April 24, 2010

Saturday, April 24, 2010
The Buck Institute for Age Research has been studying the possibility that antidepressants and mood stabilizers, like lithium for example, could have positive effects on stroke victims. The growth of new neurons has been known to diminish the effects of a stroke as well as dramatically improve impaired functions after a stroke, while those types of medications have been found to encourage neurogenesis in rodents.
"What this study shows more convincingly than in the past is that the production of new neurons after stroke is beneficial in rodents," said Buck faculty member and senior author David Greenberg, MD, PhD. "Assuming that neurogenesis is also beneficial in humans, drugs approved by the FDA for other purposes and already shown to promote new neuron growth in rodents might be worth studying as a potential treatment for stroke in humans. For example, antidepressants are often used to treat post-stroke depression, but their potential for improving outcome from stroke itself is less certain."
Researchers compared the size of a stroke and the recovery from stroke in genetically altered mice that either had the ability to grow new neurons or not. It was discovered that mice without the ability to grow new neurons suffered strokes 30% larger; whereas the mice with the ability to grow new neurons showed dramatic improvement of motor functions following a stroke.

Although this new research sounds very exciting, Greenberg cautions that people should not attempt to treat themselves until clear evidence is made official as testing has not been rigorous enough to determine if negative effects exist or whether these positive effects can be seen in humans. Testing these medications that stimulate the growth of neurons could lead to other exciting discoveries for many other age-related disorders, such as Alzheimer’s, Parkinson’s and Huntington’s disease.
“Stroke is the third leading cause of death in the U.S. and is the leading cause of serious long-term disability in this country. Treatments for stroke are limited. Clot busting drugs, which have to be given within hours of the stroke, have been of great benefit to a small number of patients, but stroke is not usually diagnosed in time for them to be used.”
What is a stroke?

A stroke (sometimes called a cerebrovascular accident (CVA)) is the rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain, caused by a blocked or burst blood vessel. This can be due to ischemia (lack of glucose and oxygen supply) caused by thrombosis or embolism or due to a hemorrhage. As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or inability to see one side of the visual field.

What factors lead to a higher risk of stroke?
  • advanced age
  • hypertension
  • a previous stroke or transient ischemic attack (TIA)
  • diabetes
  • high cholesterol
  • cigarette smoking
  • atrial fibrillation
What are the symptoms of stroke?

Symptoms of a stroke that affects the central nervous system include:
  • hemiplegia and muscle weakness of the face
  • numbness
  • reduction in sensory or vibratory sensation
Generally, the symptoms affect one side of the body and the side affected is typically opposite to the affected brain area.

Symptoms of a stroke that affects the brain stem include:
  • altered smell, taste, hearing, or vision
  • drooping of eyelid and weakness of ocular muscles
  • decreased reflexes (gag, swallow, pupil reactivity to light)
  • decreased sensation and muscle weakness in the face
  • balance problems and nystagmus (involuntary eye movement)
  • altered breathing and heart rate
  • weakness in sternocleidomastoid muscle with an inability to turn the head to one side
  • weakness in tongue (inability to protrude and/or move from side to side)
Symptoms of a stroke that affects the cerebral cortex include:
  • aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
  • apraxia (altered voluntary movements)
  • visual field defect
  • memory deficits (with damage to the temporal lobe)
  • hemineglect (a deficit in attention to and awareness of one side of space is observed when there is damage to the parietal lobe)
  • disorganized thinking, confusion, hypersexual gestures (with damage to the frontal lobe)
  • anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)
Symptoms of a stroke that affects the cerebellum include:
  • trouble walking
  • altered movement coordination
  • vertigo and or disequilibrium
What are the long-term effects?

Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion. Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include:
  • paralysis
  • numbness
  • pressure sores
  • pneumonia
  • incontinence
  • apraxia (inability to perform learned movements)
  • difficulties carrying out daily activities
  • appetite loss
  • speech loss
  • vision loss
  • pain
  • coma
  • death
Some of the mental disabilities that can result from stroke include:
  • anxiety
  • panic attacks
  • flat affect (failure to express emotions)
  • mania
  • apathy
  • psychosis
  • depression (characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal)
  • emotional lability (a rapid switch between emotional highs and lows and an inappropriate expression of emotions
  • speech problems
  • dementia
  • attention and memory problems
  • anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)
  • hemispatial neglect (inability to attend to anything on the side of space opposite to the damaged hemisphere)
  • seizures
All resulting affects of stroke are dependent on the severity of brain damage.

Antidepressants as Treatment Immediately Following a Stroke?
Stroke

© www.mentalhealthblog.com

April 18, 2010

Sunday, April 18, 2010
Richard Borgens and his team from the Center for Paralysis Research at the Purdue School of Veterinary Medicine have discovered that chitosan can repair damaged nerve cell membranes. In doing so, the repaired membranes of nerve cells can re-establish the spinal cord's ability to transmit signals to the brain, thus restoring motor abilities.

“Chitosan (pronounced /ˈkaɪtɵsæn/) is a linear polysaccharide composed of randomly distributed β-(1-4)-linked D-glucosamine (deacetylated unit) and N-acetyl-D-glucosamine (acetylated unit).” It is produced commercially by deacetylation of chitin, a derivative of glucose. Chitin can be found in crabs, lobsters, shrimps, insects, squid, octopuses and cell walls of fungi to name a few.

Firstly, the researchers converted chitin to chitosan. They then isolated and compressed a segment of a guinea pig’s spinal cord. Following this, they applied chitosan and a fluorescent dye into the cells through damaged membranes. All of the neurons in the spinal cord tissue remained unstained by the dye under the microscope. While measuring the guinea pig’s brain response, it was noted that signals could not reach the brain because of the damaged spinal cord. “However, 30•min after injecting chitosan into the rodents, the signals miraculously returned to the animals' brains.” Hence, the nerve cells had been successfully repaired.

Borgens and his team also discovered that the levels of LDH leakage from the spinal cord tissue treated with chitosan were lower than those in undamaged spinal cords. “Lactate dehydrogenase catalyzes the interconversion of pyruvate and lactate with concomitant interconversion of NADH and NAD+. It converts pyruvate, the final product of glycolysis to lactate when oxygen is absent or in short supply, and it performs the reverse reaction during the cori cycle in the liver.” Understanding the function of LDH is quite complex, however, in layman’s terms, high levels of LDH are an indication of tissue breakdown or necrosis.

In addition, the researchers uncovered that the sugar repaired any damaged portions of the cell membrane, not only the compressed portion. During their studies, they also found that chitosan could likely be used to repair mitochondrial membranes. “Mitochondria have been implicated in several human diseases, including mitochondrial disorders and cardiac dysfunction, and may play a role in the aging process.” Could further research lead to developing treatments for certain genetic disorder and neurodegenerative diseases?

Chitosan
First Evidence That Chitosan Could Repair Spinal Damage
Lactate dehydrogenase
Mitochondrion

© www.mentalhealthblog.com

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