#6: Parasitic Twin
Lakshmi Tatma was born joined at the pelvis to a “parasitic twin” that stopped developing in her mother’s womb. The twin had no head or brain, but Lakshmi absorbed the twin's limbs, kidneys and other body parts. It took doctors 27 hours to operate on Lakshmi.

During the surgery, which took place at the Sparsh hospital in Bangladore, India, surgeons removed Lakshmi’s extra limbs, transplanted a kidney from the twin and reconstructed the girl’s pelvic area. However, she will require more surgeries and rehabilitation, especially as she grows. Lakshmi was named for the six-limbed Hindu goddess who represented wealth and prosperity. Lakshmi is now attending school, and playing sports.
(Image taken from: http://www.foxnews.com/slideshow/health/2010/02/16/oddest-medical-conditions?slide=6)

#7: Foreign Accent Syndrome
This is a rare syndrome that affects only people who have had strokes – they emerge from the stroke speaking in an accent different from the one they used to speak.

It can happen if a stroke damages the parts of the left hemisphere of the brain related to speech production. Foreign Accent Syndrome was highlighted in last year’s "Canadian Journal of Neurological Sciences," when a woman from Ontario, Canada had a left-sided stroke and began speaking in an East Coast accent.
(Image taken from: http://www.foxnews.com/slideshow/health/2010/02/16/oddest-medical-conditions?slide=7)

Here is another article on other oddest medical conditions (I shared out 2 of them here):

#1: Blue Skin Disorder
A large family simply known as the "blue people" lived in the hills around Troublesome Creek in Kentucky until the 1960s. They were the blue Fugates. Most of them lived past the age of 80, with no serious illness - just blue skin. The trait was passed on from generation to generation. People with this condition have blue, plum, indigo or almost purple skin.

#2: Walking Corpse Syndrome
It is a syndrome of mental depression and suicidal tendencies, in which the patient complains of having lost everything: possessions, part of or entire body, often believing that he or she has died and is a walking corpse. This delusion is usually expanded to the degree that the patient might claim that he can smell his own rotting flesh and feel worms crawling through his skin. The latter phenomenon is a recurring experience of people chronically deprived of sleep or suffering amphetamine/cocaine psychosis. Paradoxically, being "dead" often gives the patient the nation of being immortal.

The inheritance pattern in progeria syndrome is autosomal dominant (or less frequently recessive when involving the ZMPSTE24 gene) [22,26]. All subjects with HGPS have the disease as result of a de novo mutation (the most common mutation is p.G608G), as their parents are not affected. This mutation causes aberrant splicing in exon 11 and the deletion of 50 residues close to the C terminus of lamin A, including the second ZMPSTE24 cleavage site. This deletion prevents complete processing of prelamin A, resulting in the accumulation of a farnesylated lamin A, known as progerin. Five other different de novo dominant LMNA mutations have been found less frequently: p.E145K, p.S143F, p.R644C, p. T10I and p.E578V [13]. Despite being very rare, mutations in HGPS are thought to have a paternal origin [27].

Clinical manifestations

Patients with HGPS are infants who are healthy at birth and in the course of 1–2 years present signs of progressive premature ageing. Initially, sclerodermatous plaques appear on the skin of the hip and in the upper region of the lower extremities. These areas grow more and put virtually the entire body at risk, except for the genitals and some regions of the lower limbs. The production of sweat is simultaneously decreased and alopecia becomes evident. Some late signs are hyperpigmentation in sun-exposed areas, as well as dystrophic nails [5]. The clinical manifestations of classic progeria include abnormalities in growth, skin and skeletal and cardiovascular systems, which are always present after the age of 3 years [6].

The ever present clinical features are prominent scalp veins, alopecia, bird-like facies, prominent eyes, abnormal dentition and delayed tooth eruption, micrognathia, short clavicles, horseman stance, pyriform thorax, thin legs with prominent joints, short stature and low weight for height, incomplete sexual maturation and lack of subcutaneous fat. The clinical manifestations that may be apparent or not are sclerodermatous skin, generalized alopecia, eyelashes and eyebrow alopecia, protruding ears with absent lobes, beaked nose, thin lips with centrofacial cyanosis, protracted anterior fontanel and high-pitched voice [4,7,10].

Patients who have most of the aforementioned characteristics are considered to have a classic case of progeria. However, individuals who have characteristics more or less intense of the syndrome are considered patients with atypical progeria [21].

Diagnostic methods

The diagnostic methods of HGPS are clinical (serum lipid levels, hyaluronic acid excretion, blood count), histological (biopsies from areas of abdominal skin with abnormal nuclear morphology), radiological (abnormality found in the brain, thorax, long bones and phalanges) and by screening for mutations in the gene LMNA [12-14].

No laboratory offers a specific molecular genetic testing for prenatal diagnosis of progeria. Nevertheless, prenatal testing may be offered to families in which the causative mutation of the disorder has been identified in a family member [13].

Some clinical tests for confirmatory diagnosis are sequential analysis of the gene LMNA, which reveals point mutations in approximately 90% of the patients with HGPS, and the test for uniparental disomy of chromosome 1 and deletions associated with HGPS. Imaging studies may also be performed. Radiography detects manifestations that usually occur in the skull, thorax, long bones, and phalanges [10].

Under light microscopy, histological tests using skin biopsies from HGPS patients exhibit irregular nuclear envelope outlines, indicating the massive and global alterations of chromatin functions, including alterations of gene expression [20]. Tests using keratinocytes from transgenic mice expressing progerin revealed alterations in nuclear shape such as decreased nuclear circularity, resulting in greater nuclear surface area and greater morphological diversity, thereby, microscopic analysis of the nuclear shape could be an interesting diagnostic alternative to be studied [14].

Treatment

There is no known cure for progeria. Nonetheless, there are treatments in order to improve the clinical conditions. Regular diets may be prescribed, as well as routine immunizations, inspection for cardiovascular diseases, treatment with aspirin, surgical procedures, and physical and psychological therapies. Children with HGPS must have a regular diet. Common mulltivitamin tablets are appropriately given in normal doses. Supplements with fluoride are recommended, since there are dental problems. It is advised to occasionally give small doses of aspirin to children with HGPS, aimed at reducing the occurrence of heart attack and strokes. Atherosclerosis of the coronary artery may be diagnosed with an echocardiogram (ECG), and nitroglycerin may be useful should there be development of angina. The drug doses must be based on weight and the anesthetics must be used cautiously. As these children are susceptible to fractures, they should be routinely accompanied. Due to the susceptibility to dislocation of the hip bone because of coxa valga, conservative care and surgical procedures are recommended. In relation to delay or loss of the first dentition, dental extraction may be recommended. Physical and psychological therapies are recommended to help maintain the joints with good movement amplitude, as well as to foster social interaction, respectively [21].

Another therapeutic approach involves the use of farnesyltransferase inhibitors which have been shown to reverse abnormalities in nuclear morphology in cells expressing progerin [14]. In vitro studies in fibroblasts have shown the capacity of farnesyltransferase inhibitors (FTI) to reverse nuclear alterations [28-30].

Using transgenic mice expressing progerin, an ammelioration and reversion of cardiovascular phenotype, number reduction of the spontaneious rib fractures and improved survival and growth was observed, indicating that these compounds are an interesting pharmacological alternative for future treatment of HGPS and progeroid syndromes, as well as anti-aging [14,31,32]. The promising results with FTIs led to an open-label clinical trial of the FTI use in HGPS (ClinicalTrials.gov number NCT000425607) [7].

Other possibilities of treatments studied involves the use of low levels of growth hormone, but hormonal replacement has had unsatisfactory effects in these patients [10,11]. The use RNAi or antisense strategies might be useful for reduce the progerin production in HGPS patients, but this strategy have few studies [31,33,34]. The combined use of a statin and a biphosphonate, compounds that act in the same mevalonate pathway as FTIs, but the effect of these drugs alone and combined to treat HGPS remains an open question [32].

Prognostic

The causes of morbidity in HGPS are difficulty in development, cerebrovascular events, vertigo, migraine, necrosis of the head of the femur and luxation of the hip [5].

Despite all medical and technological advances in cardiovascular surgeries (catheterization, cardiac pacemaking), improvement in patients' life expectancy has not been achieved, due to their tendency to accumulate atheromatous plaques again. The main cause of death (in 75% cases) is cardiac or cerebrovascular abnormalities which include myocardial infarction and congestive heart failure due to premature atherosclerosis [13]. Psychological support in these patients is important, as well as a good family circle, since there is no mental abnormality. However, they do have deficient body and physiopathologic control [5].

Final considerations

While there is a move towards precise molecular classification of "laminopathies" rather than the broad clinical categories in use to date, it appears essential that clinical features be documented in detail. This may help in answering parents' questions about prognosis. It may also contribute to a better understanding of the functions of lamin A, and may in the future help in determining the efficacy of pharmacogenetic interventions for Hutchinson-Gilford syndrome and other progeroid syndromes. Due the fact of the cencentration of progering is enhanced in fibroblast of older persons, HGPS and possibly other laminopathies may serve as a model for the normal ageing process.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

VSFS, RBN and GFG contributed to conception and design, designed the review, carried out the literature research, and manuscript preparation. HDMC contributed to conception and design, carried out the manuscript editing and manuscript review. All authors read and approved the final manuscript. We declare that all figures used in this article were authorized by the corresponding authors of the cited articles, Dr. Stephen G. Young and Dr. Francis S. Collins.

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