What does 'non-specific shallow cortical hyper density in left post-central gyrus' mean?

Cortical means pertaining to the outer layer or rind of the cerebrum, the cerebral cortex. This is where most of the neuron cell bodies are—the centres of thought, sensation, memory, muscle control, speech, etc. It’s the “gray matter” of the brain (most of it, anyway).

Gyrus means one of the raised folds of the cerebral cortex, the wrinkles of the brain.

Post-central refers to one of the grooves between these gyri, called sulci. I’ve marked a few gyri and sulci on the textbook photo below.

One of these is called the central sulcus. It descends from the top of the brain toward the ear and separates the frontal lobe of the brain (centre of thought, memory, judgment, emotion, etc.) from the parietal lobe.

Post central gyrus means the first gyrus behind that central sulcus. I’ve circled the labels on this textbook photo and marked that gyrus with a row of asterisks.

This gyrus is where “general” sensory signals from the body arrive (not for vision, hearing, or other “special senses”). It serves such senses as touch, pain, heat, cold, pressure, itch, tickle, stretch, etc. Sensory signals from the lowest points on the body arrive in the uppermost part of the gyrus and down in the deep groove between the right and left cerebral hemispheres. The lowest part of the gyrus receives sensory input from the face. The diagram below shows the origins of the signals that arrive at different levels of that gyrus.

Hyper density means that the image you’re referring to (a CT scan?) shows a region of brain tissue a little more dense than usual. Here is a cerebral CT scan with an arrow indicating a hyper dense region in this patient. This particular patient was a 48-year-old man experiencing atypical headaches and left-sided muscle weakness after receiving a neck injury in a hockey game.

Putting it all together, your description means that there is a hyper dense region of cerebral cortex, not far below the brain surface, in the left post central (sensory) gyrus. I’m not a physician and can’t guess at a diagnosis (even a physician couldn’t diagnose anything from this limited information), but I think the nonspecific part of this just means that the hyper density seen in that image doesn’t point to any specific diagnostic conclusion. It might not be anything to be concerned about, or it might result in some sensory effects depending on which part of that gyrus is affected.

Reference: Ken Saladin

What are the early warning signs of a possible brain tumour?

Common symptoms include:

• Headache, which can be severe and worsening with activity or in the morning
• Seizures. People may have different types of seizures. Some medicines can help prevent or control them. Motor seizures, also known as convulsions, are sudden involuntary movements of a person's muscles. The different types of seizures and what they look like are listed below:
• Myclonic
• Single or multiple muscle tweaks, jerks, cramps
• Tonic-clonic
• Decreased consciousness and body tone, followed by twitch and resting muscles called contractions.
• Loss of control of body functions, such as loss of bladder control
• Breathing may be of short duration of 30 seconds and a person's skin may be blue, purple, brown, white or green.
• After this type of seizure, a person may be sleepy and may experience headaches, confusion, weakness, numbness, and sore muscles.
• Receptive
• Changes in sensation, vision, smell and / or hearing without losing consciousness
• Complex partial
• Loss of awareness or partial or total loss of consciousness may occur
• Repetition may be associated with unintentional movements, such as repetition
• Personality or memory changes
• Vomiting or nausea
• Fatigue
• Sleepiness
• Sleep problem
• Memory problem
• Changes in ability to walk or perform daily activities

Symptoms specific to the location of the tumour may include:

• Pressure or headache near the tumour
• Loss of balance and difficulty with fine motor skills is associated with a tumour in the cerebellum.
• Changes in judgment, including loss of initiative, lethargy, and muscle weakness or paralysis are associated with a tumour in the frontal lobe of the brain.
• Partial or complete loss of vision is caused by a tumour in the occipital lobe or temporal lobe of the cerebrum.
• Changes in speech, hearing, memory, or emotional state, such as aggression and understanding problems or retrieving words can develop from a tumour in the frontal and temporal lobe of the brain.
• Touch or pressure on 1 side of the body, altered perception of weakness of the hands or feet or confusion with the left and right parts of the body is associated with a tumour in the frontal or parietal lobe of the cerebrum.
• Inability to look up may be due to a tumour of the pineal gland.
• Lactation, which is the secretion of breast milk, and menstrual changes in women, and growth in hands and feet in adults are associated with a pituitary tumour.
• Difficulty swallowing, facial weakness or numbness or double vision is a symptom of a tumour in the brain stem.
• Vision changes, including loss of part of vision or double vision, may result from a tumour in the temporal lobe, occipital lobe, or brain stem.

 Reference: Vineet Rana

Does a lack of white matter in the brain cause movement disorders?

White matter refers to the myelin sheath around a nerve.

In the picture below, the top part shows a myelinated nerve - which looks like a long sausage. The spaces between each sausage link is called a node of Ranvier. The node is an open area - the only place on the axon where the exchange of Na+ and K+ ions) necessary to propagate an action potential) can occur. This means that for the action potential to travel down the nerve, it must “re-ignite” at each node. That makes it like an express train, with the action potential jumping from node to node.

The bottom portion of the picture is an unmyelinated nerve. It is more like a local train, making all the stops. This means the impulse travels more slowly.

Because various functions require the contributions of hundreds of nerves, the slowing down of too many of them may mean the loss of the function- as happens in multiple sclerosis.

The process of myelination occurs with development. All the milestones, sitting up, standing, walking, talking etc, are a consequence of myelination. Loss of myelin means a reversal of ability. The genetic disorder adrenoleukodystrophy (ADL) portrayed in the movie “Lorenzo’s Oil” renders the victim a “basket case”, unable to move, speak, see, eat etc. It is always fatal.

A familiar example of a myelinated vs unmyelinated experience occurs in the pain system. If you hit your finger with a hammer, you first experience “fast pain” which travels quickly to your brain along a myelinated pathway. The pain is short lasting and precisely localized. It will cause you to stop hammering and to swear at yourself for being a jerk. It also gives you enough time to run to the faucet and start the cold water running in preparation for the arrival of the slow pain.

Slow pain travels along an unmyelinated system and stops off in your limbic system to make you feel sorry for yourself- maybe even cry. Because the pathway is recurrent (meaning it recycles the activity), it doesn’t go away anytime soon. In addition, it is less localized so you become protective, not just of your finger, but your whole hand. (In fact, some of these circuits cause you to withdraw your entire limb out of harm’s way and to limp).

(Because anesthesia affects unmyelinated nerves, this explains why blocking them eliminates pain)

Your question regarding which function affected with demyelination depends upon the LOCATION of the myelin loss. Whichever subway line switches from express to local, means that those passengers are the ones to be late.

An early symptom of multiple sclerosis (MS) is blurred vision when exercising (because the vision fibers are demyelinating) or dizziness when immersed in a hot tub. Heat exacerbates demyelinating disorders because the normal nerves conduct MORE efficiently when warm, giving them a greater advantage over the damaged nerves, which by contrast are slower still.

Reference: Joyce Schenkein

What are some theoretical ways that many neurological diseases could be cured? (i.e. ADHD, OCD, Tourette's Syndrome, Depression)

A genetic marker is a DNA sequence with a known physical location on a chromosome. DNA segments close to each other on a chromosome tend to be inherited together. Genetic markers are used to track the inheritance of a nearby gene that has not yet been identified, but whose approximate location is known.

ADHD (attention deficit hyperactivity disorder) runs in families. Anywhere from one-third to one-half of parents with ADHD will have a child with the disorder? There are genetic characteristics that seem to be passed down. If a parent has ADHD, a child has more than a 50% chance of having it. Researchers have been unable to identify a single cause for ADHD. A combination of genes, environmental factors, and possibly diet seem to influence the likelihood of a person developing ADHD. Researchers have found that a genetic variant on the latrophilin 3 gene (LPHN3) is associated with ADHD in several different populations. Previous studies have also shown that this gene plays a role in how people respond to the stimulant medications often used to treat the childhood behavioural disorder. ADHD is still incompletely understood, results from family, twin and adoption studies, as well as molecular genetic studies consistently indicate the strong genetic influence on ADHD with estimated heritability ranging from 75% to 91%. In the next few years, the number of genetic studies of ADHD is expected to keep increasing especially with the development of new technologies.

Experts say OCD affects an estimated 1 to 2 percent of the U.S. Population. A genetic marker that may be associated with the development of obsessive-compulsive disorder (OCD), whose causes and mechanisms are among the least understood among mental illnesses, has been identified by researchers. A significant association (on chromosome 9) was identified in OCD patients near a gene called protein tyrosine phosphokinase (PTPRD). Moreover, some cases of attention-deficit hyperactivity disorder (ADHD) have been associated with the gene (PTPRD), and OCD and ADHD have some symptoms in common. The gene also works with another gene family, SLITRK, which has also been associated with OCD in animals.

A variety of genetic and environmental factors likely play a role in causing Tourette syndrome. A small number of people with Tourette syndrome have been found to have mutations involving the SLITRK1 gene. Brain researchers say they have confirmed for the first time that a rare genetic mutation can cause some cases of Tourette syndrome, with the fault disrupting production of histamine in the brain. The authors will be investigating treatment of Tourette syndrome by drugs that target histamine receptors in the brain. Histamine is an organic nitrogenous compound involved in local immune responses, as well as regulating physiological function in the gut and acting as a neurotransmitter for the brain, spinal cord, and uterus. The specific gene in this study is called HDC (the histidine decarboxylase gene), which the researchers previously found to be mutated in a family that had nine members with Tourette syndrome.

For depression, researchers found evidence that by removing from the cohort people who have experienced major life adversities, they can unveil genetic factors associated with depression whose physiological effects may be in common to those caused by adversities. This can help researchers pin down the biological mechanisms involved in depression. A study in Nature revealed the first two genetic regions that are associated with an increased risk for developing major depression. The findings of this new study take the research a step further by factoring in people's life histories and discovered three additional genetic markers that only have a significant effect for people who have not experienced extreme adversity. These genes have functions in mitochondrial function and metabolism, so one potential direction for future research is to try and understand the link between depression and metabolism. In the future it is hoped that research such as this will help to identify high-risk individuals for early intervention and personalized medicine.

One way to help the above problems is to use gene therapy, which involves altering the genes inside your body's cells in an effort to treat or stop disease. Researchers are investigating replacing mutated genes or mutated genes that cause disease could be turned off so that they no longer promote disease, or healthy genes that help prevent disease could be turned on so that they could inhibit the disease. Along with genes, environment and diet must be looked at for each neurological disease.

Reference: Ron Kolinie

Why does our left hemisphere of brain control our right side of our body and the right our left?

Because of a phenomenon called Neuronal Decussation.

Our bodies move and work through muscle contractions. Those contractions are facilitated by neuronal impulses delivered by motor neurons that arise from the spinal cord (To be more specific, the anterior horn of the gray matter in the spinal cord). The anterior motor neurons are also called lower motor neurons because they are downstream the neuronal circuitry, below the first synapse.

These anterior horn motor neurons in the spinal cord receive information from the higher centres (the cerebral cortex) through upper motor neurons. It is because of the crossing over of the upper motor neurons to the opposite site along their course that the right hemisphere controls the left side of the body and the left hemisphere controls the right. This crossing over is known as Decussation. There is little literature on the evolutionary benefits conferred by this organisational paradigm.

The upper motor neurons predominantly include the Corticospinal Tract and the corticonuclear fibres which together constitute the Pyramidal tract.

The Lower motor neurons are motor neurons that arise from the anterior horn cells and the twelve cranial nerves. The former supply most of the body while the latter supply the head and neck.

The decussation of Corticospinal Tract occurs at the lower part of the medulla.

Decussation is not unique to Upper motor neurons. Cranial nerves like Trochlear nerves also decussate.

The decussation of the trochlear cranial nerves occur just concomitant to their emergence from the midbrain. They are the only cranial nerve to do so.

Reference: Udayabhanu Bhanja

What must a neurotransmitter cross in order to excite or inhibit an action potential in a receiving neuron?

Most neurotransmitter molecules get released from axon terminals, and the cross the synaptic cleft through diffusion. They then bind to receptors embedded in the membrane of the postsynaptic cell.

Neurotransmitters do not directly excite or inhibit action potentials per se. They can raise or lower the potential of the neuron (or more accurately, the region of the neuron near the receptor binding site). If the potential of the neuron (or a region of a dendrite containing active channels) exceeds the effective spiking threshold, then an action potential is generated.

Crash course has some good videos illustrating all this.

Reference: Yohan John

Parkinson's disease is caused by the loss of dopamine production. Are there other diseases that affect different neurotransmitters similarly?

I would be cautious with saying that Parkinson’s disease (PD) is caused by the loss of dopamine production. The pathogenesis of PD is rather complex and not yet quite understood. But let’s say the majority of the symptoms in PD can be attributed to the degeneration of dopaminergic neurons in substantia nigra (SNpc).

There are quite a few diseases with disturbances in neurotransmitter production. Here are some examples:

Huntington’s disease is characterized by the degeneration of neurons predominantly in another part of the basal ganglia - the striatum, where neurons producing gamma-Aminobutyric acid (GABA) are preferentially affected. GABA is an inhibitory neurotransmitter, and reduction in its content results in uncontrolled movement, known as chorea.

Reduction in GABA-mediated inhibition also plays a role in epilepsy.

Acetylcholine (ACh) is a neurotransmitter implicated in learning and memory processing, and cholinergic neurons (among others) are severely affected by Alzheimer’s disease. 

 Perhaps most famously, reduction in serotonin signalling is a factor in major depression, evidenced best by the effectiveness of serotonin reuptake inhibitors in treatment of depression. 

Reference: Minja Belić

How does meditation rewire the brain?

How does Meditation rewire the brain? No one know what happens to the individual neurons during Meditation.

However, we can get an idea of how rewiring of neurons occur in a stroke patient.

If the post central gyrus of right side of the brain is damaged during stroke the patient loses the ability to control the left side of his body.

Can the patient still control the left half of his body with a damaged post central gyrus of right side?

If the tone of the left side of a muscle is increased or decreased the patient will feel the altered tone on the right side, which is normal. Soon he will learn to use the muscles on the right side to control the muscles on the paralysed left side. There is undoubtedly rewiring in the brain, with the left half post central gyrus controlling both his right and left halves of the body. The patient then onwards can control both halves of his body.

I have treated a patient with almost one of the brain damaged who could lead an almost normal life. She lived independently and cooked food.

I was practicing Vedic Meditation about two decades back. One day I felt that I no more need to practice it. Yet, the effect of my Meditation two decades back is persisting perfectly.

Therefore, there is undoubtedly rewiring in the brain after Meditation. Since Vedic Meditation is based on muscle tone it is the changes in muscle tone that causes changes in control mechanisms of life that gets rewired in the brain.

Where and how these changes occurs probably science can never know because it is estimated that there are 100 billion neurons in the brain.

Reference: Rangaswamy Sundar Raj

Why does the human brain have so many deep crevasses?

The human brain has two types of crevasse, mostly seen on the surface.

The first type of crevasse is the longitudinal fissure. It is the deepest and oldest, as vertebrate brains all divided into two largely independent, cooperating hemispheres. It reaches down into the centre of the brain, where the corpus callosum connects the two hemispheres.

The second type of crevasse is the sulcus, which only descends into the brain a short ways, as shown in this picture from Gyrus.

The sulcus and gyrus result from the folding of the 465 square inch 2D surface of the cortex into a space small enough to fit in the skull. The cortex surface consists of a regular array of neurons arranged in stacks of 6 deep. In primitive vertebrates the 2D surface (with different neuron depths) was deposited directly on the inner surface of the skull during development. Since that limits the size of the brain to the size of the skull’s surface area, some vertebrate experienced a mutation that allowed a slight wrinkling that evolved into the gyri and sulci that humans (and other animals) have.