Thursday, August 03, 2017

Folliculitis

Folliculitis is a group of skin conditions where there are inflamed hair follicles. The result is a tender red spot, often with a surface pustule.

Folliculitis may be superficial or deep.

It can affect anywhere there are hairs, including chest, back, buttocks, arms and legs.

Acne and its variants are also types of folliculitis.

can be due to infection, occlusion (blockage) or irritation

Staphylococcus aureus.and Pseudomonas aeruginosa are two of the most common organisms causing bacterial folliculitis

Pityrosporum ovale, also known as Malassezia. Malassezia folliculitis (Pityrosporum folliculitis) is an itchy acne-like condition usually affecting the upper trunk of young adults.

Candida albicans can also provoke a folliculitis in skin folds (intertrigo) or in the beard area.

both of these could be secondary to antibiotic use.Stop antibiotics and use an anti fungal cream.

Tinea capitis,Microsporum canis and Trichophyton tonsurans are some common fungi causing folliculitis requiring oral anti fungal Rx for a few months.

Herpes simplex ,Herpes zoster and Molluscum contagiosum are the common viral causes.

Colonization by hair follicle mites (demodex) known as demodicosis.is seen in immuno suppressed patients.

Infestation by scabies, often leads to folliculitis, as well as non-follicular papules, vesicles and pustules.

Folliculitis may be caused by hairs regrow after shaving, waxing, electrolysis or plucking. these pustules are sterile.Irritant folliculitis In the beard area is known as pseudofolliculitis barbae. Irritant folliculitis is also common on the lower legs of women (shaving rash). It is frequently very itchy. Treatment is by stopping hair removal, and not beginning again for about three months after the folliculitis has settled. To prevent reoccurring irritant folliculitis, use a gentle hair removal method, such as a lady's electric razor. Avoid soap and apply plenty of shaving gel, if using a blade shaver.

Occlusion/ Paraffin-based ointments, moisturizers, and adhesive plasters may all result in a sterile folliculitis. If a moisturiser is needed, choose an oil-free product, as it is less likely to cause occlusion.

Chemicals/ cutting oils,Coal tar and other chemicals may cause an irritant folliculitis. Avoid contact with the causative product.

Topical steroids/Overuse of topical steroids may produce a folliculitis. Perioral dermatitis is a facial folliculitis provoked by moisturizers and topical steroids. Perioral dermatitis is treated with tetracycline antibiotics for six weeks or so.

Folliculitis due to immunosuppression

Eosinophilic folliculitis is a specific type of folliculitis that may arise in some immune suppressed individuals

Folliculitis due to drugs

Folliculitis may be due to drugs, particularly corticosteroids (steroid acne), androgens (male hormones), ACTH, lithium, isoniazid (INH), phenytoin and B-complex vitamins. Protein kinase inhibitors (epidermal growth factor receptor inhibitors) and targeted therapy for metastatic melanoma (vemurafenib, dabrafenib) nearly always result in folliculitis.

Folliculitis due to inflammatory skin diseases

Certain uncommon inflammatory skin diseases may cause permanent hair loss and scarring because of deep seated sterile folliculitis. These include:

Lichen planus/Discoid lupus erythematosus/Folliculitis decalvans/Folliculitis keloidalis

Treatment depends on the underlying condition and its severity. A skin biopsy is often necessary to establish the diagnosis.

Acne variants

Acne and acne-like or acneform disorders are also forms of folliculitis. These include:

Acne vulgaris/ Nodulocystic acne/ Rosacea/ Scalp folliculitis/ Chloracne

Follicular occlusion syndrome refers to:

Hidradenitis suppurativa (acne inversa)

Acne conglobata (a severe form of nodulocystic acne)

Dissecting cellulitis (perifolliculitis capitis abscedens et suffodiens)

Pilonidal sinus.

Buttock folliculitis

Folliculitis affecting the buttocks is quite common and is often nonspecific, ie no specific cause is found. Buttock folliculitis is equally common in males and females.Acute buttock folliculitis is usually bacterial in origin (like boils), resulting in red painful papules and pustules. It clears with antibiotics.

Chronic buttock folliculitis does not often cause significant symptoms but it can be very persistent. Although antiseptics, topical acne treatments, peeling agents such as alphahydroxy acids, long courses of oral antibiotics and isotretinoin can help buttock folliculitis, they are not always effective. Hair removal might be worth trying if the affected area is hairy. As regrowth of hair can make it worse, permanent hair reduction by laser or intense pulsed light (IPL) is best.

Secondary Syphilis

Patient is very infectious during this stage.

If left untreated or treatment has failed, about 3 weeks to 3 months after the 1st stage, a widespread skin rash occurs.

Rash may be subtle or appear as rough, red or reddish brown papules or patches. Occurs typically on the trunk and frequently affects palms and soles. May be mistaken for other conditions. The rash does not itch. It can appear more obvious with physical activity or heat. It resolves spontaneously within several weeks but can recur during the following 2 years.

Patchy hair loss.

Raw and red mucosal surfaces such as inside the mouth, throat, genital area, vagina and anus (mucous patches).

Unilateral tonsilitis, which may be ulcerated and accompanied by cervical lymph node enlargement. Can be mistaken for common tonsilitis but does not respond to usual oral antibiotics.

Grayish-white moist raised patches in the groin, inner thighs, armpits, or under breasts (condyloma latum).

Other symptoms include fever, tiredness, muscle and joint pains, headache and swollen lymph glands.

Other affected organs may include liver, kidneys, central nervous system (CNS), joints and eyes (resulting in visual impairment).

pyoderma faciale

Pyoderma faciale

This an unusual skin condition occurring usually in young adult women. It is also called "rosacea fulminan". It can resemble severe acne or rosacea.

Unlike acne, pyoderma faciale:

Starts abruptly

Rarely persists more than a year or so

Is not associated with oily skin

Does not arise from comedones

Is confined to the face

Does not affect males

Affects younger women

Is not associated with flushing

Does not affect eyes

Pyoderma faciale presents as an ugly looking and painful large red bumps (nodules), pustules and sores on very red areas of the cheeks, chin and/or forehead. The lesions may leave scars.

Despite the severity of the inflammation, there are no internal symptoms. No infective organisms are found in bacterial cultures of the affected skin.

Perioral dermatitis

Periorificial dermatitis

Periorificial dermatitis is a common facial skin problem characterized by groups of itchy or tender small red papules. It is given this name because the papules occur around the eyes, the nostrils, the mouth and occasionally, the genitals.

The more restrictive term, perioral dermatitis, is often used when the eruption is confined to the skin in the lower half of the face, particularly around the mouth. Periocular dermatitis may be used to describe the rash affecting the eyelids.

Periorificial dermatitis and its variants mainly affect adult women aged 15 to 45 years. It is less common in men. It may affect children of any age.People with periorificial dermatitis are often using topical or inhaled corticosteroids.

The exact cause of periorificial is not understood. Periorificial dermatitis may be related to:

Epidermal barrier dysfunction
Activation of the innate immune system
Altered cutaneous microflora
Follicular fusiform bacteria
Unlike seborrhoeic dermatitis, which can affect similar areas of the face, malassezia yeasts are not involved in periorificial dermatitis.This condition may be induced by:

Topical steroids, whether applied deliberately to facial skin or inadvertently
Nasal steroids, steroid inhalers, and oral steroids
Cosmetic creams, make-ups and sunscreens
Fluorinated toothpaste
Neglecting to wash the face
Hormonal changes and/or oral contraceptives
The characteristics of facial periorificial dermatitis are:

Unilateral or bilateral eruption on chin, upper lip and eyelids in perioral, perinasal and periocular distribution
Sparing of the skin bordering the lips (which then appears pale), eyelids, nostrils
Clusters of 1–2 mm erythematous papules or papulopustules
Dry and flaky skin surface
Burning irritation
In contrast to steroid-induced rosacea, periorificial dermatitis spares the cheeks and forehead.

Genital periorificial dermatitis has a similar clinical appearance. It involves the skin on and around labia majora (in females), scrotum (in males) and anus.

Complications of periorificial dermatitis

Granulomatous periorificial dermatitis is a variant of periorificial dermatitis that presents with persistent yellowish papules. It occurs mainly in young children and nearly always follows the use of a corticosteroid. There is a granulomatous perifollicular infiltrate on histopathology.

Steroid rosacea presents with steroid-induced, large facial papules, papulopustules and telangiectasia on the mid-face, including forehead and cheeks.

Rebound flare of severe periorificial dermatitis may occur after abrupt cessation of application of potent topical steroid to facial skin.

How is periorificial dermatitis diagnosed?

The presentation of periorificial dermatitis is usually typical, so clinical diagnosis is usually straightforward. There are no specific tests.

Skin biopsy shows follicular and perivascular chronic inflammation similar to rosacea.

What is the treatment for perioral dermatitis?

Periorificial dermatitis responds well to treatment, although it may take several weeks before there is noticeable improvement.

General measures

Discontinue applying all face creams including topical steroids, cosmetics and sunscreens (zero therapy).
Consider a slower withdrawal from topical steroid/face creams if there is a severe flare after steroid cessation. Temporarily, replace it by a less potent or less occlusive cream or apply it less and less frequently until it is no longer required.
Wash the face with warm water alone while the rash is present. When it has cleared up, use a non-soap bar or liquid cleanser if you wish.
Choose a liquid or gel sunscreen.
Topical therapy

Topical therapy is used to treat mild periorificial dermatitis. Choices include:

Erythromycin
Clindamycin
Metronidazole
Pimecrolimus
Azelaic acid
Oral therapy

In more severe cases, a course of oral antibiotics may be prescribed for 6–12 weeks.

Most often, a tetracycline such as doxycycline is recommended. Sub-antimicrobial dose may be sufficient.
Oral erythromycin is used during pregnancy and in pre-pubertal children.
Oral low-dose isotretinoin may be used if antibiotics are ineffective or contraindicated.
How can periorificial dermatitis be prevented?

Periorificial dermatitis can generally be prevented by the avoidance of topical steroids and occlusive face creams. When topical steroids are necessary to treat an inflammatory facial rash, they should be applied accurately to the affected area, no more than once daily in the lowest effective potency, and discontinued as soon as the rash responds.

What is the outlook for periorificial dermatitis

Periorificial dermatitis sometimes recurs when the antibiotics are discontinued, or at a later date. The same treatment can be used again.

Naevus Comediconus

What is a comedo naevus?

A comedo naevus is a hair follicle naevus. It is also known as ‘comedone naevus’ and ‘nevus comedonicus’.

A comedo naevus is an unusual type of epidermal naevus, or birthmark (hamartoma), in which there is a localized collection of dilated follicles filled with keratin. It is more accurately termed follicular keratotic naevus, as there are no true comedones.

What does comedo naevus look like?

Comedo naevus is usually present at birth or develops in early childhood. Males and females are equally likely to be affected. Lesions often grow more quickly at puberty. They can appear anywhere on the body but are most commonly found on the face, trunk, neck and upper extremities.

The lesions appear as closely grouped slightly elevated papules with central keratinous plugs so they look like comedones. They may be distributed in a linear, interrupted, unilateral or bilateral pattern and sometimes follow the lines of Blaschko.(Blaschko's lines, also called the lines of Blaschko, named after Alfred Blaschko, are lines of normal cell development in the skin. These lines are invisible under normal conditions. They become apparent when some diseases of the skin or mucosa manifest themselves according to these patterns.)

The exact cause of comedo naevus is unknown, but it is thought to be due to cutaneous mosaicism, i.e. a line of cells with a genetic error. If this error occurs early in development of the embryo, the cells may spread out to cause multiple comedo naevi.

Mutations in FGFR2 have been detected in the naevi of some patients. This is the same gene that has found to be abnormal in a more serious generalized genetic condition, Apert syndrome, so the comedo naevus may be a ‘mosaic’ of Apert syndrome (some cells have the abnormal gene, and other cells have the normal gene). Apert syndrome causes craniofacial dysostosis (abnormalities of the bone structure of skull and face) and other skeletal abnormalities. Patients with Apert syndrome often suffer from severe acne, which also arises within a comedo naevus.

What is comedo naevus syndrome

Comedo naevus syndrome is when comedo naevus is associated with other medical conditions. Like other epidermal naevi, comedo naevus is rarely associated with other abnormalities of the cell of origin, the embryonic ectoderm. These may include:

Cataracts

Skeletal anomalies especially affecting fingers and toes or the spine

Developmental delay

What is the treatment for comedo naevus?

There is no specific treatment for comedo naevus. Lesions are usually symptom less and treatment is usually sought for cosmetic purposes. Some improvement of lesions may be seen with the use of topical tretinoin, salicylic acid or ammonium lactate lotion.

Surgery and laser treatment may be used if lesions are particularly disfiguring.

What are the complications of comedo naevus?

Rarely, at puberty or later, a comedo naevus may develop inflammatory acne-like lesions within it. These can lead to cysts, recurrent bacterial infections, abscesses, and scarring. then treatment with antibiotics or surgical drainage may be required Topical and oral treatment for acne may improve the appearance.

Herpes gladiatorum

The name implies association with martial arts. In association with rugby it is called 'scrum pox'.
Transmission is primarily by direct skin-to-skin contact and abrasions may facilitate a portal of entry. The majority of lesions occur on the head or face, followed by the trunk and extremities.
A prodromal itching or burning sensation is followed by clustered vesicles on an erythematous base which heal with crusts over about one to two weeks. Less often, headache, malaise, sore throat and fever may be reported.
Recurrent episodes may follow the initial infection.
Because of its unusual location, herpes gladiatorum any be confused with impetigo, varicella, staphylococcal furunculosis, or allergic or irritant contact dermatitis.
Accurate diagnosis requires viral immunofluorescence and cultures should be obtained by gently breaking an intact vesicle and firmly rubbing the swab tip across the base of the erosion.
Treatment of herpes gladiatorum is with oral aciclovir or similar agents and is most effective if commenced at the first symptoms of an outbreak. Topical aciclovir is probably less effective. Any secondary infection should also be treated.
The virus can survive for hours to days outside the host if conditions are appropriate. Hence, all contaminated surfaces should be cleaned with antiseptic solution. In the vesicular phase and until the crusts have separated, patients should avoid sports which could involve physical contact.
Herpes simplex acquired in sport is often associated with constitutional symptoms.
Prophylactic use of valacyclovir has been shown to be efficacious in lowering the incidence of outbreaks of herpes gladiatorum among adolescents at a 28-day wrestling camp

Acne aestivalis

Acne Aestivalis

Acne aestivalis is also known as mallorca acne. Acne aestivalis is a form of light-sensitive acne. That is to say, it is triggered by sun exposure. Acne aestivalis is characterized by multiple tightly-clustered eruptions of simple red papules forming on the skin after exposure to sunlight. It should be noted that only sun exposure and its relevant ultraviolet rays will cause acne aestivalis; merely bright lights or lights from any other source will not. Acne aestivalis is frequently associated with various skin cancers, but in truth, this is because both share a common root in sun overexposure. Acne aestivalis could nearly be thought of as a warning mechanism to indicate that the individual is spending too much time in the sun.

Acne aestivalis is very distinctive from other forms of acne due to the uniform nature of its breakout, as well as the distinctly red coloration of the papules.

Individuals that sunbathe with or without skin protection are more prone to acne aestivalis than anyone else. While casual sun exposure can cause a breakout of acne aestivalis, prolonged sun exposure is far more likely to spark a case. The use of sunscreen does not assay the risk of an acne aestivalis outbreak; sun exposure writ large is the culprit in acne aestivalis’ cause. Individuals that use sunscreen are only very mildly protected with regards to acne aestivalis.

Individuals such as manual laborers who must spend multiple hours each day outdoors may be at risk as well, although this generally involves more oblique sun exposure. The more direct the sun exposure suffered, the greater the chance of an outbreak. Risk can be reduced by covering the skin with clothing, or with wide-brimmed hats for those that it would not be a safety risk for (gardeners, for instance, could wear a wide-brimmed hat to shade themselves almost entirely from the sun, while a construction worker could not do so safely).

Acne aestivalis is not a common condition. While it is not rare or unheard of, most simply don’t need to deal with it at any point in their lives. Further, individuals of darker complexions are fairly insulated against acne aestivalis; the paler the skin, the greater the risk, and vice-versa.

Individuals that are generally resistant to sunburn and other such skin conditions will not necessarily be immune or resistant in any way to acne aestivalis. Some individuals develop acne aestivalis at the same time as they burn in the sun, others develop acne aestivalis after burning. Still others develop acne aestivalis as a result of sun exposure without burning at all. In any case, acne aestivalis indicates that the individual has spent too much time in the sun and needs to extricate themselves from sun exposure as soon as possible.

Acne aestivalis is caused by sun exposure. There are no other causes known for acne aestivalis, and no contributing factors that lead to acne aestivalis specifically. Other conditions that may exacerbate other forms acne may also exacerbate acne aestivalis, but they cannot cause acne aestivalis; acne aestivalis is a stand-alone condition brought about by sunlight.

Acne aestivalis is, in general, less of a nuisance than most cases of acne. It is unsightly and can be uncomfortable, but the pustules rarely swell in the same manner as in other forms of acne, so the risk of scarring and infection is much lower. Acne aestivalis does still carry the standard suite of potential secondary effects, however: acne aestivalis breakouts are more susceptible to excoriation and subsequent infection than the rest of the skin, and if an acne aestivalis breakout is scratched or otherwise mechanically abused, permanent scarring can occur.

Acne aestivalis in and of itself is not dangerous. It is quite unsightly and a nuisance, but it is not life-threatening, nor does it pose a long-term risk to greater bodily health. That said, acne aestivalis incidence indicates a sensitivity to the sun in excess of what the body can stand. Some individuals sunburn very easily, and others do not; likewise, some individuals contract acne aestivalis very quickly, and others do not. Whether or not the rest of the skin is sunburned, an acne aestivalis breakout indicates that the afflicted has been spending too much time in direct sunlight, which can cause many more difficult health and cosmetic problems in the future, including wrinkles and rough skin. Further sun exposure may cause skin cancer. Thus, any case of acne aestivalis should be taken as a hint that the afflicted needs to change their outdoor behavior.

Acne aestivalis treatment is the standard regimen for environmental acne breakouts. First and foremost, the individual must be removed from the source of the acne. In this case, the source is the sun. While the individual does not need to begin spending all of their hours indoors, they do need to pull themselves away from sunbathing. Sunbathing more carefully with sunscreens, or stronger variations thereof will not be sufficient. They must stop sunbathing and, as best as possible, limit sunlight contact with the afflicted areas. Further treatments are symptomatic for the breakout itself, and include antibiotic regimens. These regimens vary depending upon the patient’s own tolerance and allergies for antibiotics, but are generally a very low dose.

If you have suffered a distinctive acne outbreak after sun exposure, it is entirely likely that you are suffering from acne aestivalis. If you have been spending regular time in the sun, it is more likely that you have suffered from a breakout of acne aestivalis. Furthermore, if you are Caucasian, you are at greater risk. Acne aestivalis is difficult to mistake for other forms of acne due to the nature of its red lesions. If this breakout coincides with sun exposure, cease sunbathing immediately and contact your physician as soon as possible.

Acne detergicans

. The obsessive use of soaps by patients with acne vulgaris may aggravate the disease and result in its extension to unusual locations.

Bacteriostatic substances, especially hexachlorophene, were mildly comedogenic. Conventional soaps include salts of fatty acids; the latter are known comedogens

clinical entities such as cosmetic acne, pomade acne, chloracne, Steroid acne, tar acne and acne detergicans.

Unsung Indian scientist of India Birbal Sahni (1891-1949)

Birbal Sahni (1891-1949)

Professor Birbal Sahni FRS (1891-1949). Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

The Birbal Sahni Institute of Palaeobotany, Lucknow, India. Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

Birbal Sahni the founder of palaeobotanical research in India was a dreamer and a great visionary. He was born on 14th November 1891 at Behra, a small town in Shahpur District (now a part of west Punjab in Pakistan). He was third child of his parents, Mr. Ruchi Ram Sahni and Mrs. Ishar Devi. Ruchi Ram Sahni was an enthusiastic educationist, a great patriot and a devoted social worker. He was a man of independent thinking and progressive ideas. He was a professor of Chemistry at Government College in Lahore. Mrs. Ishwar Devi was a religious lady and was devoted to her family.

Professor Birbal Sahni FRS (1891-1949) as a young student. Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

Birbal received his early education at Lahore, first at the Mission and Central Model schools and later at the Government College. He was a brilliant student and achieved many academic distinctions during his student life e.g. standing first in Sanskrit in Matriculation, attaining a province position in intermediate Science. After, completing graduation in 1911 from Punjab University (now in Pakistan), he went to Cambridge University for higher studies. He obtained his B.Sc. degree from London University and started his research under inspiring teacher Sir Albert Charles Seward whom he regarded as mentor. In 1913 he obtained first class in Part I of the Natural Sciences Tripos and completed Part II of the Tripos in 1915. In 1919 he was awarded with the degree of Doctor of Science for his research in the field of palaeobotany by the London University. He revised Lawson’s textbook of botany on the advice of his teacher.

Professor Birbal Sahni FRS (1891-1949) undertaking research. Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

Birbal Sahni had great passion for out door life and tracking. Traverses from Pathankot to the Rohtang Pass, Kalka to Chini (Hindustan-Tibet Road) via Kasauli, Subathu Simla, Narkanda, Rampur, Bushahr, Kilba Buranpas (16,800 feet high), Srinagar to the Drass Zozila pass, Srinagar to Amarkantak etc. were greatly cherished by him. It was these tracks through the Himalayas, which gave him expansive horizons, breaking through the bounds of insularity that enabled him to view paleobotanical and geological problems in their widest perspectives.

Professor Birbal Sahni FRS (1891-1949) as a great teacher. Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

Returning to India he held faculty positions at Banaras Hindu University, Varanasi and Punjab University, Punjab for a year each. In 1921 he joined Lucknow University as Professor of Botany at the age of 30 where at he later also established the geology Department and was head of both the departments.

Professor Birbal Sahni FRS (1891-1949) and wife

In the same year he married to Ms Savitri, the daughter of Mr. Sundar Das Suri She was not only the source of encouragement to him but also his strength in all walks of life. She cherished his dream of establishing an Institute of palaeobotany single handedly after his premature demise. For Prof. Sahni work was worship. As he lay on his death-bed, afflicted with cerebral thrombosis, his last thoughts were not for him or for his family but for the newly founded institute. He expressed his intense feeling to his wife before passing to eternal sleep “nourish the institute”.

He was a teacher of par excellence and had great passion for palaeobotany. He started this subject from a small corner in the Botany Department, Lucknow University and ultimately successeded in establishing a well-recognized International Institute on this subject. His love and devotion for this subject helped him to procure fossil material from many countries. He made comprehensive studies on Indian Conifers. Later, he explored wealth of fossil plants from Rajmahal Hills. He studied Ptilophyllum and other elements and found that stem Bucklandia, leaf Ptilophyllum and flower Williamsonia belong to the same plant. He made reconstruction of Williamsonia sewardiana. He discovered petrified wood of Homoxylon rajmahalense, later, which was named as Sahnioxylon rajmahalense. He also described Glossopteris angustifolia Brongniart, Palmoxylon sundram a petrified wood, Cocoswood and a water fern Azolla intertrappea. This was followed by study of Gondwana plants of Salt Range, Karewa flora from Kashmir. He instituted a new plant group ‘Pentoxyleae’ which attracted worldwide attention. His palaeobotanical studies had given support to continental drift theory. In addition he dated some of the rocks of Salt Range to about 40-60 million years, and searched the Deccan traps in Madhya Pradesh and dated them as 62 million years, concluding they belonged to the Tertiary period.

Besides this, he was greatly interested in Archaeology. He did his studies on Yaudheya Coin Moulds from Khokhra- Kot at Rohtak (1936) and from Sunhet near Ludhiana (1941). He threw light on the studies of coin moulds and published his results on “The Technique of Casting Coins in Ancient India” in masterly monograph, Memoirs of the Numismatic Society of India in 1945. This won him Nelson Wright Medal award. In his research paper he had mentioned that the aims and methods of the palaeobotanist are not essentially different from those of the archaeologist. The aim of both is historical: the interpretation and reconstruction of the past.

Besides his deep interest in science, he was fond of music and could play the sitar and violin. His other hobbies were drawing and clay modeling. Whenever time permitted, he loved playing chess. At school times he was a player of hockey and tennis. He represented India Majlis at Tennis and played against the Oxford Majlis.

Professor Birbal Sahni FRS (1891-1949) - Founder of the Birbal Sahni Institute of Palaeobotany. Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

Sahni received number of awards and prizes for his significant contributions. He was the recipient of the Barclay Medal of Royal Asiatic Society of Bengal in 1936, the Nelson Wright Medal of the Numismatic Society of India in 1945 and the Sir C. R. Reddy National prize in 1947. He was elected fellow of Geological Society of Great Britain. He also served the editorial board of the Botanical Journal Chronica Botanica. He was elected vice president of the 5th and 6th International Botanical Congress in 1930 and 1935 held at Cambridge and Amsterdam respectively. In 1936 he was elected as fellow of Royal Society of London. He was general President of the Indian Science Congress in 1940. He was a founder fellow of the National Institute of Science Academy (now Indian Science Academy, New Delhi). The University of Cambridge had recognized his researches and awarded a Sc. D. in 1929, American Academy of arts and Science elected him as its foreign honorary member in 1948. However, in 1950 destiny prevented him to preside as honorary president in International Botanical Congress, held at Stockhlom.

Professor Birbal Sahni FRS (1891-1949) adressing a scientific audience. Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

Birbal’s foremost ambition was to put palaeobotanical research in India in an organized basis. Initially he established a museum of plant fossils in 1929. In 1939 he constituted the committee of Indian Palaeobotanists named as “The Palaeobotanical Society” and convened a meeting to coordinate and develop research fields in India. The Governing body of Society resolved at 10th September 1946, to establish an Institute of Palaeobotany, which started functioning at the Botany Department, Lucknow University with Professor Sahni as his honorary Director.

Professor Birbal Sahni FRS (1891-1949) at a palaeobotany display. Image courtesy of and copyright of the Birbal Sahni Institute of Palaeobotany, Lucknow, India

The Government of United Provinces gifted a land next to Lucknow University in September 1948. He made comprehensive plan for Institute building and its construction. Pandit Jawahar Lal Nehru, the then Prime Minister of India laid the foundation stone on 3rd April 1949. Sahni in his welcome speech said:

the foundation stone symbolizes: A great fact of the antiquity of plant life on the globe, the intellect of man ever trying to bring that fact more and more clearly to light, revealing different stages not only in the evolution of the plant kingdom in more and more orderly and understandable sequence, but also the evolution of his own poor understanding of these truth. The very construction of it, the flaws and imperfections in its entire make up, the labour that has gone into its preparation are all but symbols of our imperfect and helpless efforts at constructing something new, something worthwhile.

Unfortunately Birbal Sahni passed away a week after the foundation stone laying ceremony was conducted, on 10th April 1949 and could not see his cherished dream “The Institute Grow and Develop”.

To cope with the situation governing body of the Palaeobotanical Society authorized Mrs Savitri Sahni to serve the Institute as Director. Later, in October 1949 the Institute was named after a great scientist, a devoted teacher, a loving husband and affectionate colleague. He is a constant source of inspiration and courage to us.

I would like to end this article by quoting from an obituary written by one of his student Prof. Sadasivan:

A celebrated botanist has passed away in the wake of national exuberance and I firmly believe that posterity will class Prof. Sahni with Englar, Strasburger, Goebel, DeBerry, of Germany, Guillermond of France, Scott, Seward and Bower of United Kingdom and Brongniart of Prague for his out look like these men of Science was truly

Significant research contributions:

Glossopteris angustifolia

Homoxylon rajmahalense

Williamsonia

W. sewardiana sp. nov.) from the Rajmahal Hills, India. Memoir Geological Survey of India, Palaeontologia Indica, New Series, 20 (3): 1-19.
Sahni, B. 1932c. Dadoxylon zalessky, a new species of cordaitean trees from the Lower Gondwanas of India. Record Geological Survey of India 66 (4): 414-429.
Sahni, B. 1934. The silicified flora of the Deccan Intertrappean Series- Part II. Gymnospermous and angiospermous fruits. Proceedings 21st Indian Science Congress, Bombay 3: 317-318.
Sahni, B. 1936a. The occurrence of Matonidium and Weicheselia

Azolla intertrappea

Rodites

Contribution by permission of the director of the Birbal Sahni Institute of Palaeobotany, by:

Neeru Prakash

Unsung heroes Calyampudi Radhakrishna Rao, also known as C R Rao

C R Rao

Calyampudi Radhakrishna Rao, also known as C R Rao is an Indian mathematician and statistician, who is noted for his contributions to the foundations of statistical theory and multivariate statistical methodology. C.R. Rao was born in 1920 in Hoovina Hadagali, Karnataka. He did his M.A. degree in mathematics at the Andhra University and completed his M.A. degree in statistics from Calcutta University. He earned his Ph.D. in 1948 from Cambridge University under the guidance of R.A. Fisher, the father of modern statistics.

Later, C R Rao began working at the Indian Statistical Institute, where he worked until he retired at the age of 60. Under the direction the doyen of Indian statistics, P.C. Mahalanobis, he played an important role in setting up state statistical bureaus in different states of India. Further, C.R. Rao worked towards setting up the Central Statistical Organization and the National Sample Survey Organization, due to which India has one of the world’s best national statistical systems.

Among his best-known discoveries are the Cramér–Rao bound and the Rao–Blackwell theorem on the quality of estimators. Other areas he worked in include multivariate analysis, estimation theory, and differential geometry. His other contributions include the Fisher–Rao Theorem, Rao distance, and orthogonal arrays. Today, at the ripe age of 87, he is still active as the Director of the Center for Multivariate Analysis at Pennsylvania State University.

Shanti Swaroop Bhatnagar

Indian scientists - S.S. Bhatnagar | Courtesy: Arago.si.edu — S.S. Bhatnagar | Courtesy: Arago.si.edu

Sir Shanti Swaroop Bhatnagar is a well known Indian scientist owing to the national award instituted for science & technology in his name. However, few of us know that the Council of Scientific and Industrial Research (CSIR) was established way back in 1942, much before India’s independence! Born in 1894, Bhatnagar got his B.Sc degree from Punjab University in 1913. He did his first research work for his MSc degree on the subject of surface tension.

Bhatnagar spent 16 years in Punjab University as a professor of physical chemistry and Director of University Chemical Laboratories. During this time, he did considerable work in applied chemistry, solving industrial problems such as developing process for converting bagasse into cattle feed, using Indian gum to lowering the viscosity of the mud in oil drilling operations and studying applications of magneto chemistry.

During the British Raj, the government was reluctant to set up a separate department for scientific and industrial research in India. However, Sir Arcot Ramaswamy Mudaliar, the last Diwan of Mysore kingdom, insisted on setting up a board. Due to the efforts of Mudaliar and Bhatnagar, the CSIR was established as an autonomous body in 1942. Under Bhatnagar’s able leadership, CSIR set up 12 national laboratories such as the Central Food Processing Technological Institute, Mysore, the National Chemical Laboratory, Pune, the National Physical Laboratory, New Delhi, the National Metallurgical Laboratory, Jamshedpur, the Central Fuel Institute, Dhanbad. His association with Pandit Nehru enabled him to set up so many institutes, which was termed as the ‘Nehru-Bhatnagar Effect’ by Sir C.V. Raman!

Vainu Bappu

Vainu Bappu is considered the father of modern Indian astronomy, who largely contributed to the establishment of the Indian Institute of Astrophysics. His is a case of like father like son! Bappu was born in 1927 to a senior astronomer in the Nizamiah Observatory, Hyderabad. Being a keen amateur astronomer, Bappu published various papers on variable star observations. After obtaining his Masters degree in Physics from Madras University, he joined the Harvard University on a scholarship.

At Harvard, Vainu Bappu discovered a comet named ‘Bappu-Bok-Newkirk’, after Bappu and his colleagues Bart Bok and Gordon Newkirk. He completed his Ph.D in 1952 and joined the Palomar observatory on the prestigious Carnegie Fellowship. There, Bappu and Colin Wilson discovered a relationship between the luminosity of particular kinds of stars and some of their spectral characteristics, which is today known as the Bappu-Wilson effect.

On his return to India, Bappu was appointed to head a team of astronomers to build an observatory at Nainital. He worked towards building a large indigenous optical telescope and a research observatory in India led to the founding of an optical observatory of Kavalur. In 1979, he was nominated as the President of the International Astronomical Union. Due to his efforts, India’s largest optical telescope, the Vainu Bappu Observatory was established in 1986, just after his death!

Yash Pal

Prof. Yash Pal is an Indian astrophysicist who has made significant contributions to the study of cosmic rays, high-energy physics, astrophysics, and science education. Born in 1926 in Jhang in Pakistan, he got his Masters degree in physics from Panjab University in 1949. Later in 1958, he did his Ph.D from the Massachusetts Institute of Technology, specializing in astrophysics.
Yash Pal started his career at the Tata Institute of Fundamental Research, Mumbai, as a member of the Cosmic Rays group.

In 1973, Yash Pal became the first Director of the Space Applications Centre in Ahmedabad when the government set up the Department of Space. He later served on various administrative assignments such as the Secretary General of the UN Conference on Peaceful Uses of Outer Space, Chief Consultant for Planning Commission, Secretary for Department of Science & Technology, and Chancellor of Jawaharlal Nehru University. However, his role as the Chairman of the University Grants Commission (UGC) during 1986–1991 was the prominent one.

As the UGC Chairman, Yash Pal initiated numerous innovative programmes to improve the standards of higher education in India. During this period, he also made regular appearances on a TV show known as “Turning Point” on Doordarshan, which explained the great discoveries of science and explained scientific concepts in layman’s language. Similarly, he worked on “Race to Save the Planet”, an international TV series that examined the major environmental issues facing the world. No wonder he received the Kalinga Prize, awarded by UNESCO for the popularisation of science in 2009!

Red Ear Syndrome Download PDF

Steven D. Waldman MD, JD

Atlas of Uncommon Pain Syndromes, Chapter 18, 46-47

ICD-9 CODE 350.1

ICD-10 CODE G50.0

The Clinical Syndrome

Red ear syndrome is an uncommon primary pain disorder thought to be a variant of one of a group of three headache syndromes known as the trigeminal autonomic cephalgias ( Table 18-1 ). Whether red ear syndrome is in fact a distinct pain syndrome resulting from auriculo-autonomic dysfunction or simply a constellation of symptoms that occurs on a continuum along with the other trigeminal autonomic cephalgias is a point of ongoing debate among headache and pain management specialists. As with most headache and facial pain syndromes, the exact cause of the pain of red ear syndrome is unknown; however, the pathogenesis of this uncommon cause of head and face pain is thought to be dysfunction of the trigeminal autonomic reflex. The rapid onset of ear redness and associated pain may be caused by an antidromic release of vasoactive peptides from the terminal afferent fibers of the third cervical nerve root, which provides sensory innervations to the pinna of the ear.

TABLE 18-1

The Trigeminal Autonomic Cephalgias

•
Cluster headache
•
Paroxysmal hemicranias
•
Short-lasting unilateral neuralgiform headache with conjunctival injection tearing (SUNCT)

As its name implies, the pathognomonic finding of red ear syndrome is in fact a unilateral red ear ( Figure 18-1 ). This redness involves the entire ear, including the pinna, and is associated with neuralgia-like pain reminiscent of sudden unilateral neuralgiform conjunctival injection tearing (SUNCT) headache (see Chapter 7 ). The pain and erythema associated with red ear syndrome have a rapid onset to peak, with attacks lasting 15 seconds to 5 minutes and the frequency of attacks ranging from 20 to 200 attacks per day. In some patients, these attacks can be triggered by sensory stimulation of the affected area, such as when brushing the hair. Although in many ways similar to SUNCT headache (i.e., unilateral, rapid onset to peak, short duration of attacks, pain-free periods between attacks), many dissimilarities also exist, including the location and pronounced autonomic phenomenon manifested by the red ear.

Signs and Symptoms

Patients with red ear syndrome present with the complaint of severe paroxysms of sudden onset of unilateral ear redness associated with pain involving the ipsilateral ear. The pain is neuralgiform in quality and severe to excruciating in intensity. Like trigeminal neuralgia, the pain of red ear syndrome rarely switches sides. Red ear syndrome occurs slightly more frequently in males. It can occur at any age, with a peak incidence in the fifth decade.

Testing

Magnetic resonance imaging (MRI) of the brain provides the clinician with the best information regarding the cranial vault and its contents. MRI is highly accurate and helps identify abnormalities that may put the patient at risk for neurological disasters secondary to intracranial and brainstem pathology, including tumors and demyelinating disease. Magnetic resonance angiography (MRA) also may be useful in helping identify aneurysms that may be responsible for the patient’s neurological findings. In patients who cannot undergo MRI, such as patients with pacemakers, computed tomography (CT) is a reasonable second choice. Radionuclide bone scan and plain radiography are indicated if a fracture or bony abnormality such as metastatic disease is considered in the differential diagnosis.

Screening laboratory tests consisting of complete blood cell count, erythrocyte sedimentation rate, and automated blood chemistry should be performed if the diagnosis of red ear syndrome is in question. Additional testing to rule out collagen-vascular disease is indicated if polychondritis is suspected.

Differential Diagnosis

Red ear syndrome is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography, and MRI. Pain syndromes that may mimic red ear syndrome include erythromelalgia of the ear, polychondritis, cluster headache, temporal arteritis, trigeminal neuralgia, demyelinating disease, primary stabbing headache, SUNCT, and chronic paroxysmal hemicranias. However, because of the overlapping features of all headache and facial pain syndromes, red ear syndrome easily can be mistaken for another type of headache or facial pain. Trigeminal neuralgia is more common and is characterized by trigger areas and tic-like movements. Demyelinating disease is generally associated with other neurological findings, including optic neuritis and other motor and sensory abnormalities. The pain of chronic paroxysmal hemicrania lasts much longer than the pain of red ear syndrome.

Treatment

The treatment of red ear syndrome is analogous to the treatment of trigeminal neuralgia, although the pharmacological management of this uncommon headache disorder is disappointing. The use of anticonvulsants such as lamotrigine and gabapentin represents a reasonable starting point. High-dose steroids tapered over 10 days also have been anecdotally reported to provide relief. For patients who do not respond to these treatments, a few case reports suggest that daily ipsilateral C2-C3 facet joint blocks with local anesthetic and steroid may provide relief of both the pain and the autonomic dysfunction. Underlying sleep disturbance and depression associated with the pain of red ear syndrome are best treated with a tricyclic antidepressant compound, such as nortriptyline, which can be started at a single bedtime dose of 25 mg.

Complications and Pitfalls

Failure to diagnose red ear syndrome correctly may put the patient at risk if intracranial pathology or demyelinating disease, which may mimic the clinical presentation of red ear syndrome, is overlooked. MRI is indicated in all patients thought to have red ear syndrome. A careful evaluation of the ear to rule out localized pathological conditions is also indicated, as is laboratory testing for collagen-vascular disease if polychondritis is suspected.

CLINICAL PEARLS

Given the poor response to treatment with drugs traditionally used to treat trigeminal neuralgia, facet block of the ipsilateral C2-C3 facet joints with local anesthetic and steroids should be considered in patients thought to have red ear syndrome. Given the uncommon nature of this headache syndrome and its overlap with the other trigeminal autonomic cephalgias and other more serious forms of intracranial pathological conditions such as tumors and vascular abnormalities, red ear syndrome must remain a diagnosis of exclusion. All patients thought to have red ear syndrome require MRI of the brain with and without gadolinium contrast material and thorough otic and neurological evaluation. Cervical facet block should be performed only by clinicians familiar with the regional anatomy.