Lumber Degenerative Disk Disease

As humans age, our minds age as well as our body… Really?? Ok, so my point is when our bodies change the our weight distribution on our spine does too. So it only makes sense that many Americans, especially with our obesity percentages *don’t even get me started*, end up with lower back pain. This lower back pain can very easily develop, or stem from, lumbar degenerative disk disease, also known as LDDD. Did you know that the anterior portion of your lumbar spine bears over 90% of the weight we put on the spine? It’s pretty much the Hercules of our body. Therefore, the intevertebral discs act as primary cushions to provide relief and stability to this area.
This pathology has three main stages. The first stage shows small tears around the outer annulus which can be accompanied end plate separation which can then lead to blood supply interruption. These changes could be a result of harmful repetitive movements. The second phase is also known as the unstable phase. This phase is characteristic of loss of disc space height. Herniated disks fit in this category. The third phase is basically just a more intense version of the first two stages. There is further disk space narrowing , further endplate destruction. Which means the pain is greater in this phase as well.
Nearly 13 million of doctors’ visits a year are related to lower back pain. The cause of this pathology is unknown. Treatment that does not include surgical intervention include physical rehabilitation, relative rest, and education. Surgery includes fusions and disk arthroplasty.

http://www.spineuniverse.com/displaygraphic.php/866/ag_290300falatyn_fig2L-BB.gif

http://asme.files.wordpress.com/2007/08/disc.jpg

Dissections in the carotid artery

Carotid Artery Dissection
So I feel like I’m preaching to the choir when I talk about this subject, so I will try and throw in a few fun facts for you. ;) Dissection occurs when there is an initial tear in the intima of the vessel. Which is…the innermost lining of the vessel! From this dissection, stenosis or complete occlusions can very easily occur because there is blood flowing out of the inner AND the outer layers of the vessel. Oh and it gets better. From there, those nasty little occlusions can then lead to production of emboli, which can then shower into the brain and cause an ischemic stroke. Oh and I forgot to mention that complete occlusion can lead to ischemia in the carotid itself. But when that happens the brain is like ok, I can deal and circulates in other areas for the weaker area. It’s the beauty of a bilateral circulation system.
There are two types of carotid artery dissection: spontaneous and traumatic. Spontaneous occurs in about 3 cases out of 100,000. In those with spontaneous dissection cases, some were associated with hereditary connective tissue disorder, or a history of stroke. But these incidences vary. The traumatic side of it is when the neck is severely injured. I wonder how much head banging that would take. Good thing I don’t act like I can do it. Anyway, about .67% of injuries of people in vehicle accidents end up having some kind of carotid injury AND from these 76% had dissections.
Some signs and symptoms of this pathology are neck pain, decreased pupil size, vision loss, and stroke.
Treatments for dissections include of course the thrombolytic medications if an occlusion occurs, observation, or stent placement. From what I gather though, these are treatments assuming that there was some sort of outcome from a dissection.

http://www.medscape.com/content/2004/00/49/79/497907/art-smj497907.fig1.gif

http://www.vascularweb.org/graphics/Article_Contribution_Images/Spontaneous_internal_carotid_ar-9_7_2004_Figure2.jpg

Tuberculosis!!!! Of the Neck!!!

Ok, so we all have heard of this pathology, considering with get shots for this more often than most of us would like. But TB of the neck? So, I’m going to refer to this pathology by its other name considering TB of the neck is just long, so the other name that it’s known for is called

‘Scrofula’. That’s just more fun to say anyway.
So basically what it is is an infection of the lymph nodes in the neck. About half of these patients are known as ‘immunocompromised’. Currently it affects about 5% of the population said to have some form of tuberculosis.

Signs and symptoms to look for with scrofula are chronic, painless abscesses on the neck. They are also known as ‘cold abscesses because they are do not take a reddish color or even the color of skin, but have a bluish, purple tint. This pathology can also cause fever, chills, and weight loss in almost half of these patients. As the lump gets bigger the skin might stretch to its max and bust open causing an open wound. Diagnosis is done by needle biopsies.

So what is there to do about it? Well, surgery doesn’t usually work out to well for the fact that in that kind of environment it is very easy to spread that infection, so the best way to fight it is antibiotics. With this kind of treatment, recovery is pretty much 100%!
http://www.isradiology.org/tropical_deseases/tmcr/chapter5/large5/05-104A.jpg

http://rad.usuhs.mil/medpix/tachy_pics/thumb/synpic44129.jpg CT

Achondroplasia

Achondroplasia is basically is of the most common forms of dwarfism. So obviously is marked by short arms, short legs, and a rather large forehead (frontal bossing). Midface hypotonia *decreased muscle tone* is another characteristic that is an obvious sign, especially in childhood. Spinal curvatures are also common. Motor skills are usually delayed, but life span and intelligence are usually normal. Though in rare cases, this deformity could block an infant’s airway or cause compression on the spinal cord.

This pathology is due to genetics believe it or not! Well, to be more specific, a mutation a certain gene; to be even more specific, the gene FGFR3. So in order to detect this certain mutation, ‘molecular genetic testing’ must be done. This testing is in fact 99% efficient in detecting this mutation. Another form of diagnosis includes radiology, such as CT or MRI. But if it is undetectable in these modalities, then the molecular genetic testing would be done.

This condition is irreversible, but there are ways of monitoring it. It is important to monitor height, weight, and head circumference. It is also important for MRI and CT evaluation to make sure there is no spinal cord compression or severe hypotonia.

Interesting to know, out of the children who are diagnosed with achondroplasia, 80% have both parents of normal stature, which means that the gene mutations or mostly spontaneous. But if a parent has the condition, the infant has a 50% of inheriting it. If both parents have it, the infants chances are increased to 75%.


Below is a T1 weighted MRI image of an infant with achondroplasia. notice the distinct frontal bossing.http://radpod.org/wp-content/uploads/2007/03/achondroplasia_arrows.jpg

Below is a father and a son out exercising, both diagnosed with achondroplasia.http://www.sciencemuseum.org.uk/on-line/genes/images/1-3-5-1-4-2-1-1-1-0-0.jpg

Juvenile Nasopharyngeal Angioblastoma

Juvenile Nasopharyngeal Angioblastoma is a benign tumor of the nasal cavities occurring almost entirely in males anywhere from 14 to 18 years old. The article goes on further more to say that if a female is diagnosed that this particular diagnosis should be questioned and undergo chromosomal studies…wow I know, right? It is most commonly found in the back of the nose and upper throat. This noncancerous growth is not common and occurs in about 1 in 60,000 nose and throat patients. Instead of invading surrounding tissue, it adds pressure which therefore distorts and displaces. This causes necrosis of tissue by pressure. Intracranial extension happen in about 10 to 20% of cases. How the tumor occurs no one knows for sure, but scientists predict it derives from sex-steroid tissue located in the nasal cartilage.

Symptons include bloody snot from the nose, rhinorrhea (more commonly called a runny nose), loss of hearing, eye pain, and double vision.

Treatments vary for this disease. To reduce the size of the tumor, doctors can use hormonal treatments, chemotherapy, or external beam irradiation. Surgery greatly depends on the location and the size of the tumor. CTs and MRIs help map out the possibility of this option, as well as help diagnose this disease.


Below is a junvile boy with angiofibroma. Notice the bulge of his eyes and middle of his face due to the pressure of the tumor.
http://eyepathologist.com/images/KL18434.jpg

This is a contrast ehanced axial MR image of the tumorright behind and into the nasal cavity.
http://www.radpod.org/wp-content/uploads/2007/07/juvenile_angiofibroma_gd_ax.jpg

Retinoblastoma

Retinoblastoma is a type of intraocular cancer that occurs most often in children. Only about 300 children are diagnosed in the US per year. Basically it forms in the retina and is caused by a mutation in the genes. The chemicals in our DNA are vital to how our cells will function. For example, a chemical called ‘oncogenes’ tell cells how fast to divide. Then there is a chemical known as the ‘tumor suppressor’ chemical. Mutations in these genes can tell them to do the opposite, this turning off the ‘tumor suppressor’ chemical, which can very easily cause cancers.

Retinoblastoma itself affects the tumor suppressor gene Rb. This is the gene that stops uncontrolled cell growth. So when that gene becomes ineffective, if unchecked the cells can then very easily become cancerous.

Nearly three-fourths of children who are diagnosed have a white pupil, also known as leukocoria. They may also have symptons such as poorly aligned eyes are red and swollen eyes. These symptoms mentioned in the previous sentence could also be mistaken for other pathologies, such as congenital cataract, or coats disease. The main way to tell the difference is through testing; blood tests, CT’s, digital photography, or biopsy. Though biopsy is a 100% effective, doctors tend to veer away with this form of diagnosis because it could potentially spread the cancer cells elsewhere.

Since the nineteen seventies doctors and scientist have developed treatments that have gone from total eye removal, to chemo-based therapy treatments, or radiotherapy. The chemo can shrink them and from there they can use laser therapy or freezing therapy.

Notice in the picture below of a axial CT image the calcification.
http://www.eyecancer.com/ViewImage.aspx?sImgSource=2005719183420.gif&sDesc=A+CT+scan+of+a+retinoblastoma+demonstrates+calcification+within+the+right+eye+(arrow).


These are "seeds" of the disease showing through the iris.
http://www.eyecancer.com/ViewImage.aspx?sImgSource=2005719183229.gif&sDesc="Seeds"+of+retinoblastoma+have+migrated+onto+the+iris+surface.

This is the white pupil appearence 75% of children with this disease get.

http://www.eyecancer.com/Patient/Condition.aspx?nID=53&Category=Retinal+Tumors&Condition=Retinoblastoma

Craniopharyngioma

Craniopharyngioma is a looooong word, but this is the pathology I chose to do! Whoo hoo!
Ok, so basically this is a tumor that develops most commonly in childhood and adolescence. If not then, it could also occur in adults over fifty. So hopefully we are all ok for now. These tumors make up 2-4% of all cranial tumors. Apparently they can get HUG, up to 3 cms to be a little more exact. There are not usually caught until they start to put pressure on other structures. These structures are then affected making the idea of a tumor plausible. Eyesight might be affected for example because the optic nerve lies just anterior to where the pituitary gland lies. Researches think these tumors might arise from embryonic cells from an imperfect involuted anterior pituitary gland; these cells eventually from the craniopharyngioma. They are benign, so the greatest damage is how they affect the structures around it, such as optic chiasm, arteries within the cranium and even the brain itself.

Symptons of this tumor really vary, depending on what structures it’s putting pressure on. If it is putting pressure on the pituitary gland itself, hormone deficiency would most likely follow, which in turn might affect growth depending on your stage in life. If it’s affecting the pituitary stalk diabetes could develop along with milk coming from the breast. More common symptons include vomiting, personality changes, and confusion.

Diagnoses can really only be made with a CT or MRI of the pituitary gland with and without contrast.

Treatment is almost always surgery. The goal is to get it out, while keeping the other structures fully intact. Whenever they can’t fully remove it, radiation therapy is an option to control the size of the tumor. CTs and MRIs should be done yearly after the surgery to ensure the tumor has not grown back.

Below is a coronal CT post contrast. Notice the bright appearance of the tumor.
https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjIt-_8_gOqP77872PywczgP_BN3W1QgMpuQzosLQ60FK89Ko61_YRvcKhd2ihvzT8J2g8ef649OIxxBIBbXKxJ5SfG8gJV4PZk_TLsMQJON7XjfSF9Q0pD3ii9eDV9BSCfU4qabQqQz2kN/s320/cranio.jpg


Below is an MRI T1 sagittal post contrast view of a childs brain.
bp0.blogger.com/.../ZVpdGq_3FeU/s320/cranio.jpg

Ramsey Hunt Syndrome!!!

Soo, Ramsey Hunt Syndrome involves the facial nerve, which we know is also known as the 7th cranial nerve, located just anterior and inferior to the pons. This nerve controls facial muscles and taste sensation. Basically you get Ramsey Hunt Syndrome by the chicken pox virus. After the symptons of chicken pox of subsided the virus itself, the varicella-zoster virus lies dormant within the nerves. There is no certain amount of years that triggers the virus, but it is most common in people over 60. In time the virus reactivates itself and infects the nerve, which causes the pathology. This virus is actually related to the herpes family of viruses, which cause sores on the mouth and genital herpes. It is also the same virus that causes shingles.

Symptoms of this pathology are fairly visible. A couple that stand out in my mind are painful red rash on your tympanic membrane, your external acoustic canal, and the roof of your mouth. You might also experience muscle weakness in your face. The palsy will be on the affected side of the ear. A constant feeling of unbalance (vertigo), change in taste, or tinnitus might also be symptons. The earlier you recognize these symptons as a problem the better. The earlier you catch it, the lesser chance you have of long-term conditions. Within seven days ensures the highest probability of a healthy recovery.

Doctors can most of the time be able to diagnose the pathology with the history of the patient. They may also may take fluid samples of blisters, or a blood test, though the fluid from the blisters is a more accurate diagnosis.

If the pathology is caught early enough, medications are given to fight the infection of the virus. Antiviral medications, corticosteroids to fight swelling and pain, diazepam for vertigo, or pain relievers are given. If a person suffers from facial palsy, physical therapy would be offered to regain strength in those facial muscles. The success rate of treatment depends on how far Ramsey Hunt Syndrome is progressed. There’s really nothing one can do to prevent the disease from coming on, but there are ways to try and lessen the discomfort. Make sure to keep the rash clean, apply cold compress to the rash, and keep good oral hygiene.


Below is a picture from a sagittal view of where the facial nerve is located in the head. It also give you an idea of how extentsive the nerve branches out into the face.
http://www.mayoclinic.com/health/ramsay-hunt-syndrome/DS00878

Below is a T1 axial MRI view of an enlarged right facial nerve. Notice the difference from the right and the left nerves. The right is clearly visible over the left.

http://images.google.com/imgres?imgurl=http://www.medscape.com/content/2001/00/40/58/405875/art-fp1405.10.fig1.jpg&imgrefurl=http://medgenmed.medscape.com/viewarticle/405875_print&usg=__yPd_TCX458RjFh54tCAGfeuI66c=&h=334&w=400&sz=28&hl=en&start=1&tbnid=fsrLF3ZujstMeM:&tbnh=104&tbnw=124&prev=/images%3Fq%3Dmri%2Bof%2Bramsey%2Bhunt%2Bsymdrome%26gbv%3D2%26hl%3Den%26sa%3DG

Leigh's Disease

Ok so I researched a pathology by the name of Leigh's disease. To be quite honest, the reason why this pathology caught my interest is because my middle name is Leigh! Anyway, from what I understand Leighs disease affects the nerves in your brain, it affects how they function, which obviously makes this a fatal disease. MOST the time the disease will show itself within toddler stages; 6 months to two years old. Rarely the disease can begin in teenage to young adult years, but it is possible.

What happens is the nerve cells die because the mitochondria (powerhouse of each cell) is affected. Some symptons that I think are unique to this disease are a childs sucking inablity, constant crying, and lack of motor skills.More obvious symptons are seizures and vomitting. Lacitic acidosis, which is lactic acid built up in the brain is a sympton as well. This leads to kidney failure.

Unforunately there is no cure for Leigh's disease. The best medicine can do right now is the use of vitamin B-1. Vitamin B-1 is what nerve cells require to maintain function.
It is quickly degenerative. Since mitochondrian ablilities inherited from the mother,Leigh's disease is also inherited from the mothers side by a DNA mutation. Most do not live to their teens, although it is possible. Though the appearance of Leigh's disease is not strikingly obvious, it is pictured below.




http://www.ispub.com/xml/journals/ijra/vol3n1/mri-fig2.jpg
Ok here is a normal T1 weighted image of a brain. Notice the size of the gyrus, ventricles, and cerebellum.

http://rad.usuhs.mil/medpix/tachy_pics/thumb/synpic39123.jpg

I apolgize about the blurriness but this is a T1 weighted image of a child with Leigh's disease. Although the difference is not dramatic, there is volume loss in the cerebellum and gyri. The ventricles are also abnormally larger.

http://healthlink.mcw.edu/article/921774134.html

http://www.bbc.co.uk/health/conditions/leigh1.shtml