Porencephaly is a very rare disorder of the central nervous system resulting in cerebrospinal fluid in cavities or cysts within the brain.   The localized encephalomalacia (brain softening) is usually because of hemorrhage or inflammation of that portion of the brain.  A less common form is inherited. [2]

It is possible that the fetus essentially had a stroke. It may develop before or after birth. It is usually found in infants or very young children. These cavities or cysts may be mild enough to not be noticed. Or they may be severe enough to show physical and mental disorders. [1]

Symptoms of Porencephalic Cyst

Some patients show no symptoms at all.  Muscle spasms and seizures are common early signs.  Delayed language development, muscle development, and mental incapacity are also common. Head size and shape may vary from very small (microcephalic) to expanding (hydrocephalic) due to the size and location and growth of cysts.[10]

Diagnosis of Porencephaly

Porencephaly is usually identified before the infant reaches the age of one year. Patients may live into their twenties in some cases.[1] The two types of porencephaly are developmental or congenital. Within the developmental type there are several additional sub categories. [10]

Porencephaly Radiology

To confirm the diagnosis of porencephaly cyst requires several tests and exams.  The examination of the infant with magnetic resonance imaging, ultrasound and CT scans can reveal the presence of these porencephalic spaces or cysts, even in a pre-natal state  after 20 weeks of gestation. [10]

Porencephaly MRI

Picture 1 : MRI (T2)

Picture 2: MRI (T1)

Porencephaly CT

Porencephaly Cyst : Modality: CT (non-contrast)

Images source : radiopaedia.org/articles/porencephaly

Porencephalic Cyst

As early as 1859 porencephalic cysts were first seen and discussed by R. Heschl, though this precedes the development of the highly technical diagnostic tools available today.

In determining what kind of developmental cyst is present, physicians consider these differential imaging characteristics:

• Arachnoid cyst - extra axial, including gray matter beneath
• Interhemishperic cyst
• Neuroglial cyst - without communication between ventricles or subarachnoid space
• Holoprosencephaly - normal separation of the hemispheres has failed.

MRI : Difference between Neuroglial cyst and Arachnoid cyst

Modality: MRI (T2)

This is valuable information for the purposes of diagnosis. However, the prognosis and treatments remain essentially the same. The amount of impairment is dependent upon the size and location of the cysts. Treatment is essentially supportive for the infant. [10]

Porencephaly vs Schizencephaly

Schizencephaly and Porencephaly are both rare disorders in the brain.  In fact, schizencephaly is a type of porencephaly. Patients have abnormal clefts or slits in their cerebral hemispheres.   If the clefts are in both hemispheres, most likely they will have central nervous system dysfunction, minimal language skills and speech will be delayed.

If they have smaller splits or clefts in only one hemisphere they may have weakness on one side of the body and may not be mentally impaired.  Other characteristics of  schizencephaly  include:

• mental retardation
• microcephaly,
• hemiparesis (weakness or paralysis which affects only one side)
• hypotonia (reduced muscle tone)
• quadriparesis (paralysis or weakness affects all arms and legs)
• hydrocephalus
• seizures.

This is a significant, though rare birth defect. One type of schizencephaly has  a genetic origin. Other causes may be exposure to toxins,  particular medications  or cocaine use by the mother during pregnancy, or some unidentified external environmental abnormality or an unidentified vascular injury.  Other signs indicate neurons have not succeeded in migrating to their proper place in the brain.

Treatments for patients with schizencephaly include physical therapy, medications to minimize seizures, and if necessary,  a shunt to remove excess fluids from the brain. The prognosis for patients with schizencephaly will depend almost entirely upon the size and number of clefts and how much neurological damage has happened.  [16]

The significant difference between schizencephaly and porencephaly that one is  believed to be a primary developmental disorder where the neurons do not reach their destination, schizencephaly.  The other, porencephaly, is a consequence of injury to brain tissue that causes it to soften or dissolve.  These spaces can resemble each other.  Some researchers theorize that they both have primary developmental disorders but at different stages of the development of the brain.   It often requires magnetic resonance imaging (MRI) to examine the brain tissue along the edge of the cleft.  In porencephaly it is usually white matter and scar tissue but in schizencephaly the cleft is lined with gray matter [17]

Porencephaly Cyst Treatment

Treatment for porencephaly is much the same as it is for schizencephaly. Since the degree of impairment depends entirely upon the size, location and number of cysts, and the patients are, for the most part, infants, physical therapy is provided. If  epileptic symptoms are present, treatment for seizures is given. If needed, a shunt is provided to remove excess fluids from the brain. [5]

Research

Research is focused upon developmental issues and processes of the brain during the prenatal state. Much of the research investigates normal brain development, thus gaining insights into where things are different in these rare disorders. [2] In addition, since there are some cases of inherited porencephaly, there is genetic research underway to examine the genes involved.

It is described as an autosomal  dominant trait, though these studies are in early stages. [6] A distinct genetic form of porencephaly occurs due to mutations of the COL4A1 gene. [9]

References

1. http://en.wikipedia.org/wiki/Porencephaly
2. http://www.ninds.nih.gov/disorders/porencephaly/porencephaly.htm
3. http://www.ninds.nih.gov/disorders/cephalic_disorders/detail_cephalic_disorders.htm
4. http://ghr.nlm.nih.gov/condition/familial-porencephaly
5. http://www.medterms.com/script/main/art.asp?articlekey=15543
6. http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert…0
7. http://www.ajnr.org/content/19/1/135.full.pdf
8. http://www.bridges4kids.org/Disabilities/Porencephaly.html
9. http://www.webmd.com/brain/sporadic-porencephaly
10. http://radiopaedia.org/articles/porencephaly
11. http://www.encyclopedia.com/topic/Porencephaly.aspx
12. http://neuropathology-web.org/chapter3/chapter3fPorencephaly.html
13. http://www.healthline.com/galecontent/porencephaly
14. http://www.rightdiagnosis.com/p/porencephaly/intro.htm
15. http://dictionary.reference.com/browse/porencephaly
16. http://www.ninds.nih.gov/disorders/schizencephaly/schizencephaly.htm
17. http://www.healthline.com/galecontent/schizencephaly

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The exploding head syndrome sounds like it comes from a science fiction movie, but it is a real phenomenon which remains a medical mystery.  People experience a loud and frightening noise, like a loud bang, a shotgun, a roar, thunder, etc. It happens either while the patient is falling asleep or right after falling asleep. The sound is sudden and awakens them.  Fear and anxiety follows, along with a surge of adrenaline.  It is a common sleep disorder which is not harmful but it is stressful and disturbing for the patient.  [1]

Actually it seems that most people have this sort of incident at some time during their lives. It is startling or terrifying depending on the patient. There are other sleep disorders that have similar effects: sleep twitches, restless legs, sense of falling. These are referred to as sleep-related myoclonus. [2]

Symptoms of Exploding Head Syndrome

The basic symptoms of exploding head syndrome are the sudden awakening right after falling asleep. The person is usually agitated and often frightened. No pain is involved. The reason for the rude awakening is the loud sound or the noises the person heard. These sounds are entirely internal.

There is no evidence of an external source. The symptom of loud noises is reported by the patient with varying frequency and intensity. It may happen only once in their lifetime.

Who has Exploding Head Syndrome?

The typical patient is an adult over fifty years of age. Though younger men and women in high stress work environments have experienced it also. Women are more likely to report this syndrome. Some people fear they are going insane and are reluctant to tell anyone about the episodes.  Children as young as ten have also reported it.[5, 6]

Causes of Exploding Head Syndrome

• The cause of exploding head syndrome remains a physiological mystery.
• External stress factors in the patient’s life seem to be major contributors. There is no known connection to any serious medical condition.
• Extreme fatigue is a factor. Withdrawing from certain prescription medications can contribute in some cases.
• Possible cause may be movement within the middle ear or some stimulation in the temporal lobe where hearing occurs.  [4]

Diagnosis of Exploding Head Syndrome (EHS)

The puzzling thing is the patient may have once incident or many recurring episodes of exploding head syndrome. They may go for years with no episodes and then have another one. [4]

This syndrome is self reported. A good medical history of the patient is helpful, though there are no major health complications related to EHS.  An examination at a sleep center can include a wide range of monitors to determine if there are any other sleep disorders.

Sleep Paralysis and Exploding Head Syndrome

Both sleep paralysis and exploding head syndrome are types of parasomnia.  Parasomnia is a condition or behavior which happens around sleeping times. Both are self reported. Neither has an obvious external cause. Both are a disruption in the normal transition from being awake to being asleep.  Sleep paralysis happens during REM sleep and is a state of not being able to move or speak.   [8]

Treatment of Exploding Head Syndrome

There are ways to minimize the impact of exploding head syndrome and the first step in treating this disturbing sleep syndrome is to recognize that it is not a symptom of a serious condition. Learn to relax when it happens.

• Relax
• Reduce Stress
• Maintain a Balanced Diet
• Sleep regularly and routinely.
• Seek professional help.

Stress is unavoidable, but learning how to de-stress yourself and striving for a more balance life can help reduce these incidents.
Believe it or not, what you eat and drink during the day helps your body deal with routine stress and helps your body during your sleep times. Try to set a sleep schedule and keep it regular. Most adults need a minimum of six hours of sleep each night. It may take you 8 hours to reach that goal when you consider time to unwind and relax before sleep.

If your exploding head syndrome is causing sleep deprivation, it is time to see a doctor who can deal with this condition. There are prescription medications that can reduce the frequency and the intensity of these incidents if the home remedies and lifestyle changes do not help.   [2]

Research on Exploding Head Syndrome

Some research has used recordings during the patient’s sleep. EEG and EKGs and other monitoring devices are used at sleep centers to study what is happening in the patient’s head and body when they experience the exploding head incidents.  There are some changes in EEG recordings and no evidence that epilepsy is involved.

Researchers indicated that once the patients understood the benign nature of the incidents they began to experience relief.  Clomipramine is prescribed with reasonable success.  It appears that this syndrome is more directly related to the person’s emotional condition and stress during their regular awake times. [3]

References

1. http://www.aan.com/news/?event=read&article_id=11104
2. http://www.huffingtonpost.com/2011/12/23/exploding-head-syndrome-tips_n_1167768.html
3. http://www.ncbi.nlm.nih.gov/pubmed/1896728
4. http://en.wikipedia.org/wiki/Exploding_head_syndrome
5. http://www.sleepassociation.org/index.php?p=explodingheadsyndrome
6. http://www.riversideonline.com/health_reference/Nervous-System/AN00929.cfm
7. http://www.rightdiagnosis.com/e/exploding_head_syndrome/intro.htm
8. http://sleepdisorders.about.com/od/commonsleepdisorders/a/Exploding_Head_Syndrome.htm

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Odontoma is a specific type of tumor that is benign and located in your mouth. It is made of all or some of the tissues that make your teeth. However, these tissues may or may not be arranged in the form of a tooth.  It may not be visible to the naked eye.  It is a mass of enamel, dentin, pulp and cementum that usually grows at the same rate as teeth. However, this mass is disorganized and any one of the components may become the dominant part.[1]

Odontoma is most often found in people around age 14 as a tooth that has not emerged. [3] More complex odontoma are found in males up to age 30. [7 ] Though more recent data indicates these tumors are found in both genders. [11]

Types of Odontoma

There are  two general types of odontoma, some are more serious than others: Common odontoma and complex odontoma. These are further defined by specific components. They are described in part by their location and origin:

• Ameloblastic [2]
• Compound
  
• Radicular
  
• Temporal
  

Picture : Odontoma

Image source : course.jnu.edu.cn

Symptoms of Odontoma

There are many symptoms of Odontoma but they are often overlooked or misdiagnosed. One that is serious is difficulty with swallowing. (dysphagia).  If a tooth is delayed when it ought to be erupting, that is another sign that something is not right. If you have a lump in your gum that could be a symptom of odontoma.  Some may be confused initially with an impacted wisdom tooth.

You could also have a primary tooth that is not coming out as it should. Also, if the bone beneath your tooth is enlarged, your dentist will notice this as a possible sign of odontoma.[4] These are some reasons why you need to keep a good connection with your dentist. That way the dentist becomes familiar with your teeth and oral conditions.

Diagnosis of Odontoma

Odontoma does not usually show external symptoms. These tumors are revealed when the x-rays are examined by the dentist. Although it is true that a delayed tooth or absent tooth may suggest there is a need for further examination. [5]

The presence of an a tumor of dental origin requires further examination to determine what type of tumor it is before further action is taken. In addition, a histological diagnosis of the tissues that were extracted provides valuable information to the dentist.

Odontoma Histology

No one really knows why an odontoma forms. The most likely reasons are trauma and/or infection at the site. Some dentists and researchers believe they are hereditary or they develop because of genetic mutations.[7] One example of an inherited syndrome is known as Gardener Syndrome. It is responsible for a wide range of tumors in the body, including occasional odontoma.[8]  When examined at the cellular level, all of the dental tissues are found, but in an abnormal combination.

Pulp, dentin, enamel and cementum may sometimes resemble a tooth like structure in a compound odontoma. These denticles are found in a surrounding supporting layer of fibrous cells. Since it is decalcified, the enamel looks like spaces around the tiny tooth structures.  [11]   Looking closer, you can see the calicified material either as a solid mass or as multiple, small tooth-like bodies visible by x-rays. Because it is easily separated from its bony location it can be distinguished from other possible tumors.[7]

A complex odontoma has no specific sequence for all of the dental tissue. It does not resemble normal tooth structure. At the cellular level it appears as mostly tubular dentin that encloses hollow spaces. These circular spaces are decalcified but they once held enamel. On the edges there may be a thin layer of cementum which forms a capsule like tissue surrounding the mass. [11]

Histology Picture 1 : ODONTOMA (Complex) Histological features

Histology Picture 2 : ODONTOMA (Compound) Histological features

CT Findings for Odontoma

CT findings refers to the images found by x-rays enhanced by computer tomography(a layered sectional view). These advanced technological images help the dentist see what is inside the tumor before engaging in surgery to remove it.  They are each unique in formation and each arrangement of dental tissue can determine what kind of structure it has. Sometimes a complex odontoma can extend into the nasal cavity and require special attention.[9]

It is important to perform a complete examination beyond a simple x-ray to obtain this additional information.  Sometimes magnetic imaging is recommended (MRI) to gain a thorough analysis of a complex mass.

CT Picture 1 : Adenomatoid Odontogenic Tumor (Axial CT scan in left maxilla in 17 year old girl)

Image source : American Journal of Roentgenology [10]

CT Picture 2 : Ameloblastic Fibroodontoma (Axial CT scan of right maxilla in 10 year old boy)

Image source : American Journal of Roentgenology [10]

CT Picture 3 : Calcifying Odontogenic Cyst (Axial CT scan of mandible in 17 year old girl)

Image source : American Journal of Roentgenology [10]

Treatment of Odontoma

The only real treatment of an these dental tumors is removal by surgery. An early discovery and treatment will be beneficial to the patient. It is a benign tumor made of dental tissue and it is a fairly simple extraction in most cases. A speedy recovery is generally expected. [6]  Some complex tumors can result in complications after extraction. So it is essential to stay in contact with your surgeon. [7]

Research on Odontoma

How often are each of these dental abnormalities found?  Which are more common?  After reviewing 104 cases, 67 were identified as compound and 32 were diagnosed as complex.  It is rare to find both types or multiple odontomas. Only 5 such cases were found in this study.[ 7]

Odontoma Video

References

1. http://medical-dictionary.thefreedictionary.com/odontoma
2. http://medical-dictionary.thefreedictionary.com/…loblastic
3. http://en.wikipedia.org/wiki/Odontoma
4. http://www.rightdiagnosis.com/o/odontoma/intro.htm
5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996496/
6. http://www.ncbi.nlm.nih.gov/pubmed/11340730
7. http://www.SciRP.org/journal/ojst/
8. http://en.wikipedia.org/wiki/Gardner’s_syndrome
9. http://www.thefreelibrary.com/Complex+odontoma+of+the+nasal+cavity%3a+a+case+report.-a0179614104
10. http://www.ajronline.org/doi/full/10.2214/ajr.177.4.1770937
11. http://dentallecnotes.blogspot.in/2011/07/oral-pathology-lectue-note-odontogenic_23.html

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Acanthosis nigricans is a condition where there is an occurrence of discoloration in the skin. This discoloration normally occurs in areas where there are folds, such as the folds in the side of the neck as well as the posterior folds. Moreover, it has been recognized that indeed, the condition highly predisposes children to develop diabetes.

As an added tidbit of information, the first recorded incident of acanthosis nigricans is dated back in the late 1880s in Germany. It was first observed by Unna and Pollitzer. Although in the earlier part of 1880s, a suspected case of acanthosis nigricans was discovered by Addison; however, he misdiagnosed it as a case of Addison’s disease. Moreover, in the early part of the 1900s, about fifty individuals were identified to have been affected by the disease with a tendency to develop internal cancerous growth.

Epidemiology

To date, the precise incident rate of acanthosis nigricans is still not known. However, the cancerous variation of the condition has a fewer incidence than the benign ones. Moreover, acanthosis nigricans has been found to be more common in individuals with darker pigments of their skin; however, the cancerous variation of the condition has no known partiality to any skin color or race.

Also, the condition (both the benign and cancerous ones) has no known partiality to gender as it occurs equally among both sexes. Acanthosis nigricans also has no specific age at which it occurs. The condition can appear at any stage of an individual’s life span; although, it is usually observed in the adulthood stage.

Causes of Acanthosis Nigricans

The exact cause of acanthosis nigricans has not yet been fully elucidated to date. The condition usually occurs at a young age, usually before an individual reaches the fourth decade of life. Moreover, the condition is highly linked with obesity or the condition where there is excessive accumulation of fat in the body that may pose significant health risks to an individual.

Other than that, acanthosis nigricans may also be a hereditary condition. In addition, the condition is also said to be caused by problems in the endocrine system such as Cushing’s syndrome, Acromegaly, Hyperthyroidism, Hypothyroidism and Diabetes Mellitus.

The most frequent etiologic factor associated with acanthosis nigricans is insulin resistance. When there is insulin resistance, the levels of insulin floating around the body will consequently increase. Due to this phenomenon, the excess insulin may accumulate in the skin resulting to skin hyperplasia or the anomalous augmentation of growth.

Pathophysiology

Basically, acanthosis nigricans may be predisposed by the factors mainly responsible for the propagation or increase in production of keratinocytes (main cell types of the epidermis) and fibroblasts in the dermis. Below, the pathophysiology of benign and malignant acanthosis nigricans will be further discussed.

Benign acanthosis nigricans

In the non-cancerous form of acanthosis nigricans, the condition may be instigated by insulin itself or the insulin-like growth factor that initiates the increase in production of cells in the epidermis. Other key players are receptors such as the fibroblast growth factor as well as the epidermal growth factor. In patients having excessive fats in the body, the insulin-like growth factor 1 has a very high tendency to increase, as a result the insulin’s capability to produce accelerated cell growth as well as cell differentiation, is also higher. This is because; the insulin’s high affinity to the insulin-like growth factor causes the increase in the growth of the cell and its differentiation.

Currently, there have been two identified classifications of the condition’s manifestations, which are namely the anomaly in the growth factor of the fibroblast and the syndromes associated with insulin resistance. Moreover, the three usual elements associated with the condition are craniosynostosis, hyperinsulinemia and excessive accumulation of fats in the body.

In addition, other causative factors of acanthosis nigricans are friction and perspiration as evidenced by its dominance in areas of the body where there is presence of folds.

Malignant Acanthosis Nigricans

A factor called transforming growth alpha has been cited as the most likely factor to cause the occurrence of cancerous forms of acanthosis nigricans. Evidences like normalization of the said factor’s level in the blood after the elimination or removal of the tumor in the body has supported the idea that indeed it may be the one responsible for the progression of benign acanthosis nigricans to malignant ones.

Extrinsic factors such as medications have also been cited as causative factors for malignant acanthosis nigricans. Medications, especially the ones that utilize parenteral routes may have the tendency to activate insulin-like growth factors in the injection site.

Moreover, there are a lot of disorders that are highly associated with acanthosis nigricans. Examples of these disorders are Acromegaly, Barter syndrome, Bloom syndrome, Dermatomyositis, Phenylketonuria, Pituitary hypogonadism, Rud syndrome, Wilson syndorme as well as Lupus erythomatosus among others.

Signs and Symptoms

Initially, the first clinical manifestation that can be observed in acanthosis nigricans is the darkening of the skin with accompanying thickening of the area. There may be itching and it can then progress to dark macules. Lastly, it may then develop into a very tangible plaque when touched. In malignant forms of acanthosis nigricans, these skin manifestations may appear before, on or after the tumor presentation. Moreover, in malignant acanthosis nigricans, the itching may be considerably higher.

As  stated above, frequent locations of the condition are in areas of the body where there are folds such as the neck, groin and armpit; with the back side of the neck being the most frequent site in children. In addition, lesions of the condition may also develop in moist areas of the body such as the mouth and the mucosa of some parts of the gastrointestinal tract including the esophagus. In other cases, even the areola may be affected.

Types of Acanthosis Nigricans

There are nine known types of acanthosis nigricans, which will each be discussed below.

Obesity-related type

The obesity-related type is the most frequently occuring type of acanthosis nigricans so far. Lesions usually develop in older people than in younger ones. Although, not all may have resistance of insulin, it is usually common in this type and since it is obesity related, the symptoms may consequently disappear as the weight is trimmed down.

Syndromic type

As can be inferred from the name itself, this type of acanthosis nigricans is linked with a syndrome. For instance, there are two types of syndromes that are associated with acanthosis nigricans, which are namely the types A and B. The first type is associated with hereditary links, especially common in young women with abnormally elevated levels of testosterone. The second type, on the other hand, is linked with various conditions such as Hashimoto thyroiditis, Sjogren syndrome, Scleroderma and SLE among others.

Acral type

This type of acanthosis nigricans happens in individuals who are relatively healthy, other than, of course, their acanthosis nigricans condition. This type is mostly common in dark skinned individuals such as the African American race.

Unilateral type

This type of acanthosis nigricans is hereditary and is usually acquired through an autosomal dominant manner. In this type, the lesions may develop in various stages of an individual’s life span, may it be in the infancy or in the adulthood stage. Moreover, these lesions have a tendency to have a continuing growth before it stops to its optimal size.

Generalized type

This type of acanthosis nigricans is uncommon and has no known predisposition to cancerous acanthosis nigricans.

Familial type

This type of acanthosis nigricans is also usually uncommon and just like the unilateral type; it is usually acquired through an autosomal dominant manner. Moreover, the lesions usually develop from early childhood and usually stops during the teenage years.

Drug-related type

This drug-related acanthosis nigricans may be linked to the use of various medications such as corticosteroids, nicotine as well as insulin among others, with the nicotinic acid being the most frequently linked drug to the development of the condition. However, the drug-related acanthosis nigricans along with its associated lesions may disappear after the discontinuation of the related medication.

Malignant type

Obviously, the malignant type is the worst type of acanthosis nigricans that an individual could possibly have. Although there are a lot of possible associations with various carcinomas, the most frequently associated carcinoma is the ones that are in the gastrointestinal tract, especially gastric adenocarcinoma. Moreover, the mouth, including the lips may be severely affected.

Mixed type

As can be inferred from the name itself, the mixed type of acanthosis nigricans is characterized by a combination of two or more of the above-mentioned types.

Differential Diagnosis

Differential diagnoses should also be done to rule out other similar disorders such as Pellagra, Hemochromatosis and Addison’s disease among others.

Procedures and Tests

It may be helpful to perform tests to measure the level of glycosylated hemoglobin in the individual’s body, as well as, test for glucose tolerance. In some cases, a biopsy performed in the skin may be necessary as the need of it may arise.  Moreover, it may also be necessary to test for the level of plasma insulin in the body to consequently discover or come into light the occurrence of insulin resistance in an individual.

Treatment for Acanthosis Nigricans

Medical Management

To date, there is still no routine treatment regimen for the management of acanthosis nigricans. Usually, the objective of most medical managements is to cure the causal or primary disease condition that leads to the development of acanthosis nigricans, in the first place. Moreover, the accompanying lesions in the condition usually do not pose a significant health risk and its management is solely for cosmetic matters only. However, the following may be helpful in the resolution of acanthosis nigricans:

• As stated above, obesity or the excessive accumulation of fats in the body is one of the main factors to the development of acanthosis nigricans. Hence, a healthy reduction of weight as well as healthy control of glucose intake may be helpful in the resolution of the condition.
• On the other hand, in the case of drug-related acanthosi nigricans, the discontinuation of the causative medications may be necessary in order to resolve the appearance of acanthosis nigricans.
• Experts also suggest the inclusion of fish oil in the diet of the patient, as it may help in the resolution of the generalized type of the condition.
• There are also topical creams that have posed promising results. Examples of these topical creams are keratolytics such as ammonium lactate, as well as depigmenting topical soluctions, usually in triple combination. The use of sunscreen in a daily manner may also help in the resolution of acanthosis nigricans.
• Aside from topical agents, there are also oral medications that posed promising results in the resolution of acanthosis nigricans. Examples of these oral medications are metformin, isotretinoin, as well as etretinate.
• Type A syndromic forms may also be treated with the utilization of metformin and contraceptives taken orally.
• Lesions may also be significantly reduced by using available laser therapies such as dermabrasion among others.
• For malignant acanthosis nigricans however, the first line of treatment is surgical intervention. The tumors are surgically removed. Moreover, cyproheptadine is usually used for the management of malignant types of acanthosis nigricans as it may hamper or hinder the liberation of tumor materials.
• Lastly, the utilization of Psoralen in combination with ultraviolet A may help relieving symptoms of malignant acanthosis nigricans.

Also, as acanthosis nigricans involve various systems in the body, like the endocrine system, a collaborative team effort may be necessary to achieve optimal management of the patient. Because of this, different specialists may be needed such as the family physician, dermatologist for the skin care, geneticist to determine familial or genetic links, oncologist for malignant cases of acanthosis nigricans and the endocrinologist for the management of endocrine signs and symptoms.

Patient Education

An integral part of the medical management for acanthosis nigricans is patient education. The patient should be informed that acanthosis nigricans is not a disease in itself, but a resulting condition of another causative disease. Proper diet and healthy reduction of weight should be included in educating the patient.

Prognosis

The malignant type of acanthosis nigricans have shown poor prognosis, with an estimated life span of two years upon onset of malignant signs and symptoms.

Acanthosis Nigricans Pictures

Picture 1 : Acanthosis Nigricans on axilla (on of the most common sites)

Image source : Wikipedia.org

Picture 2 : Acanthosis Nigricans on neck (on of the most common sites)

Picture 3 : Acanthosis Nigricans on body

References

http://en.wikipedia.org/wiki/Acanthosis_nigricans

http://emedicine.medscape.com/article/1102488-overview

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Cherry angiomas are quite common types of vascular lesions that appear on the skin. They are usually dilated capillaries or the excessive clumping of blood vessels. They may appear as cherry-red papules or purplish in color. Cherry angiomas are also known as Campbell De Morgan spots after the British surgeon who first took notice of these clusters of lesions. Senile angioma is another name given as its proliferation increases over age.

Cherry angiomas are known to increase with age, specifically after 40 years old. The exact cause is still unknown but it can appear to any areas of the skin.

What are the Characteristics of Cherry Angioma?

• Cherry angiomas usually appear like bright cherry-red papules or are purplish in nature.
• They would occur in any surface area of the skin but is most common on the trunk or the torso. The face, scalp, neck, arms and legs are also probable sites for the development of cherry angiomas. The papules seldom appear on the hands and feet.
• The papules may be flat topped and may start as small dots or pinheads.
• They are usually quite smooth or they can be elevated and stick out from the skin.
• Cherry angiomas may increase in size and diameter. They would also tend to expand in thickness as it continues to grow larger.
• Some cherry angiomas may adapt a mushroom or dome shape as it becomes larger.
• Polypoid angioma is the name given to several adjoining angiomas.
• Cherry angiomas are usually painless and not harmful. However, large cherry angiomas may bleed excessively if injured because of the proximity of the blood vessels of the angiomas to the skin.

Causes of Cherry Angioma

• The cause of the development of cherry angiomas is idiopathic in nature though they have been linked with genetic tendencies. This lack of information is probably due to the disinterest regarding the subject as these lesions are usually benign and rarely indicate malignancy.

• Cherry angiomas usually occur after 40 years of age though they may start appearing as early as 30 years old. However, there may also be incidences when they start to appear spontaneously in younger people.

• There are two mechanisms involved that may lead to the possibility of cherry angiomas:

• Angiogenesis refers to the growth and formation of new blood vessels from current and existing blood vessels.
• Vasculogenesis, on the other hand, refers to the formation of new blood vessels as they are and without any pre-existing blood vessels.

• Certain chemicals and compounds have also been linked with the development of cherry angiomas. These include but are not limited to bromides, butoxyethanol, cyclosporine and mustard gas.

• An increase in mast cells, which are cells usually rich in histamine and heparin, has also been associated with the proliferation of cherry angiomas.

Exams and Tests for Diagnosis

Diagnosis for cherry angiomas is usually made on the basis of the physical appearance of the lesion growth. A skin biopsy may be indicated to confirm the diagnosis. Usually there are no other laboratory studies that may be required unless histopathologic confirmation is necessary to rule out malignancies.

Treatment and Removal

Cherry angiomas may or may not be treated as they are usually harmless or painless. The main reasons, however, for their removal is for aesthetic purposes as well as if the lesions tend to bleed frequently.

There are several treatment options for the removal of cherry angioma:

Cryosurgery

This is the use of extremely cold temperature to eradicate abnormal tissue. Ice crystals would form around the cells until such time that the cells would tear apart. The blood vessels of the abnormal tissue are also damaged when they become frozen. Argon, carbon dioxide, liquid nitrogen, dimethyl ether – propane are the most common chemical compounds that are used for this procedure.

It is not as invasive as other procedures and causes minimal pain and scarring. Localized pain and redness may be managed with analgesics like acetaminophen, aspirin and ibuprofen. In addition, it is a cost effective therapy. The risks associated with cryosurgery are damage to the nerve tissues and scarring.

Electrosurgery

This procedure utilizes the application of an electric current to the abnormal tissue to destroy it. Electrosurgical devices are used and alternating current is used in directly heating the tissue. The risk of scarring may be avoided if done by a skilled professional.

Electrocautery

This procedure uses heat conduction by an electric current through a heated metal probe. This procedure is different from electrosurgery due to the differences in the electric current used. However, the use of electrocautery has been controversial because of the toxicity of the surgical smoke emitted during the procedure.

Pulsed Dye Laser

This procedure makes use of an organic dye as the active laser medium. The dye would usually come in a liquid preparation but can also come in solid or gas state.

Intensed Pulse Light (IPL)

This procedure utilizes various wavelengths in targeting various skin treatments including removal of vascular lesions. It is much more commonly used as a form of hair removal technique. However, there may be contraindications for the application of this treatment, which include seizures, sunburn, hypertrophic scarring and moles.

Shave Excision

This is done by removing the lesion through the use of a blade. Bleeding may be stopped through the use of aluminum chloride or electrocautery.

Natural Remedies for Cherry Angiomas

There are also natural remedies, which may be used in treating cherry angiomas. These remedies utilize natural ingredients provided by nature.

1. Sandalwood powder may be mixed with fresh basil leaves to make a paste.
2. Crushed leaves of strawberry may also be used.
3. Witch hazel is also helpful in eliminating bacteria after a shower.

Although cherry angiomas are usually not dangerous and need not necessarily be treated, it is important to have them checked by a dermatologist if multiple angiomas are noted in a short span of time. This is important to rule out internal malignancies. In addition, it is important to remember that the cherry angiomas should not be punctured because of their risk to bleed profusely.

Cherry Angioma Pictures

Picture 1 : Cherry Angioma photo

Picture 2 : Cherry Angioma

Picture 3 : Cherry Angioma image

Picture 4 : Cherry Angioma on shoulder

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Arthrogryposis is a non progressive neuro-musculoskeletal, congenital disorder characterized by various joint contractures. It is also known as arthrogryposis multiplex congenital (AMC). Contractures, muscle weakness, stiffness, poor mobility or immobility and fibrosis are usually the presenting signs and symptoms of this condition. The term “arthrogryposis” is derived from the Greek terms “arthro,” which means joint and “gryp” meaning curved.

Classification (Types)

Arthrogryposis consists of various subgroups (types) depending on the signs and symptoms as well as the causes. The different classifications of arthrogryposis would also depend on the joints affected. Some of the most common classifications include but are not limited to:

• Arthrogryposis ectodermal dysplasia
• Arthrogryposis multiplex
• Gordon Syndrom
• Illum Syndrome

Arthrogryposis Picture

Picture : Arthrogryposis

Image source : gfmer.ch

Causes of Arthrogryposis

The exact cause of arthrogryposis is unknown though there are various theories surrounding the condition. In addition, there is said to be no link as to it being a genetic or hereditary condition though there is a rare autosomal recessive trait of the disease.

The following theories are thought to be connected to the condition:

• Obstructions to uterine movement during pregnancy.

This results to arthrogryposis as there is limitation for normal joint movement of the fetus. The development of the joints may be normal but due to the lack of movement, extra connective tissue tends to grow and develop around it.  The tendons are also not fully stretched to their normal length because of the lack of movement.

Obstructions during pregnancy may be caused by the inadequate shape of the uterus of the pregnant woman or if there is a lack amniotic fluid.

• Fetal hyperthermia.

Fetal hyperthermia may take place if the pregnant woman develops fever during the pregnancy. This could also be the result of a contracted viral infection like German measles or could also be caused by prolonged soaks on hot tubs.

• Failure of the nervous system and muscular system to develop.

Impairment of the nervous system and muscular system to develop fully and appropriately could also lead to arthrogryposis. Usually, it is the spinal cord and the central nervous system which fails to develop fully. Nervous system impairment could include spinal muscular dystrophy, spina bifida and brain defects while neuromuscular ailments would include multiple sclerosis, myasthenia gravis and myotonic dystrophy.

• Maternal conditions during pregnancy.

Excessive alcoholism, smoking and exposure to certain drugs like phenytoin (Dilantin) have also been linked to the development of arthrogryposis.

How is Arthrogryposis Diagnosed?

• Up to date, there is still no prenatal diagnostic tool that is available.
• Taking a look into the medical history and performing physical examination can help the doctor make a diagnosis.
• Radio-graphic examination is usually utilized to confirm diagnosis for Arthrogryposis.
• Blood tests, muscle findings and other imaging studies may also be utilized to confirm diagnosis and to rule out other medical conditions.

Signs and Symptoms

There are different clinical manifestations for Arthrogryposis. Signs and symptoms would usually depend on the joints and muscles involved.

• Muscle weakness
• Limited mobility or immobility of the joints
• Possible displacement of the hip joints
• Facial deformities may also be present
• Inward rotation of the shoulders
• Abnormal extension of the elbows
• Abnormal flexion of the wrists and fingers
• Clubfoot

Treatment and Therapy

Unfortunately, there is no cure for arthrogryposis but improvement to the quality of life is possible. Treatment would usually need a multidisciplinary approach depending on the problem. In addition, responses to treatment would also be individualized with each patient responding or reacting to treatment differently.

• Surgery may be indicated for children depending on the problem. Orthopedic surgical operation can help improve mobility and correct joint problems by releasing muscle tensions and bony fusions as well as tendon transfers. Facial deformities may also be corrected.Children with cardiac anomalies like congenital heart defects would also require corrective heart operation.

• Physical therapy is also necessary to strengthen, stretch and provide mobility training to improve movements. Some doctors prefer physical therapy to be done prior to surgery as this would allow them physical assessment on the allowable range of motion the child is capable of. Parents are usually taught this therapy session as this would allow them to be performed even at home and several times a day. Physical therapy session eventually progresses on depending on the child’s developmental stage and should therefore be a continued process.

• Occupational therapy is also indicated to help in the improvements of activities of daily living and fine motor skills. These activities would include feeding, bathing and dressing. Fine motor skills are also the focus with occupational therapy.

• Psychological therapy may also be indicated in cases with depression and low self-esteem among children.

• In addition, there are different adaptive tools especially made for children with arthrogryposis that can help parents in managing their children. These include but are not limited to standers, pedi wraps, crutches, gait-trainers, walkers and mouth sticks.

• Water rehabilitation is another therapy gaining popularity as an exercise alternative for children with arthrogryposis. Water helps in relieving painful joints by decreasing pressure on weight bearing joints, muscles and bones. Moreover, water promotes relaxation at the same time provides resistance during motion exercises.

• Hippotherapy or horse-riding therapy is another alternative mode of therapy which is utilized because of the similarities associated with human movement of the pelvis to that of the horse’s gait when walking. This form of therapy has found to be beneficial in improving function, posture and mobility of the joints and muscles.

Complications

The most common complications of the condition include pulmonary hypoplasia, scoliosis, delayed physical growth, abdominal hernias and mid facial hemangiomas.

Prognosis and Life Expectancy

Children with Arthrogryposis would continue to have limited muscular and joint mobility because of the condition but since it is non-progressive, the condition would not worsen. Since there is no cognition and speech problems, children with this condition can continue to have substantial life improvements and have the potential to lead rewarding and independent lives unless altered by other medical conditions.

Arthrogryposis is a medical condition that is best left treated and managed by doctors. It requires multidisciplinary effort to be able to achieve the best outcome for those affected with the condition but prognosis is usually good especially if problems are addressed at an early age.

Please note : The life span for an person with this condition is usually normal, but when associated with Nervous system and Heart problems, it can be altered.

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Corticobasal degeneration, otherwise termed as, Corticobasal ganglionic degeneration or CBGD, is a kind of neurodegenerative disorder concerning a certain protein, called tau. In the disorder, there is an abnormal or unhealthy assembly of the tau protein in an individual’s brain.

This phenomenon is medically referred to as tauopathy that ultimately leads to the deterioration or the degeneration of the individual’s brain. Generally, the main parts of the brain that are directly involved are the basal ganglia and the cerebral cortex. Moreover, corticobasal degeneration is also a progressive disorder; meaning, it worsens as time passes by.

As an added information, a group of physicians led by doctor Rebeiz in the late 1960s first observed the occurrence of corticobasal degeneration in three affected people exhibiting the hallmark characteristics of the disorder.

Epidemiology

Corticobasal degeneration is a rather uncommon disease and usually occurs in people in their advanced age, usually in the sixth decade of life. However, the youngest age recorded to have had the disease was at 28 years old. Both sexes, males and females may be affected by the disorder; however, the disorder is more likely to occur in the female population more than the male population.

Recent studies show that the disorder’s prevalence most likely fall under a 5 to 7 per 100,000 individual rate and have multiplied in great amounts since the disorder’s discovery. This multiplication in number is indicative of a more sensitive diagnosis or simply, corticobasal degeneration is more frequently occuring in the present days.

Moreover, corticobasal degeneration has no known racial partiality; meaning, it can occur equally through different races.

Causes

The definite cause of corticobasal degeneration has not yet been fully elucidated; however, some reports have identified familial or genetic factors. The particular gene of interest that has been the focus of research studies, associated with corticobasal degeneration is the gene in chromosome 17.

Pathology

Corticobasal degeneration affects both the subcortical as well as the cortical parts of the human brain. Moreover, glial cells as well as nonpyramidal neurons and pyramidal neurons are also affected. As mentioned above, corticobasal degeneration is characterized by an abnormality called tauopathy. Presently, the disorder is categorized under the classification 4-repeat tauopathy.

This distinction is the main factor that sets corticobasal degeneration apart from its similar diseases such as Alzheimer’s disease and progressive supranuclear palsy. The basal ganglia and the cortex of the brain are characterized by puffed-up neurons as well as achromasia or the lack of staining in the cytoplasmic area. In addition, a loss of neurons both in the cortical as well as in the subcortical area may also occur due to the disease. In addition, histologic findings reveal atrophy in the frontoparietal area as well as entanglement of neurofibrils.

Picture : Corticobasal degeneration in 84 year old woman

Note : A: Coronal T1-weighted image  B: Macroscopic specimen (subthalamic nuclei showing brownish changes) C: Microscopic examination (gliosis is seen)

image url : ajnr.org

Symptoms and Signs

Corticobasal degeneration may be categorized into two. It may be a syndrome of motion problems as well as cognitive difficulty, or it may be a disease entity per se. Regardless, these motion and cognitive problems are usually utilized as early indicators that the disease is present. Moreover, motion problems are usually assymetrical in nature; meaning, what happens in one side of the body won’t necessarily happen on its counterpart. For example, a motion problem on the right hand may not necessarily occur in the left hand and vice versa.

In addition there are four signs and symptoms (both motion and cognitive) that are major characteristics associated with corticobasal degeneration. These signs and symptoms are apraxia, alien hand syndrome, aphasia and parkinsonism. Each of these four characteristics will be further discussed below.

Apraxia

Apraxia is a condition wherein an individual loses the ability to perform tasks that are normally familiar and are previously done without difficulty. In the case of corticobasal degeneration, ideomotor apraxia most likely occurs; this apraxia may affect both of the upper and lower extremities. For example, an individual may have difficulty to initiate a simple act of walking, as both feet may seem to be glued in the ground. In addition, apraxia may also occur and affect fine motor movements normally performed by the hands as well as the digits.

Alien hand Syndrome

Alien hand syndrome is fairly common in people with corticobasal degeneration. From the word itself, an individual may sense a feeling of alienation from his or her own hands. This happens because the individual affected may have a difficulty, or entirely lose the ability to control his or her own hands, hence the feeling of alienation. Moreover, alien hand syndrome in corticobasal degeneration is asymmetrical in nature. As explained above, asymmetrical means that an alien hand syndrome in the right hand do not necessarily entail an alien hand syndrome in the left hand or vice versa. Lastly, alien hand syndrome do not occur without reason. It actually is caused by an outside stimulation or otherwise known as external stimuli.

Aphasia

Aphasia in corticobasal degeneration is characterized by the inability to initiate a verbal act. In other words, the individual loses the capability to speak a word or to converse in a dialogue, resulting to defected patterns of speech and essential words in a sentence necessary to form a coherent thought are being omitted. As the disease progress into its late course, the individual ultimately loses the capability to utter a word.

Parkinsonism

The most common sign and symptom of Parkinsonism in corticobasal degeneration is the rigidity of the limb. Other common signs and symptoms are various disorders of the individual’s gait and bradykinesia. As in other manifestations of corticobasal degeneration, Parkinsonism is also assymetrical in nature and most likely affects the individual’s limbs.

Other motor and cognitive signs and symptoms found in corticobasal degeneration are as follows:

• Presence of depression,
• Amnesia,
• Impairment in judgment,
• Impaired movements of the eye (usually horizontal and upgrade impairments),
• Problems in gait,
• Involuntary or uncontrolled jerking of the muscles or medically referred to as myoclonus,
• Sensory loss of a cortical origin, and;
• Spatial neglect

The presence of major hallucinations however, is indicative that the patient do not actually have corticobasal degeneration, instead the patient may have Lewy body disease (diffused).

Diagnostic Tests and Laboratory Studies

The diagnosis of corticobasal degeneration is rather uneasy to do, due to the fact that its signs and symptoms very much resembles that of other diseases such as Alzheimer’s disease, Parkinson’s disease, as well as Pick complex disease. Moreover, in order to do a correct and accurate diagnosis, experts have developed a standard set of signs and symptoms or characteristics that are present in each stage of the disease as it progresses. This is done because the disorder is progressive in nature and different signs and symptoms may occur at each stage.

As it is said, corticobasal degeneration very much resembles other diseases such as Alzheimer’s disease, Parkinson’s disease, as well as Pick complex disease. That is why it is important and essential to do differential diagnoses to separate corticobasal degeneration from the three mentioned diseases. This is done to ensure proper and appropriate medical management for the respective disorders. However, other than those mentioned diseases, differential diagnoses are also done to differentiate corticobasal degeneration from the following disorders:

• Cardioembolic stroke,
• Thalamic stroke,
• Epilepsia partialis continua,
• Huntington disease,
• Creutzfeldt-Jakob disease,
• Hydrocephalus,
• Neuroacanthocytosis,
• Wilson disease,
• Whipple disease,
• Thyroid disease, and;
• Striatonigral degeneration

Laboratory studies are also performed for various purposes such as determination of cognitive causes. These laboratory studies are the following:

• Ceruloplasmin,
• Level of B-12 in the body,
• Tests for thyroid function,
• Complete blood count, and;
• Electrolyte levels

Magnetic resonance imaging or MRI of the brain is also performed to determine the size and form of the midbrain (if corticobasal degeneration is present, the midbrain size should be fairly normal), determine cortical atrophy and evaluation of the basal ganglia, whether if it exhibits atypical signal.

Other tests performed are tests for the evaluation of the patient’s neuropsychological state as well as electroencephalography.

On the other hand, other procedures that are performed are lumbar puncture for the evaluation of the cerebrospinal fluid, jejunal biopsy, PCR test or polymerase chain reaction test to determine presence of Tropheryma whippleii and brain biopsy.

Medical Management and Treatment

Presently, there is unfortunately no definitive cure for the disorder, as its definitive cause has not yet been fully elucidated. However, essentially, the medical management for corticobasal degeneration is divided into three evaluations, which will be discussed below.

First evaluation

During the initial evaluation, the medical care focuses on alleviating or treating presenting signs and symptoms or the symptomatic approach to treatment. Discontinuation of various medications may be necessary such as ceasing anticholinergic drugs to prevent damage in memory and attention function of the individual. However, if the patient already has memory loss, patient may be prescribed with Vitamin E as well as antioxidants. Aside from that, medications that may possibly cause Parkinsonism are also ceased. Moreover, if symptoms of rigidity are already debilitating to the patient, a regimen for levodopa may be started. Also, if the dystonia of the limb are already painful, injections of botulinum toxin may be instituted.

Second evaluation

During the follow-up evaluation, or the second part of the medical management, treatment of associated systemic situations identified in the serologic examinations may be started. If in the second evaluation, rigidity is still present, indicating that the levodopa treatment is ineffective, then discontinue the regimen and institute other line of medications such as dopaminergic drugs in the third line.

Third evaluation

In the third and last evaluation, systemic situations that have presented further through the course of the disease are being recognized and treated appropriately. Modifications in dopaminergic regimen may also be done if prior dopaminergic drugs are rendered ineffective.

Moreover, the activity of the patient is not limited or restricted; however, physical assistance may be needed as the disease progresses to its late stage.

Supportive therapies

Along the course of the three evaluations, supportive therapies are done to aid in the medical management of corticobasal degeneration. Examples of these supportive therapies are as follows:

• Electroencephalography or EEG for the identification of myoclonus,
• Consultation to various specialized therapists such as speech, physical as well occupational therapists for the planning of appropriate physical activities, safety assessment and evaluation of possible assistive devices if needed for the patient,
• Management of associated dementia by providing reading materials (online materials such as the CGBD caregivers report are very helpful to families with members having corticobasal degeneration) and referring the patient and significant others to a case manager or other resource persons for the management of associated dementia,
• Spinal tap may also be done to rule out Whipple disease; however, proper evaluation and great care should be practiced since a spinal tap may cause subdural hematoma if the patient has cerebral atrophy,
• Lastly, brain biopsy may also be done if the patient and his/her significant others so desire

Diet

Patient with corticobasal degeneration may develop dysphagia or the difficulty to swallow, hence proper adjustment regarding the patient’s diet may be necessary. Depending on the extent of the dysphagia, the patient may be subjected to a soft food diet to a thickened liquids diet.

The patient may also experience constipation, hence proper diet adjustment considering constipation may also be necessary such as increase in fluid intake and intake of high-fiber foods. Medications such as laxatives and stool softeners may also be prescribed as well as promotion of the patient’s physical activity.

Follow-up

Regular follow-up should be done to monitor the patient as well as the condition’s progress and to adjust medication regimens such as dopaminergic therapies.

Prognosis

As mentioned above, corticobasal degeneration is a progressive disease, hence, both the cognitive as well as the motor problems of the patient worsens as time passes by. According to recent records, the individual affected by corticobasal degeneration has roughly eight to ten years of life from the onset of the disease.

Normally, the patient does not die due to the disorder per se, but due to the complications that comes along with the disease such as complications in the respiratory system (aspiration pnuemonia) and various infections.

References

http://en.wikipedia.org/wiki/Corticobasal_degeneration

http://emedicine.medscape.com/article/1150039-overview

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