brain pathology

The large haemorrhage in this adult brain arose in the basal ganglia region of a patient with hypertension. This is classed as a haemorrhagic stroke. The other form of stroke is an ischemic stroke, which results from a blood clot blocking the flow of blood into areas of the brain. 

The brain above illustrates the degenerative changes and atrophy caused by Creutzfeld-jakob Disease, a form of transmissible spongiform encephalopathy. When ‘mad cow disease’ is transmitted to humans it is classified as a varient of CJD. Typically CJD is transmitted through exposure to infected tissue usually through medical procedures, however there can be a other causes - such as hereditary CJD. A person is infected with a type of protein known as a ‘prion’, these occur normally within humans but the infectious form is folded in an abnormal way, which then alters normal, healthy prions in the cells of the host.  It is thought that the neuronal loss and damage is caused by a build up of these proteins in the brain.

CJD is marked by a quick onset of neurological symptoms and a rapidly progressing dementia and decline of neurological functioning. Initially, individuals experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. People with the disease also may experience insomnia, depression, or unusual sensations. As the illness progresses, mental impairment becomes severe. Individuals often develop involuntary muscle jerks called myoclonus, and they may go blind. They eventually lose the ability to move and speak and enter a coma. CJD is fatal, and there are no treatments for the condition. 

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I’ve been on zombie dates before where the gentleman zombie and I weren’t rocking the same brain. I was a pathological liar, he was a hypochondriac. He was gay, I was a nympho. So, how about we hop on the same brain train? Mmm, this spoon-feeding thing makes me think you ate my mom’s brain. That’d make for an uncomfortable night. Come on.

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Neurocysticercosis is an infectious parasitic diseases that results from ingestion of the eggs of pork tapeworm, known as ‘Taenia solium’. This is the most common parasitic infection of the central nervous system, and also the most common form of acquired epilepsy in many developing countries. The images above show the cysticerci (larval tapeworm contained within a sac) within the brain, 

The most common presentation of symptomatic neurocysticercosis involves epilepsy, which is present in 70% of cases. Other symptoms include headache, dizziness, stroke, and cognitive decline. It is worth noting, however, that people with neurocysticercosis can be entirely asymptomatic. The treatment depends on whether the parasite is active, and where in the brain is affected - but this can include anything from anticonvulsants, anti-parasitics,  anticysticercal drugs and surgery.

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Brain pathology
Neuropathologist dissecting a human brain for gross pathology. By studying the shape and structure of a brain, most brain disorders can be diagnosed. For instance, Alzheimer’s disease causes shrinkage and the fissures appear to grow. A stroke causes localised brain tissue death, and Creutzfeldt-Jakob disease gives the brain a spongy appearance with evident holes. This type of pathology is carried out not only to try to find causes of death, but also in research into all brain disorders.

Elderly discovered with superior memory and Alzheimer’s pathology

Well-established research suggests extensive plaques and tangles in the brain result in the death of neurons and are an indicator of Alzheimer’s dementia.

But surprising new Northwestern Medicine research on the brains of individuals 90 years and older who had superior memories until their deaths revealed widespread and dense Alzheimer’s plaques and tangles in some cases, considered full-blown Alzheimer’s pathology.

“This is amazing,” said Northwestern Medicine lead investigator Changiz Geula. “We never expected it. It tells us there are some factors that are protecting their brains and memories against the Alzheimer’s pathology of plaques and tangles. Now we have to find out what those are.”      

The Northwestern findings are the first to indicate that full-blown Alzheimer pathology also can exist in brains of elderly who show superior cognitive performance.

Geula presented the results of the study Monday, Nov. 14, at the Society for Neuroscience 2016 Annual Conference in San Diego. He is a research professor at the Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University Feinberg school of Medicine.

Extensive plaques and tangles in the brain result in the death of neurons and are an indicator of Alzheimer’s dementia. The fact that some elderly with the pathology still had superior memory points to mechanisms that protect their neurons and memory.

Discovery of these mechanisms is likely to help the development of therapies against Alzheimer’s disease, Geula said.

“Now we have to search for factors that protect these elderly against memory loss,” Geula said. “We will look at genetic, dietary and environmental influences that could confer protection for neurons against Alzheimer’s pathology.”

If scientists can find a protective environmental factor, it could help the normal elderly and those with the Alzheimer’s pathology, Geula said.

A number of recent studies suggest some elderly individuals harbor extensive Alzheimer pathology in the brain without any evidence of the cognitive decline seen in Alzheimer’s disease.

Northwestern scientists studied the brains of eight individuals older than 90 who were selected for superior performance in memory tests compared to their same-age peers who had a normal memory test performance. Three of those brains qualified pathologically as having Alzheimer’s disease, despite superior memory performance of the individuals when they were alive.

When Geula and colleagues examined nerve cells in the hippocampus, the part of the brain that is responsible for memory formation, they found cells in this area were relatively intact in brains of elderly with full Alzheimer pathology and superior memory performance.

They also examined five brains of Alzheimer’s dementia patients with full Alzheimer’s pathology. Those brains showed significant cell death in the hippocampus. A similar pattern was observed in other areas of the brain that control cognitive function.

“These findings clearly demonstrate the brains of some elderly are immune to the toxic effects of plaques and tangles,” Geula said.

To count the neurons, they examined a series of tissue sections, which were stained to visualize neurons. Then, using a microscope, they counted the number of neurons in sections of the hippocampus and the frontal cortex. When plaques and tangles appear in the frontal cortex, it means Alzheimer’s pathology has spread throughout the brain.

Geula’s lab is now embarking on a large-scale study to determine the factors, including genetic factors, that help protect the brains of some elderly against Alzheimer pathology.

Gene Discovered Associated With Tau Pathology

Investigators at Rush University Medical Center and the Brigham and Women’s Hospital in Boston reported the discovery of a new gene that is associated with susceptibility to a common form of brain pathology called Tau that accumulates in several different conditions, including Alzheimer’s disease, certain forms of dementia and Parkinsonian syndromes as well as chronic traumatic encephalopathy that occurs with repeated head injuries.

Published in Molecular Psychiatry, the manuscript describes the identification and validation of a genetic variant within the protein tyrosine phosphatase receptor-type delta (PTPRD) gene.

“Aging leads to the accumulation of many different pathologies in the brain,” said co-principal investigator Dr. David Bennett who directs the Alzheimer Disease Center at Rush. “One of the most common forms of pathology is the neurofibrillary tangle (NFT) that was at the center of our study,” he said. “The NFT is thought to be more closely related to memory decline than other forms of aging-related pathologies, but there are still very few genes that have been implicated in the accumulation of this key feature of Alzheimer’s disease and other brain diseases.”

Using autopsies from 909 individuals participating in studies of aging based at Rush University, the team of investigators assessed the human genome for evidence that a genetic variant could affect NFT.

“The variant that we discovered is common: Most people have one or two copies of the version of the gene that is linked to accumulating more pathology as you get older,“ said lead author Dr. Lori Chibnik of Brigham and Women’s Hospital. "Interestingly, tangles can accumulate through several different mechanisms, and the variant that we discovered appears to affect more than one of these mechanisms.”

The reported results offer an important new lead as the field of neurodegeneration searches for robust novel targets for drug development. This is especially true given the recent disappointing results in Alzheimer’s disease trials targeting amyloid, the other major form of pathology related to Alzheimer’s disease.

Tau pathology is more closely connected to loss of brain function with advancing age and may be more impactful as a target. The advent of new techniques to measure Tau in the brains of living individuals with positron emission tomography offers a biomarker for therapies targeting Tau.

“This study is an important first step,” Dr. De Jager, co-principal investigator at Brigham and Women’s Hospital, notes. “However, the result needs further validation, and the mechanism by which the PTPRD gene and the variant that we have discovered contribute to the accumulation of NFT remains elusive. Other studies in mice and flies implicate PTPRD in memory dysfunction and worsening of Tau pathology, suggesting that altering the level of PTPRD activity could be helpful in reducing an individual’s burden of Tau pathology.”

Tau pathology is one of the defining features of Alzheimer disease, which is the most common form of dementia in older age. While symptomatic treatments exist, there are currently no preventive therapies. PTPRD is an intriguing new candidate that deserves further evaluation in the search for Alzheimer’s disease therapies.

Pathologization

I wrote this in response to a post I saw in the actuallyautistic tag. The original poster deleted it before I got around to reblogging, but I wanted to post my response anyway. 

I’m not going to screenshot their post, because that seems a little rude, but basically they were saying that there is a difference between autism, which is a “healthy variation” in a person’s brain, and mental illnesses, which are “pathologies”. They were also saying that the word “neurodivergent” was created to describe this distinction, which it wasn’t, but that’s sort of beside the point. 

Here’s my response.


I get that by creating a dividing line between “healthy variations in brains” and “pathologies” you’re trying to protect autistic people from harm. You’re trying to protect us from being forced into abusive therapy or pseudoscience “cures”. So you want to convince people that autism isn’t a disease at all, because if it isn’t a disease, it doesn’t need to be cured or treated, right?

The problem I have with that is:

It’s not as simple as “If you have a disease, then you need treatment; if you don’t have a disease, then treatment is bad.”

Even people who really unarguably do have diseases, in the sense that they have symptoms that prevent them from living their lives and that could be successfully treated or cured, still need protection from being given harmful treatments or being forced into treatment against their will.

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The pathologization of autism is a problem not because “pathologies” and autism are two separate things, but because too many people think “this person has a pathology” gives them a blank check to do anything to that person in the name of treatment.

People ignore the pathologized person’s feelings or opinions. They assume that what the pathologized person says about their treatment isn’t meaningful or trustworthy. They assume that intensive medical intervention to cure the person as fast as possible should be the number one priority, even if that intervention has severe side effects. They don’t let the pathologized person make their own decisions about whether the benefits outweigh the side effects or not.

These kinds of assumptions are what make “pathologization” harmful.

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The issue isn’t whether someone’s condition is technically a disease or not. The issue isn’t the language that we use to describe diseases / disorders / conditions / disabilities / pathologies etc.– being aware of the implications of words is important but just changing the word won’t necessarily change people’s ingrained assumptions.

The issue is that whatever label we use, some people see that label and mentally reclassify a person, with rights and agency, into an object to be cured above all else.

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The things we are pushing for as autistic people– to be listened to when we say certain treatments are harmful, to be allowed to refuse treatment, to be viewed as people rather than objects of pity or fear– are also really important and necessary things for people who do consider themselves to have diseases, who could be cured, and who do want treatment (on their own terms.)

There’s no reason to tie our fight for these things to a distinction between “natural difference” and “pathology”. In fact, I think it’s very counterproductive. It isolates us from a lot of people who are working for the very same things. And personally I doubt whether any amount of saying that autism isn’t a pathology will stop people from perceiving us that way.

We need to, and I believe we can, fight this battle on both fronts, so to speak– we can say that autism cannot be cured and does not need to be treated, and also say that people who do want medical treatment should have a choice in how they get it and be treated respectfully while they get it.

Gross Pathology of Melanoma Tumor of the Brain

Melanoma is a cancer of the melanocytes (pigmented cells). While the majority of melanocytes are in the basal layer of the epidermis, giving us our skin pigment, they also exist in the meninges, uvea (in the eyes), inner ear, bones, and colon. As most melanomas are a result of UV radiation damage of melanocytes, the skin is the most common origin of this form of cancer. However, any melanocyte can give rise to it.

While most skin cancers are survivable and detectable, melanomas originating in the skin are the most deadly, causing 75% of all deaths related to skin cancer. Their 5-year survival rate is still over 91% if treated early, however. When not treated in a timely manner, or when originating elsewhere in the body, melanomas frequently spread to the thyroid, brain, and colon.

Reeve Collection at the National Museum of Health. Date unknown.

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Multiple Sclerosis

  • is a chronic demyelinating condition, affecting white matter of brain, spinal cord and optic nerves, distribution is non-uniform
  • typical age of onset is 20-40yrs old, the course of the disease is often unpredictable, periods of remission, interspersed with acute relapses which may leave lasting neurological deficits
  • the above images show classic bilateral periventricular plaques, which appear bright on MRI

Hello, my favorite brainy people of the internet!
We’ll be talking about some brain tumors today.
All of the mnemonics might not work for you, so take only what you need :)

Glioblastoma Multiforme:
It is the most common malignant CNS tumor in adults. It has a butterfly appearance as it commonly crosses the corpus callosum. Areas of necrosis and hemorrhage are present. (This was asked as a MCQ in my exam!) GFAP positive.

Glioblastoma Multiforme mnemonic:
GlioBUTTERFLYoma multiforme.
G for Glioblastoma, G for GFAP.
G for gangrene (Lame way to remember about the hemorrhage and necrosis!)

Meningioma:
A whorled appearance is seen, histopathologically. It commonly presents in women and expresses estrogen receptors. It can calcify resulting in psammoma bodies.

Meningioma mnemonic:
M flipped upside down looks like a W for whorled, women.

Psammoma body mnemonic:
PSaMmoma
Papillary carcinoma of the thyroid
Papillary renal cell carcinoma
Prolactinoma
Serous cystadenocarcinoma of the ovary
Somatostatinoma
Meningioma
Mesothelioma

Oligodendroglioma:
Fired egg appearance or chicken wire capillary pattern seen on histology. It commonly involves the white matter of frontal lobe resulting in seizures.

Oligodendroglioma mnemonic:
Eggs look like O.. OligOdendrOgliOma. Fried eggs leads to a fried brain. Fried brains cause seizures.

Pilocytic astrocytoma:
It’s a benign tumor of astrocytes, most common tumor in children. It involves the cerebellum (below the tentorium). Rosenthal fibers are eosinophilic, corkscrew fibers found in pilocytic astrocytoma. Pilocytic astrocytomas generally form sacs of fluid (cysts).

Pilocytic astrocytoma mnemonic:
PiloCYSTIC astrocytoma.
AstROSEcyte. ROSEnthal fibres!

Schwannoma:
Often localized to CN VIII, found in cerebellopontine angle, S-100 postitive. Histologically, shows cellular Antoni A area and paucicellular Antoni B area.

Schwannoma mnemonic:
For Schwannomas I remember the bird, “SWAN”
S-100 positive
Well circumscribed
Acoustic Schwannomas are common (More common than Trigeminal Schwannomas!)
ANtoni A and ANtoni B
Neurofibromatosis type 2 has bilateral Schwannomas.

Pituitary adenoma:
It’s a prolactinoma, most often. Derived from Rathke’s pouch. Can cause bitemporal hemianopia.

Pituitary adenoma mnemonic:
P for Prolactinoma!

Craniopharyngioma:
Is a benign childhood tumor, derived from remnants of Rathke’s pouch. It is the most common childhood supratentorial tumor (Infratentorial is pilocytic astrocytoma, remember?) Tooth enamel like calcification is seen. Can cause bitemporal hemianopia.

Craniopharyngioma mnemonic:
CRaniopharyngioma!
C for Children, Calcification.
R for Rathkes pouch!

Ependymoma:
Ependymal cell tumors most commonly found in 4th ventricle and thus can cause hydrocephalus. Characteristic perivascular pseudorosettes seen on histology. Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus.

Ependymoma mnemonic:
Epic Ependymoma. (Sounds similar, yaay!)
E for ependymal cells.
P for pseudorosettes.
I for inside the cavities of the brain (How I remember involvement of the ventricles!)
C for ciliary bodies.

Hemangioblastoma:
Most often cerebellar, associated with von Hippel-Lindau syndrome, can produce erythropoeitin causing secondary polycythemia.

Hemangioblastoma mnemonic:
HEmangioblastoma! H for Hippel. E for EPO.

That’s all!

This post was requested by Kay =)
I covered most of them for you, lemme know which else do you need!

-IkaN

Kernicterus 

  • post-mortem specimen showing bilirubin deposition in the basal ganglia (yellow deposits)
  • a complication of neonatal jaundice, long term complications include learning disability, hearing loss, movement disorders
  • avoided through the use of phototherapy and exchange transfusion to reduce hyperbilirubinaemia
Study Tips: Underlining Medical Texbooks

Why is underlining so important?

  • It forces you to stay focused and concentrated on what you’re reading
  • You will easily find important information in the next reading/ review
  • You can literally see connections and links between different information and paragraphs and remember them more efficiently

My underlining method

When i write down my notes from the textbook, I generally use symbols like arrows, circles and this kind of sketches to help me connect all the information, using different colors as well. 

>> Read before underlining

>> Try not to underline the whole sentence, if not necessary, but just important phrases

LINK TO –> MY STUDY TIPS

With cerebral fat embolism syndrome (FES), there is loss of consciousness. Note the multitude of petechial haemorrhages, mostly within white matter. Cerebral oedema and herniation may follow. Overall, few persons with a history of trauma will develop fat embolism, but it is difficult to predict which patients will. Protean manifestations include: hypoxaemia, mental status changes, petechiae, fever, tachycardia, and thrombocytopenia.

Fat embolism occurs in almost 90% of all serious traumas, including long bone fractures, but fewer than 10% are symptomatic or develop into FES. The two main complications of fat embolism are pulmonary fat embolism, which can lead to sudden death, and systemic fat embolism which causes multiple, system wide, small infarctions.