenerated nerves of mammals.

Action Potentials↗
PubMed1980

Pattern of myelin breakdown during sciatic nerve Wallerian degeneration: reversal of the order of assembly.

Myelin sheaths of rapidly growing rats were sequentially labeled with the 3H and 14C isotopes of leucine as precursors of protein synthesis. The two injections were separated by time intervals ranging from 2 to 12 d. Wallerian degeneration was initiated by sciatic nerve neurotomy at 2 or 10 d after the second injection of radioactivity. After 5 d of degeneration, myelin was purified and the ratio of isotopes was determined in the delipidated protein. Regardless of the order in which the two isotopes were administered, the relative recovery of radioactivity resultant from the second injection was greatly reduced in degenerating nerves compared with sham-operated controls. Radioactivity incorporated from the first injection was also reduced, but to a lesser extent. Consequently, the isotope ratio corresponding to the first/second injection was greater in degenerating nerves than in controls, and the ratio increased in proportion to the time interval separating the two injections. The magnitude of the effect of degeneration was only slightly greater when degeneration was initiated 2 d after the second injection than when initiated 10 d after the last injection. Consequently, myelin disintegration rather than diminished incorporation of radioactivity accounts for the losses of radioactivity. Furthermore, the pattern of myelin degeneration preferentially involves the last myelin to be formed.

Animals↗
PubMed1997

MR changes in the calcarine area resulting from retinal degeneration.

PURPOSE: To study MR images for atrophic changes in the calcarine area resulting from retinal degeneration. METHODS: MR images from nine patients with retinal degeneration confirmed by ophthalmologic examination and from 30 healthy volunteers were reviewed. The causes of retinal degeneration were hereditary pigmentary degeneration of the retina (four patients), high myopia (two patients), and chorioretinal atrophy (three patients); all patients had visual disturbances and visual field abnormalities. To estimate the morphological changes of the calcarine area, the widths of the right and left calcarine fissures were measured on T1-weighted sagittal images and compared with images from age-matched control subjects. RESULTS: The calcarine fissures were significantly dilated in the patients with retinal degeneration. The anterior and middle points, which represent the peripheral visual field center, were more dilated than the posterior point. CONCLUSION: The MR findings suggested calcarine atrophy related to retinal degeneration. Transneuronal degenerative changes may occur in the calcarine area after retinal degeneration.

Aged↗
PubMed1995

A comparison of driving in older subjects with and without age-related macular degeneration.

OBJECTIVE: To determine the effects of age and central vision loss on driving skills. METHODS: Ten subjects with age-related macular degeneration and average binocular visual acuity of 20/70, and 11 age-similar subjects with normal vision, were examined with a battery of cognitive and visual tests, an interactive driving simulator, and an on-road driving test. Data were collected on the frequency of real-world accidents and convictions for traffic violations. RESULTS: There were no significant differences between the two groups on any of the cognitive tests. The age-related macular degeneration group demonstrated poorer performance on the driving simulator, including delayed braking response times to stop signs, slower speeds, and more of both lane boundary crossings and simulator accidents. The age-related macular degeneration group also demonstrated poorer overall on-road test performance, including having significantly more points deducted for driving too slowly and for not maintaining proper lane position. However, these effects on the simulator and the on-road test did not translate into an increased risk of real-world accidents for the age-related macular degeneration group. Significantly more control subjects than patients with age-related macular degeneration were involved in self-reported accidents, and significantly more control subjects had state convictions for traffic violations. There was evidence of compensation in the age-related macular degeneration group in four major areas: (1) not driving in unfamiliar areas; (2) traveling at slow speeds; (3) self-restricting their nighttime driving, and (4) taking fewer risks while driving (eg, not changing lanes). There was also evidence of compensation in the older control group. CONCLUSIONS: Vision, simulator, and on-road test variables combined with subjective risk taking predicted self-reported real-world accidents in a logistic regression analysis. However, risk taking, rather than simulator or road-test performance, was the most significant predictor for both patients with age-related macular degeneration and the control group.

Accidents, Traffic↗
PubMed1998

Long-term degeneration in the cochlear nerve and cochlear nucleus of the adult chinchilla following acoustic overstimulation.

Adult chinchillas were exposed once to an octave-band noise, centered at 4 kHz, and allowed to survive for 16 days or for 1, 2, 4, and 8 months. Axonal degeneration was mapped in the cochlear nucleus, using the Nauta-Rasmussen silver method, and related to hair cell damage and to loss of myelinated nerve fibers in the osseous spiral lamina of the cochlea. Axonal degeneration in the dorsal cochlear nucleus had already reached a peak by 16 days and disappeared after 1 month. Meanwhile, myelinated nerve fiber degeneration in the cochlea extended basally, followed 2 weeks to 2 months later by spread of axonal degeneration into the corresponding high-frequency region of the ventral cochlear nucleus. Axonal degeneration occurred early in the low-frequency region of the ventral cochlear nucleus, followed 2-4 weeks later by spread of myelinated fiber degeneration into more apical regions of the cochlea. New degeneration of axons in the cochlear nerve and in the ventral cochlear nucleus continued to occur for up to 8 months after stimulation. These findings imply that plastic changes in the central auditory pathways could play a role in the long-term effects of cochlear damage and acoustic overstimulation, possibly leading to a chronic neurodegenerative condition in the ear and in the brain.

Acoustic Stimulation↗
PubMed2002

Medial forebrain bundle axotomy during development induces apoptosis in dopamine neurons of the substantia nigra and activation of caspases in their degenerating axons.

There is growing evidence that programmed cell death may play a role in degenerative neurologic disease. The caspases are a family of cell death proteins that mediate proteolytic cascades in the death process. Although there is clear evidence that caspases play a role in the destruction of the components of the neuronal soma, it has been controversial whether they play a role in the degeneration of axons that accompanies the death of the cell body. It is important to define the molecular mechanisms of axonal degeneration, because terminal degeneration may occur early in neurodegenerative disease. We have therefore investigated whether caspases play a role in axonal degeneration in the dopaminergic nigrostriatal system following axotomy of the median forebrain bundle during development. We find that this lesion induces apoptosis in midbrain dopaminergic neurons at the level of the cell soma. Concomitantly with this induction of apoptosis, degeneration of dopaminergic axons occurs and is characterized by the formation of axonal swellings and spheroids. Immunohistochemical analysis reveals that the activated form of caspase-3 and a caspase cleavage product of beta-actin are abundantly expressed in these degenerating fibers. We conclude that caspases are activated in degenerating dopaminergic axons as the somata undergo programmed cell death in this model. These results raise the possibility that caspase activation may occur in other programmed cell death contexts for these neurons, and, if this is so, then their inhibition may be a useful therapeutic target.

Animals↗
PubMed1988

Capsaicin-induced neuronal degeneration: silver impregnation of cell bodies, axons, and terminals in the central nervous system of the adult rat.

Capsaicin is a neurotoxic substance valued in neurobiological research because of its ability to selectively damage small unmyelinated primary sensory neurons. Previous work has indicated that systemic capsaicin administration causes permanent neuronal degeneration in neonatal rats, but evidence that capsaicin has a similar effect in adults is equivocal and incomplete. Therefore, we used silver impregnation, a method that labels degenerating neurons, to examine the central nervous system of adult rats after systemic capsaicin treatment. Adult rats were injected with a single intraperitoneal dose of capsaicin (50 or 90 mg/kg) or vehicle solution and killed 6, 12, 18, 24, 48, 96, or 240 hours later. Sections of brain and spinal cord were stained with the Carlsen-de Olmos cupric silver method. As reported previously, stained sections revealed degeneration in areas known to be innervated by small-diameter primary sensory fibers: the substantia gelatinosa of the spinal cord dorsal horn and spinal trigeminal nucleus, the solitary nucleus and tract, and the lateral borders of the area postrema. In addition, axon and terminal degeneration was observed in several discrete forebrain and hindbrain areas not previously associated with capsaicin-induced degeneration in either adult or neonatal rats: the inferior olive, the olivary pretectal nucleus, the interpeduncular nucleus, the suprachiasmatic nucleus, and the lateral septum/medial accumbens region. Furthermore, degenerating cell bodies were observed in the intrafascicular nucleus of the ventromedial midbrain tegmentum, in the supramammillary nucleus, and in the posterior hypothalamic area. Unilateral nodose ganglionectomy produced terminal staining on the denervated side very similar to that induced bilaterally by capsaicin. In addition, unilateral nodose ganglionectomy 1 month prior to capsaicin injection greatly attenuated staining in the ipsilateral nucleus of the solitary tract, confirming the hypothesis that capsaicin damages vagal sensory neurons innervating this nucleus. Capsaicin-induced damage in adult rats was long-lasting, since the second of two capsaicin treatments spaced 4.5 months apart produced no additional degeneration.

Animals↗
PubMed1992

Age-related changes in capsaicin-induced degeneration in rat brain.

Previous results indicate that the pattern of capsaicin-induced degeneration in the rat central nervous system is age-related. Experiments utilizing capsaicin's selective neurodegenerative effects to study the function of central neural circuits will therefore require a detailed understanding of capsaicin's central neurotoxicity in rats of different ages. The goal of this experiment was to characterize the degeneration induced in the rat brain by systemic treatment with capsaicin at different ages (10, 15, 20, 25, 30 or 75 days, or 11 months), using a cupric silver stain to label degenerating neurons. Results revealed degenerating cell bodies in the ventromedial brainstem in capsaicin-treated rats of all age groups, though they were more numerous in adult rats than in pups. In addition, many areas contained capsaicin-induced nerve terminal degeneration both in rat pups and in adult rats. These areas were the substantia gelatinosa of the spinal cord dorsal horn; the solitary tract; the nucleus of the solitary tract, visceral portion; the area postrema; the trigeminal nerve and spinal trigeminal nucleus; the medial nucleus of the inferior olive; the rostral, dorsomedial and dorsolateral interpeduncular subnuclei and overlying interfascicular nucleus; the supramammillary area; the lateral septal nucleus; the bed nucleus of the stria terminalis, anterior medial portion; the optic nerve and tract; the suprachiasmatic nucleus, ventroposterolateral portion; the magnocellular subnucleus of the ventrolateral geniculate nucleus; the intergeniculate leaf; the medial pretectal nucleus and the olivary pretectal nucleus. In several, but not all of these areas, the apparent density of degenerating terminals was significantly less in adult rats than in pups. In other brain sites, capsaicin-induced degeneration was observed only in rats younger than 30 days of age. These areas were the lateral habenula, medial part; the sphenoid nucleus; and the stria medullaris. Still other brain sites lost their sensitivity to capsaicin sometime between 30 and 75 days of age. These areas were the bed nucleus of the stria terminalis, medial posteromedial part; the medial preoptic nucleus, central part; the septohypothalamic nucleus; the ventral reuniens area; and the ventromedial hypothalamic nucleus. Adult rats 75 days and 11 months of age did not differ detectably in their response to capsaicin. Thus, loss or attenuation of capsaicin sensitivity is not progressive throughout life. It does not occur in all capsaicin-sensitive sites. Where it does occur, loss of sensitivity occurs prior to adulthood and follows a distinct and reproducible time course that may differ for different sites.

Aging↗
PubMed1992

Degeneration of photoreceptors in rhodopsin mutants of Drosophila.

Five different, well-characterized mutants of the R1-6 rhodopsin gene (ninaE), which corresponds to the rod opsin gene of vertebrates, have been examined morphologically as a function of age (up to 9 weeks) to determine whether or not the photoreceptors degenerate and to assess the pattern of degeneration. Structural deterioration of R1-6 photoreceptors with age has been found in all five mutants. The structural pattern of degeneration is similar in the five mutants, but the time course of degeneration is allele dependent and varies greatly among the five, with the strongest alleles causing the fastest degeneration. The degeneration appears to be independent of either the illumination cycle to which the animals are exposed or the presence of screening pigments in the eye. Although the degeneration first appears in R1-6 photoreceptors, eventually R7/8 photoreceptors, which correspond to cones of vertebrates, are also affected. In many of these mutants, striking proliferations of membrane processes have been observed in the subrhabdomeric region of R1-6 photoreceptors. It is hypothesized that (1) this accumulation of membranes may be caused by the failure of newly synthesized membranes that are inserted into the base of microvilli to be assembled into R1-6 rhabdomeres and (2) this failure may be caused by the extremely low concentration of normal R1-6 rhodopsin in the ninaE mutants.

Aging↗
PubMed1993

Septal efferent axon terminals identified by anterograde degeneration show multiple sites for modulation of neuropeptide Y-containing neurons in the rat dentate gyrus.

The ultrastructure and cellular associations of septal efferent terminals identified by anterograde degeneration with neurons containing neuropeptide Y (NPY) in the rat dentate gyrus were examined quantitatively. For this, the septal complex (i.e., medial septal and diagonal band nuclei) of adult male rats was injected with the neurotoxin ibotenic acid (1%; 150 nl) and following a 2-4-day survival period, the hippocampal formation was processed for the electron microscopic immunocytochemical demonstration of NPY using the avidin-biotin complex method. Terminals with the morphological characteristics of anterograde degeneration, in particular an increase in osmiophilia, and neurons containing NPY-like immunoreactivity (NPY-LI) were most abundant in the hilus of the dentate gyrus. In this region, degenerating terminals (n = 109) were usually small (0.2-0.4 microns in diameter) and formed both asymmetric and symmetric synapses with small (distal) dendrites. The degenerating terminals contacted either single NPY-containing (19%) perikarya or dendrites or unlabeled (48%) perikarya or dendrites. Some degenerating terminals contacted the same perikarya or dendrites as an NPY-containing terminal (11%); these neurons were either immunoreactive for NPY or unlabeled. The remaining degenerating terminals were either directly apposed without glial intervention to unlabeled and NPY-labeled terminals (11%) or lacked associations with any neuronal processes in the plane of section analyzed (11%). The findings demonstrate that ibotenic acid injections in the septal complex can identify septal efferent terminals by degeneration and provide cellular substrates for the direct synaptic regulation as well as presynaptic modulation of hippocampal NPY-containing neurons by septal efferent terminals.

Animals↗
PubMed1993

Stage-specific binding of peanut agglutinin to aggregates of degenerating photoreceptor cells in the rd mouse retina.

Peanut agglutinin, a lectin with high binding affinity for galactose-galactosamine disaccharide, was used to monitor changes in the photoreceptor cell layer of mice with inherited retinal degeneration. Mice homozygous for the retinal degeneration (rd) gene exhibit a rapid loss of rod photoreceptor cells in the first postnatal month. Previous studies have shown that aggregates of peanut agglutinin-binding cells are observed in the outer nuclear layer in the retinal degenerative mouse at between postnatal days 10 and 18, a period during which massive photoreceptor degeneration occurs in this mutant. This study was performed to determine whether these peanut agglutinin-positive cell clusters represent degenerating photoreceptor cells or, alternatively, macrophages that have migrated into the photoreceptor cell layer. Electron microscopic cytochemistry, using horseradish-peroxidase-conjugated peanut agglutinin, was used to trace cellular processes of peanut-agglutinin-stained cell clusters. Additionally, macrophage-specific antibodies were employed to determine whether macrophages were present in the clusters. The cell clusters did not react with macrophage-specific antibodies. However, processes of cells in peanut-agglutinin-bound clusters could be traced by electron microscopic serial sections to both the outer limiting membrane and the outer synaptic layer. These results provide strong evidence that peanut-agglutinin-bound cells seen during this stage of degeneration in the rd mouse are degenerating photoreceptor cells. Since peanut agglutinin has been shown to bind preferentially to cone, but not to rod, photoreceptor cells, the results also suggest that the clusters may be aggregates of degenerating cones.

Animals↗
PubMed1979

Types of degenerating geniculocortical axon terminals and their contribution to layer IV of area 17 in the squirrel monkey (Saimiri).

Radiofrequency lesions were made in the lateral geniculate nuclei of six squirrel monkeys. The resulting degenerating terminals and their postsynaptic structures in layer IV of area 17 were quantitatively categorized on photomontages covering large areas of neuropil. Two to five days after the lesion, numerous axon terminals were affected by a variety of degenerative changes, i.e., enlargement and distortion of synaptic vesicles, neurofilamentous hyperplasia, electron-lucent and electron-dense reactions. Based on the aggregation of electron-dense material beneath the postsynaptic membrane, the degenerating terminals were considered to be of the asymmetric type. Among the degenerating boutons were the largest axon endings that occur in layer IV. Three days postoperatively, degenerating boutons contributed an average of 16.2% to the total synapse population; five days postoperatively, the average had increased to 19.3%. The percentage of degenerating boutons on individual montages, however, amounted to as much as 29%. This amount probably reflects more closely the actual contribution of the geniculocortical fiber system to layer IV of striate cortex. The postsynaptic structure most frequently contacted by degenerating axon endings was the dendritic spine, followed by dendrites of small diameter. To account for the diversity of degenerative changes in the same fiber system, we offer the tentative suggestion that heterogeneously degenerating axon terminals arise from a heterogeneous population of neurons in the lateral geniculate nucleus, i.e., from magnocellular versus parvocellular laminae.

Animals↗
PubMed1995

Mechanisms of macrophage recruitment in Wallerian degeneration.

Monocytes/macrophages are important effector cells in myelin removal during Wallerian degeneration. Experiments with the mouse mutant C57BL/Ola revealed prolonged axonal survival and reduced phagocytic cell recruitment after nerve transsection. In the present study, we compared the course of Wallerian degeneration in peripheral nerves of C57BL and C57BL/Ola mice in vivo and in vitro. In vivo experiments confirmed earlier investigations describing a delayed degeneration in the C57BL/Ola mutant compared with C57BL mice which were used as control animals without abnormal degeneration. Quite different results were seen in experiments in vitro: degenerating nerve segments of C57BL/Ola mice revealed pronounced axonal breakdown even in the absence of non-resident phagocytic cells. There was no difference in vitro compared with degenerating nerves from C57BL mice. The differences observed between the in vivo and in vitro situations suggest that axonal breakdown plays an important role in the initiation of macrophage recruitment to degenerating peripheral nerves.

Animals↗
PubMed1975

Spongy degeneration in the central nervous system of domestic animals. Part III: Occurrence and pathogenesis hepatocerebral disease caused by hyperammonaemia.

Severe spongy degeneration of the central nervous system (CNS) was seen in 11 cattle, 19 sheep, 4 pigs and 1 goat, associated with a variety of hepatic diseases, particularly those caused by hepatotoxic pyrrolizidine alkaloids. It was also seen in a milder form in 2 of 8 horses examined, 1 dog of 5 dogs examined, and in 1 rabbit only of a large number of laboratory animals examined. This paper reports results of experiments which confirmed initially that the CNS disease cold be caused by pyrrolizidine alkaloid intoxication. This was done by poisoning lambs with lasiocarpine. As the disease was seen in hepatoses not caused by pyrrolizidine alkaloids, the hypothesis that CNS spongy degeneration in lambs could follow any hepatic disease irrespective of its cause, was tested by poisoning lambs with allyl formate, an hepatotoxin chemically unrelated to pyrrolizidine alkaloids. Three of 4 lambs poisoned by the allyl formate showed spongy degeneration in their brains. As the CNS spongy degeneration was an apparent form of hepatocerebral disease, an experiment was conducted to show that the neural disease in sheep was caused by hyperammonaemia. CNS spongy degeneration developed in the brains of all sheep infused intravenously with ammonium acetate, and advanced spongy changes developed in the sheep infused for more than 3 days. The cerebral changes were probably temporary, since sheep infused for 5 days and retained for 3 weeks showed marked regression of vacuolation. Hyperammonaemia caused by intravenous ammonium acetate infusion is a simple, rapid model of CNS spongy degeneration. The syndrome, CNS spongy degeneration caused by hepatic failure and hyperammonaemia, is probably one of the morphologic expressions of hepatocerebral disease in domestic animals and could be an analogue of similar congenital and hepatocerebral diseases in man.

Acetates↗
PubMed1984

Senile reticular pigmentary degeneration.

Of 104 consecutive patients with senile reticular pigmentary degeneration (207 eyes), 85 patients (82%) were more than 60 years old (mean age, 69.2 +/- 8.54 years). Forty-nine (47%) were men and 55 (53%) were women. Peripheral visual fields were not characteristically constricted. Although most eyes tested had visual acuities of 20/50 or better, 69 eyes (33%) had visual acuities of 20/100 or worse. A total of 136 eyes (66%) had senile macular degeneration at the time senile reticular pigmentary degeneration was first diagnosed, whereas only 43 control eyes (21%) from the same referral population also had senile macular degeneration (P less than .001). Macular degeneration was the primary cause for reduced vision when it was noted. In no instance could reduced visual acuity or constricted visual fields be attributed to the senile reticular pigmentary degeneration alone. Senile reticular pigmentary degeneration on routine ophthalmoscopy should alert the clinician to the possibility of co-existing macular degenerative disease.

Aged↗