It is ingrained in humans to love light and, indeed, since mankind's first wanderings
from the caves, worship of the sun has been a fundamental tenet that many
societies hold even to the present.
The properties of the sun that have inspired such reverence include its light (visible
radiation) and its warmth (infrared radiation). Additional portions of the solar
spectrum that cannot be perceived directly by the senses (ultraviolet) are capable of
evoking both physiologic and pathologic events in the skin.
Sunlight is the ultimate source of energy and is vitally important to life as we know
it. However, absorption of incident solar energy by components of the skin can
cause a variety of pathological sequelae.
Despite the undeniable importance of cutaneous exposure to ultraviolet radiation for
vitamin D homeostasis, there is little evidence to indicate that there are additional
beneficial effects of such exposure. Indeed, overwhelming evidence exists to support the
concept that the skin is damaged in many different ways by its direct exposure to natural
or artificial UVR. Some exposure is virtually unavoidable over a lifetime and is
dramatically dissimilar in different populations depending upon climate, geography,
occupation, and recreational activities. The consequences of this exposure are also
influenced by factors such as the degree of melanin pigmentation. The effects of UVR can
be divided into two general types, acute and chronic. Acute effects include sunburn, and
chronic effects include, among others,
the development of certain forms of skin cancer. In addition, the skin is a major site of
immunologic activity, and UVR is capable of affecting the immune system via its effects on
the skin. The skin is also susceptible to degenerative changes evoked by chronic UVR.
These changes are a major component of the constellation of physical changes perceived as
skin aging but, which in reality, are due to chronic photodamage.
Expanding knowledge about the hazards of exposure to sunlight and UVR has been
accompanied by improved approaches to photoprotection, including the development of more
effective sunscreen formulations. In addition, there is increasing interest in
pharmacologic agents such as the retinoids that may be capable of inhibiting the
development of or possibly even reversing certain chronic effects of cutaneous sun
exposure.
Marked morphologic changes in all parts of the skin, except perhaps the subcutaneous
tissue, are recognized as consequences of exposure to UVR. These changes underlie the
clinically observed sagging, wrinkling, leathery texture, and blotchy discoloration of
skin typically associated with actinic damage. It is unclear how much exposure and how
much time is required to effect these changes, although it is evident that clinically
normal appearing skin can show pathologic signs of sun damage upon histologic and
ultrastructural examination. It is known that individuals with fair complexions are more
susceptible to this damage.
In addition to certain genetic and metabolic disorders that are precipitated by UVR,
there are many photosensitive diseases of unknown cause. These include lupus erythematosus
and polymorphous light eruption, which are elicited by certain wavelengths of the UVR
spectrum. Photosensitivity disorders may also occur due to the interaction of UVR with
many commonly used drugs, as well as chemicals used in industry and consumer products.
There is extensive epidemiological evidence supporting the direct role sunlight plays
in human skin cancer. Basal cell carcinomas (BCC), the most common skin cancers in
Caucasians, are found primarily on sun-exposed areas such as the head and neck where a
dose-response relationship exists. Furthermore, patients with skin cancer generally have
decreased melanin pigmentation and associated photo-protection; people with light
complexion and who sunburn easily have a higher incidence of tumors. There is even
stronger evidence for the role of sunlight in causing SCC's. Although both BCC's and SCC's
are more prevalent in geographic
areas of high sun exposure, there is a much greater increase in SCC with decreasing
latitude and increasing sun exposure. A reasonable correlation exists between sunlight
exposure and melanoma, but the relationship is not as clear as with NMSC. It should be
emphasized that the incidence of NMSC and melanomas has been steadily increasing. Unlike
NMSC, melanomas occur most frequently on the upper back in males and lower extremities in
females. Melanoma incidence does not follow a pattern of increased risk with cumulative
UVR exposure whereas the incidence of NMSC does.
There is evidence that vitamin D synthesis is inhibited by the use of sunscreens. In
the United States, this does not represent a health hazard for the pediatric population
that receives adequate vitamin D supplementation in milk. In other countries this may not
be the case. Deficiencies in elderly populations may exist.
Susceptibility to damage by UVR may be influenced by genetic and acquired disorders,
genetic traits, age-related factors, and the use of some medications.
Genetic abnormalities can increase the susceptibility to UVR damage. These include
disorders manifested in utero that may be lifelong or that may appear shortly after birth.
Among them are disorders of keratinization and pigmentation. Several inherited disorders
in which there is marked susceptibility to UVR in early childhood include xeroderma
pigmentosum, Bloom's syndrome, Rothmund-Thomson syndrome, the porphyrias, phenylketonuria,
dysplastic nevus syndrome, and the basal cell nevus syndrome.
There are also numerous and diverse acquired diseases that manifest increased light
susceptibility. Examples include persistent light reaction, photosensitive epilepsy,
actinic reticuloid, polymorphous light eruption, solar urticaria, hydroa aestivale, hydroa
vacciniforme, actinic prurigo, lupus erythematosus, dermatomyositis, Darier's disease, and
disseminated superficial actinic parakeratosis.
Significant factors that influence susceptibility to UVR damage include race, ethnicity,
eye and hair color, and the tendency toward formation of freckles and nevi. One approach
to categorizing humans in terms of susceptibility to UVR is typing according to history of
sunburning and tanning. Six skin types have been defined. Type I individuals always burn
and never tan; type VI individuals always tan and never burn. The age of an individual may
be correlated with factors that influence the susceptibility to UVR. These may include
age-related structural differences in the skin, behavioral differences (e.g., adolescent
risk taking) and, hypothetically, age-related immunological differences.
Numerous systemic medications may augment UVR susceptibility. Increased UVR damage may
occur with the use of oral antibiotics, antihypertensives, psoralens, immunosuppressive
agents, nonsteroidal anti-inflammatory drugs, and numerous other agents. In addition, a
number of topical medications and industrial chemicals may increase the susceptibility to
damage by sunlight. These include topical psoralens, tretinoin, and other photosensitizing
and depigmenting agents.
Studies show that tanning-bed light can burn both skin and eyes, alter immune system
function, cause skin to age prematurely (photoaging) and produce non-melanoma skin
cancers. Tanning beds also bring about various forms of photosensitivity, including
photo-drug reactions involving many commonly used medications, and polymorphous light
eruptions, commonly known as "sun poisoning." Even short-term indoor tanning may produce
redness, itching and dry skin.
Photosensitive epilepsy is the most common form of stimulus induced epilepsy.
Photosensitivity is sensitivity to radiant energy, light. Light flickering, flashing or
reflecting triggers a seizure. Types of seizures caused by photosensitivity are:
tonic-clonic, absence, complex partial and mixed epilepsy in which several types of
seizures occur at various times. The diagnoses of photosensitive epilepsy (PSE) must be
confirmed by an abnormal EEG induced by intermittent photic stimulation (IPS).
Fast paced screen changes, bright screens, flickering patterns all have been shown to
trigger seizures. Current television commercials and programs use one or a all of these
effects. These effects are also used in movies.
The longer the exposure to these triggers, the greater the chance of inducing a
seizure. Flash rates, brightness and screen change rates, in television and movies, all
contribute to this trigger. In general, flash rates above 5 per second, screen changes
above 3 per second are risky. Changes in contrast & luminance are always risky.
Until the 1970's there were no large drug studies in photosensitive epilepsy. Sodium
Valproate (Valproic Acid) was shown to be effective in treating photosensitivity. Sodium
Valproate should be avoided during pregnancy. A connection between Sodium Valproate and
spina bifida was confirmed in 1984. Consult your doctor!
Suggestions for dealing with photosensitivity are:
watch television in a well lit room
if you are exposed to an unexpected "light" trigger, cover one eye with the palm of your
hand
polarized sun glasses (blue or green) provide some protection outdoors; ordinary sun
glasses are useless
limit exposure to flourescent lighting
Only two drugs have been shown to be effective in treating PSE. Clonazepam is usually
too sedative. Since Sodium Valproate is relatively free from side effects and highly
effective in reducing photosensitivity, some form of this drug should be used. Discuss
this with your neurologist.
