Benign Fibrous Histiocytoma or Dermatofibromas  is a rare tumor of mesenchymal origin. First described in 1958 by Dahlin. They are composed of two cell types, namely atypical fibroblasts and histiocytes, arranged in a storiform pattern. Lipid-filled cells may be conspicuous and occasionally are the major component. These types of benign fibrous histiocytomas are known as xanthomas or fibroxanthomas. Benign Fibrous Histiocytomas are microscopically very similar to non-ossifying fibroma. It is essentially a non ossifying fibroma that grows in and unusual location or in an unusual age group.

Causes

Is it a Dermatofibroma or a Mole?

The cerebral cortex of the brain has 4 lobes on each side: the frontal lobe, the temporal lobe, the parietal lobe and the occipital lobe. Each of these regions carries out specific functions, and damage to any of these areas results in corresponding impairment. The frontal lobes are relatively large compared to other regions of the brain, and the extensive functions controlled by the frontal lobe reflects that large size.

Occipital Lobe Strokes:

Fig: branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus.

Of the 4 major lobes of the brain, the occipital lobe is the smallest—but in our daily lives, we perhaps lean on it the most. The lobe is located at the back of the skull, thus the name (“occipital” comes from the Latin for “back of the head”).

The occipital lobe’s purpose is to receive visual stimuli from the eyes, process the information, and forward the information to the frontal lobe (which will formulate a response). Put simply, the occipital lobe controls our ability to respond to things we see. However, that role is far more complex than we may understand at first.

While sight is probably our most valued senses, it’s also the one that’s most taken for granted. Because we use our sight so instinctively, we often forget about how incredible our sight truly is. Take a second and look at an object in the distance. A simple task, yes?

Except in that split second it took you to pick an object, your brain not only focused your center of vision on it, but it processed its contour, distinguished it from the objects around it, located its distance away from you, identified its size relative to the objects around it, and probably understood its relative size to you.

That’s a great deal of information to receive and process correctly in a split-second, but it’s what your occipital lobe does thousands of times every day. All told, your “ability to see” is actually a series of abilities that is made possible by the different parts of the occipital lobe.

CONSCIOUS & UNCONSCIOUS PROCESSING

Because our understanding of the world around us leans so heavily on sight, we associate our ability to see with our conscious decisions. For example, there are laws nationwide that address the problem of distracted driving. Lawmakers are facing a whole new generation of people behind the wheel who do not place their complete, conscious focus on the road.

Now, Plasticity Brain Centers is certainly not recommending texting while driving or anything similar, but sight depends on far more than conscious attention. In addition to the things you are focusing on, the occipital lobe is constantly processing visual stimuli that you may not be consciously aware of. This can result in something truly remarkable known as “blindsight.”

SEEING /WITHOUT SEEING: DAMAGE TO THE OCCIPITAL LOBE:

The condition we call “blindness” has two possible, general causes. The common one we know of is caused by damage to the eyes themselves. Because the receptors are damaged, the functioning occipital lobe receives no stimuli, so the brain cannot formulate a response to the outside world. In some of these cases, the occipital lobe becomes an additional site of processing for aural stimuli—which is why blind people seem to have incredible hearing or can respond to obstacles through sound.

However, the less common cause of blindness is a result of damage to the occipital lobe. For example, lesions on the occipital lobe can result in a “hole” in your vision known as a scotoma. Extensive damage can result in total blindness. Unlike other lobes of the brain, damage to one side of the occipital lobe can result in damage to both eyes’ fields of vision.

However, in these cases, the eyes are still completely functional. They continue to receive information, except the occipital lobe is not processing it correctly. While this results in a kind of blindness, some processing can still occur that isn’t consciously understood. For example, studies have been conducted on patients who are blind in one eye due to occipital lobe damage. Despite not being consciously aware of what they are seeing, these patients were able to navigate obstacles or detect movement without perceiving what they were seeing.

Treatments 

Plasticity Brain Centers leverages the complex relationship between receptors (eyes, skin, tongue, nose, ears), stimuli, and their corresponding lobes (occipital, parietal, temporal, frontal) through clinical neuroscience. In other words, we use receptors of different kinds to create tests and targeted therapies for the damaged parts of our patients’ brains.

For damaged or underperforming occipital lobes, we employ visual stimuli such as eye movement training, visual search exercises, hand-eye coordination exercises, or light therapy to rebuild or create pathways between neurons. These pathways can bypass damaged tissue or rebuild old pathways in order to restore visual processing power.

Our therapies can improve a patient’s ability to perceive depth, distinguish objects from their surroundings, identify objects or people more quickly, and track objects with their sight more accurately. By understanding the state of your occipital lobe, we can more precisely identify why your sight is suffering and how we can restore function to the visual processing part of your brain.

Any time an internal body part pushes into an area where it doesn’t belong, it’s called a hernia.

The hiatus is an opening in the diaphragm — the muscular wall separating the chest cavity from the abdomen. Normally, the esophagus(food pipe) goes through the hiatus and attaches to the stomach. In a hiatal hernia (also called hiatus hernia) the stomach bulges up into the chest through that opening.

There are two main types of hiatal hernias: sliding and paraesophageal (next to the esophagus).

In a sliding hiatal hernia, the stomach and the section of the esophagus that joins the stomach slide up into the chest through the hiatus. This is the more common type of hernia.

Leprosy is an infectious disease that causes severe, disfiguring skin sores and nerve damage in the arms, legs, and skin areas around the body. You can catch it only if you come into close and repeated contact with nose and mouth droplets from someone with untreated leprosy. Children are more likely to get leprosy than adults.

Fig: Leprosy on hand and leg

Causes: Leprosy is caused by a slow-growing type of bacteria called Mycobacterium leprae .

Symptoms:

Leprosy primarily affects the skin and the nerves outside the brain and spinal cord, called the peripheral nerves. It may also strike the eyes and the thin tissue lining the inside of the nose. The main symptom of leprosy is disfiguring skin sores, lumps, or bumps that do not go away after several weeks or months. The skin sores are pale-colored.

Nerve damage can lead to:

• Loss of feeling in the arms and legs
• Muscle weakness

It usually takes about 3 to 5 years for symptoms to appear after coming into contact with the leprosy-causing bacteria. Some people do not develop symptoms until 20 years later. The time between contact with the bacteria and the appearance of symptoms is called the incubation period. Leprosy’s long incubation period makes it very difficult for doctors to determine when and where a person with leprosy got infected.

Types of Leprosy:

• A mild, less severe form of leprosy. People with this type have only one or a few patches of flat, pale-colored skin (paucibacillary leprosy). The affected area of skin may feel numb because of nerve damageunderneath. Tuberculoid leprosy is less contagious than other forms.
• Lepromatous. A more severe form of the disease. It has widespread skin bumps nd rashes(multibacillary leprosy), numbness, and muscle weakness. The nose, kidneys, and male reproductive organs may also be affected. It is more contagious than tuberculoid leprosy.
• People with this type of leprosy have symptoms of both the tuberculoid and lepromatous forms.

Diagnosis:

Affected skin send it to lab for biopsy. A skin smear test may also be done. With paucibacillary leprosy, no bacteria will be detected. In contrast, bacteria are expected to be found on a skin smear test from a person with multibacillary leprosy. 

Treatments: 

Treatment depends on the type of leprosy that you have. Antibiotics are used to treat the infection. Long-term treatment with two or more antibiotics is recommended, usually from six months to a year. People with severe leprosy may need to take antibiotics longer. Antibiotics cannot treat the nerve damage.

Anti-inflammatory drugs are used to control nerve pain and damage related to leprosy. This may include steroids, such as prednisone. Patients with leprosy may also be given thalidomide, a potent medication that suppresses the body’s immune system. It helps treat leprosy skin nodules. Thalidomide is known to cause severe, life-threatening birth defects and should never be taken by women who are pregnant or women who may become pregnant. 

Leprosy Complications

Without treatment, leprosy can permanently damage your skin, nerves, arms, legs, feet, and eyes. Complications of leprosy can include:

• Blindness or glaucoma.
• Disfiguration of the face (including permanent swelling, bumps, and lumps).
• Erectile dysfunctionand infertility in men.
• Kidney failure.
• Muscle weakness that leads to claw-like hands or an inability to flex the feet.
• Permanent damage to the inside of the nose, which can lead to nosebleedsand a chronic, stuffy nose.
• Permanent damage to the nerves outside the brainand spinal cord, including those in the arms, legs, and feet.

Nerve damage can lead to a dangerous loss of feeling. A person with leprosy-related nerve damage may not feel pain when the hands, legs, or feet are cut, burned, or otherwise injured.

Spinal muscular atrophy (SMA) most often affects babies and children and makes it hard for them to use their muscles. When your child has SMA, there’s a breakdown of the nerve cells in the brain and spinal cord. The brain stops sending messages that control muscle movement.

When that happens, your child’s muscles get weak and shrink, and he can have trouble controlling head movement, sitting without help, and even walking. In some cases, he can have trouble swallowing and breathing as the disease progresses.

Woman with muscular atrophy

Diagnosis

SMA can sometimes be hard to diagnose because the symptoms may be similar to other conditions. To help figure out what’s going on, your doctor may ask you:

• Has your baby missed any developmental milestones, such as holding his head up or rolling over?
• Does your child have trouble sitting or standing on his own?
• Have you seen your child have trouble breathing?
• When did you first notice the symptoms?
• Has anyone in your family had similar symptoms?

Treatment

The FDA has approved one medication to treat SMA: nusinersen (Spinraza). Studies show it helps about 40% of people who use it by slowing down the advance of the disease and making people stronger.

Doctors inject nusinersen into the fluid around your child’s spinal cord. The procedure for the shot-including preparation and recovery time — can take at least 2 hours. Your child will need multiple shots.

Nusinersen is a type of gene therapy. It belongs to a group of drugs called antisense oligonucleotides that have small bits of man-made genetic material. They work by “modulating,” or adjusting, the SMN2 gene.

Everyone who has spinal muscular atrophy has at least one copy of the SMN2 gene, and some people have more. The SMN2 gene isn’t doing a good job of making a key protein that allows the cells that control muscles to work. Adjusting this gene can let it make more protein or a better-quality protein.

Besides adjusting the SMN2 gene, researchers are studying another type of gene therapy that involves replacing or correcting the SMN1 gene. Since spinal muscular atrophy is caused by a mutation — or change — in the SMN1 gene, doctors are checking to see if replacing or fixing it will treat the disease.