Category Archives: Neuroscience/Neurology

The Brain: Language

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Our language abilities result from intricate coordination of many brain areas. Learning more about the function of each of these areas allows physicians to find the root of language impairments. Aphasia is the impaired use of language but not necessarily all aspects of it.

Norman Gershwind, an American behavioural neurologist, noted the order and way in which we interpret language. First we hear or read language, which is received by the visual cortex as written words. These written words serve as visual stimulation. Then, the angular gyrus transforms the visual stimulation into an auditory code. Next, Wernicke’s area interprets the auditory code. Broca’s area, controlling our speech muscles via the motor cortex enables us to reply based on the interpreted information.

Citation:

Myers, David G. Psychology . 6. Worth Publishers, 2001. Print.Myers, David G. Psychology . 6. Worth Publishers,2001. Print.

The Brain: Plasticity

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Brain plasticity is the brain’s capacity for modification as evident in brain reorganization following immense learning, birth or damage. The younger we are, the greater our brain plasticity. As infants our brain’s capacity to change in response to stimuli is the greatest. This is due to the basic fact that as infants we have the immense responsibility to organise the world around us. Our neuroplasticity enables us to learn and begin to take in our surroundings. This plasticity is also seen in response to the learning and memorisation we experience through adulthood. Finally, however, brain plasticity is also seen following great brain damage. Plasticity enables our brains to compensate for lost function by emphasising remaining function. Infants and children have the greatest capacity to rebuild after brain damage as they still hold greater plasticity.

Master “stem cells” than can develop into any type of brain cells have been found in fetal brains. This discovery has raised hopes immensely of recovery mechanisms that would be able to mend damaged brains.

The Brain: Lateralisation of Brain Function

“The great pleasure and feeling in my right brain is more than my left brain can find the words to tell you.” – Roger Sperry

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The left hemisphere of our brain functions in reading, writing, speaking, arithmetic, reasoning and understanding. It is considered the major hemisphere because it has proven far easier to comprehend and study. Our right brain to this day is still very much misunderstood.  We do know that the right hemisphere is immensely important to our creativity, expression and social skills such as recognising faces and tone of voice. However, diseases that afflict the right side of our brain still befuddle scientists today.

Popular psychology and self-help books discuss the left versus brain dominance. Creative, free-spirited people who have excellent social skills but are poor at maths are considered right brain dominant; whereas, logical, analytical, linear people lacking creativity are considered to be left brain dominant. Like most self-help fads, there is some truth behind these claims. Most people generally rely on one side of the brain more than the other whilst thinking. This is known as brain lateralisation, a term that grew out of work by American neurobiologist, Roger W. Sperry. That is to say that, people that rely more on their left brain whilst thinking do posses a more logical, linear, objective perspective than those who rely on their right brain more. However, it is important to understand that all humans rely on both hemispheres for day to day activities and hardly anyone displays solely the characteristics of one hemisphere.

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The left and right hemispheres are connected by a large band of neural fibres called the corpus callosum. It allows for messages to be carried between the two hemispheres. Sperry along with other psychologists, Myers and Gazzinga, concluded through the splitting of the corpus callosum of animals left them relatively normal. These findings were then applied as a form of treatment for extreme cases of epilepsy – a neurological disorder marked by sensory disturbance, loss of consciousness and convulsions as a result of excessive nerve firing in the brain. In these extreme cases of epilepsy the excessive firing would start in one hemisphere but cascades into a storm of firing across the corpus callosum to the other hemisphere. A surgery in which the corpus callosum was split was seen as the only alternative to treat the worst symptoms. The surgery enabled the patients to carry out normal life without the constant life-threatening symptoms; however, through these experimental surgeries the function of the corpus callosum was discovered.

Sperry and Gazzangia found that the corpus callosum did, in fact, have significance.  It enables communication between the two hemispheres. Each hemisphere continues to learn after the operation; however, the two hemispheres remain unaware of any learning and experience of the other side.

Citations:

Cherry, Kendra. “The Anatomy of the Brain.” The Four Lobes (2012): n. pag.About.com Psychology. Web. 03 Sept. 2012. <http://psychology.about.com/od/biopsycholog

Myers, David G. Psychology . 6. Worth Publishers, 2001. Print.Myers, David G. Psychology . 6. Worth Publishers,2001. Print.

The Split Brain Experiments”. Nobelprize.org. 8 Sep 2012 http://www.nobelprize.org/educational/medicine/split-brain/background.html

 

Mental Retardation and Dendritic Spines

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Dendrite is Greek for “tree-like” and to explain what they do in the simplest terms possible, they receive electrochemical signals from other neurons and then pass these signal down to the soma or neural cell body. Dendrites play a critical role in determining the frequency of the action potential, which drives the electrical signal down axons of the body of the neuron towards the axon terminals. Dendrites are so essential that their architecture is a great indicator of the complexity of our neural connections. In fact, our brain function depends on strong synaptic connections, connections which are cultivated during infancy and early childhood.

Unfortunately, as with all things complex, sometimes something goes wrong in the developing process. Mental retardation occurs when there is a disruption in this early refinement of dendrites that results in cognitive impairment severe enough to disrupt adaptive behaviour. There is a wide array of genetic disorders and poor environmental conditions that can result in mental retardation. For example, Down Syndrome and PKU (both genetic disorders), accidents during pregnancy and childbirth, maternal infections with rubella, Fetal Alcohol Syndrome and environmental impoverishment. Poor environmental conditions in young children such as poor nutrition, isolation and neglect can even result in brain damage severe enough to cause damage to these sensitive dendrites.

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Healthy dendrites have spines that look like small balloons that hang of the dendrite. In cases of mental retardation dendritic spines are very thin and long, resembling the dendritic spines of a fetus. This is clearly seen in the top most image, a) and c) are healthy dendrites. This clear difference reflects the failure of normal circuits in the brain’s development. Studies by Marin-Padilla and Purpura have discovered a correlation between extent of dendritic spine damage and degree of mental retardation.

Citations:

Bear, Mark F., Barry W. Connors, and Michael Paradiso. “Neurons and Glia.”Neuroscience: Exploring the Brain. Baltimore, MD: Lippincott Williams & Wilkins, 2006. 43. Print.

Images courtesy of google images.

 

The Oxygen Consumption Controversy

Raichle et al. 

When Raichle et al. conducted their PET study in 80s and discovered increased blood flow to the V1 he also measured oxygen consumption and glucose consumption. He found that blood flow increased by around 50%, glucose consumption increased by around 50% but there was hardly any change in oxygen consumption (Jones, 2013). This is inconsistent with modern findings. Take the dip shown in fMRI studies, there is clearly a change in oxygenation levels. The increase in doexyhemoglobin is seen as a evidence for oxygen consumption and the overshoot of oxyhemoglobin is seen as evidence of increased blood flow. As mentioned in part 2, this dip is associated with a greater spacial resolution than during any other part of the hemodynamic response (ibid). However, in some studies this dip is not present.

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However, recent PET scans have been able to show an increase in oxygen consumption. The best explanation for this missing data is flaws in the PET scan itself. PET scans have poor spatial and poor temporal resolution, which means if oxygen were to be picked up due to spatial or temporal differences (differences in location and processing speed) it would be very difficult to pick it up.

Hypercapnia 

Hypercania, fortunately, is a more reliable way of measuring for oxygen consumption. Hypercapnia is the term used for elevated levels of carbon dioxide in the blood stream. As carbon dioxide is a waste product of aerobic metabolism (oxidative or cellular respiration), if we change the amount we breathe in or use oxygen there will be an increase carbon dioxide levels. All parts of the body that can detect carbon dioxide other than the brain maintain neural activity when we become hypercanic. As a result, hypercania acts as a ‘control’ condition for comparing blood oxygenation increase following increased cerebral blood flow to blood oxygenation increase due to neural activity.

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Basically:

Cerebral blood flow increase due to hypercania will result in an oxygenation increase.

Cerebral blood flow increase due to increased neural activity will have a lower oxygenation increase. This is because oxygen has been consumed for the increased neural activity to be possible.

The Diffusion Limited Theory

Buxton & Frank (1997) decided to tackle why if oxygen consumption increases by so much, why does cerebral blood flow need to increase even more. Buxton & Frank (1997) believed the answer to that question was a gradient. In order to get more oxygen to the brain, you either need more oxygen in the blood than in the brain or less oxygen in the brain than in the blood. This creates a gradient that will allow oxygen to diffuse from the blood to the brain. As the level of available oxygen (oxygen tension) in the brain at rest is almost or around zero, the only way to create a viable gradient is to increase the amount of oxygen in the blood vessels namely through blood flow.

Buxton and Frank believed the disproportional amount of oxygen consumption compared the blood flow is due the high speed of the blood flow. The blood passes through the brain too quickly for all the oxygen to be consumed. As a result, we have a high speed flow to continuously supply oxygen where necessary, but this unfortunately is not very efficient as the process of consuming the oxygen compared to the flow is disproportionate.

JONES, M. (2013). Referencing and citation – Harvard style, from PSY108 Neuroscience and Evolution. University of Sheffield, Richard Roberts Building on 8th March. Available from: Blackboard.

 

Animal Models in Neuroscience

Invertebrate Models 

The squid giant axon is pretty well renowned for his its applications neuroscience research. J Z Young discovered the giant squid axon and giant squid synapse and was the first to apply it neurophysiological research. The giant squid (loligo pealii) was and is still considered to extrodinarly vital to neuroscience research because of the sheer size of its axon (<1mm). It’s size makes it easy to dissect and support. External and internal perfusion with varying saline levels allowed scientists to determine ion flows in action potential.  Using the giant squid axon, Alan Lloyd Hodgkin and Andrew Huxley won the Nobel Prize in Physiology or Medicine in 1963 for developing Hodgkin–Huxley model mathematical model that describes how action potentials in neurons are initiated and propagated.

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In electrophysiology, worms are used as a model for cellular death (apoptosis) and development and are also studied because of their relatively large axon. The C.elegans a nematoda (roundworm) is often studied because its genome, nervous system and genetic regulation of behaviour has been fully mapped. Specifically, these roundworms are an ideal model for apoptosis.

Fruit flies or drosophilia melangosaster have probably come up a fair few times if you have ever taken biology. Fruit flies are used in neuroscience for the identification of genes regulation nervous system development. In particular, the role of pax-6 in the development and evolution of the eye.

Vertebrate Models 

Frogs 

Italian physician Luigi Galvani in his frog studies showed that muscles can be caused to twitch when electrically stimulated.

German physician and physicist Hermann von Helmholtz isolated the nerve conduction velocity to be between a range of 24.6 – 38.4 meters per second.

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Ross G. Harrison was the first person to make observations of axonal growth whilst studying tadpoles in vitro.

Katz and Miledi whilst studying frogs observed the role of calcium ions in the release of neurotransmitters.

The neuropsychologist Roger W. Sperry, known for his split-brain research that lead his Nobel Prize in 1981, observed rats and frogs discovering how nerves pathfind.

Birds

The domestic chicken (gallus domesticus) have been used again and again the study of brain development because of how easy they are to study. Chickens are so easy to study because of how ‘simple’ it is for scientists to manipulate the embryo. Being able to manipulate the embryo means the scientists have been able to transplant genes, tissue and nerve growth factors to study the effects.

Konrad Lorenz an Austrian zoologist,ethologist, and ornithologist studied imprinting in chicks, which is when an animal comes to believe the first person, thing or animal they see is there mother.

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English biologist Steven Rose also used chicks to study passive avoidance learning, which is when a person or animals learns to stop doing a certain behaviour when it results in punishment.

Nichole Le Douarin transplanted regions of nervous system between quails and the domestic chicken to create a chimera, which has led to critical insights into the development of the nervous system and the immune system. Other notable researchers that have worked with the domestic chicken are Viktor Hamburger and Rita Levi-Montalcini.

Mammals and Non-Human Primates

Hitzig and Fritsch both German physicians used dogs to map out the motor cortex of dogs.

Using cats, dogs and apes English neurophysiologist, histologist, bacteriologist, and a pathologist Sir Charles S. Sherrington made huge progress to our current knowledge of reflexes, motor control and localisation in addition to coining the term synapse.

German pharmacologist Otto Loewi who discovered of acetylcholine, used dogs to study chemical neural transmissions. This discovery came from the stimulation of the vagus nerve releasing vagustoff, which caused a reduction  in the heart rate. This vagustoff was later confirmed to be acetylcholine. English neuroscientist Henry Hallett Dale later expanded on this discovery to study the release of ACh from the motor nerves in cats, dogs and frogs. He came up with Dale’s principle that individual nerves release a single neurotransmitter, which of course, was later proved false.

British physiologist John Langley named the autonomic nervous system and studied cats, dogs and rabbits to formulate the receptor theory.

American psychologist Karl Lashley searched for the engram (physical embodiment of memory) using ablations in rats to see how it would affect their memory performance in maze tasks.

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To famous psychological experiments involving mammals are those of American psychologist B.F. Skinner and Russian psychologist Ivan Pavlov. Pavlov conducted studies on dogs and coined the term what is now known as classical or passive conditioning via the pairing of stimuli. B.F. Skinner using a ‘Skinner Box’ and rats coined the term active or operant conditioning via reinforcement.

Kuffler (Hungarian-American neurophysiologist), Hubel (Canadian neurophysiologist) and Weisel (Swedish neurophysiologist) worked together on cats and monkey brains to map out receptive fields related visual processing.

Mice transgenics have also widely been used to study molecular dissection of behaviour and diseases in particular in relation to reward systems and development abnormalities.

Non-human primates are of particular interest to neuroscientists because they are of few animals with brains similar to ours, in particular they have a frontal lobe.

Neuroscience: The Action Potential

Action potential is something I find a lot of people who study psychology or neuroscience struggle with. For me, I just could never remember where it was sodium or potassium on the inside or outside of the cell membrane. Luckily, action potential is not as difficult to understand when you break it down into its major subsections.

Introduction

Action potentials are generated by neurons and are always consistent in size and duration; their strength does not diminish as it propagates down the axon. The strength of the action potential is determined by the frequency it propagates down the axon; the frequency and pattern of the action potentials generate a code used by neurons to transfer information appropriately from one location to another. Neuroscientists use an oscilloscope to study action potential as it sensitive to changes in voltage over time. The action potential works its way down the axon until it reaches the axon terminal. At the axon terminal, a synaptic transmission is initiated.

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Generating the Action Potential and All-or-None 

The perception of any sensation such as warmth or pain as well as any movement is the direct result of action potential. Depolarization of the neuron is what is necessary for an action potential to be generated, and it can arise in a variety of ways depending on the kind of neuron. The most common way to depolarize a neuron is by entry of sodium ions. The important thing is that the stimulus is strong enough to depolarize the neuronal membrane. Action potential works on what is known as all-or-none response, meaning it works on a threshold basis. As it is consistent in size, it relies on the stimulus exceeding a threshold called generator potential in order to fire, rather than the strength of the stimulus itself. This may seem confusing because yes, the strength of the stimulus must exceed the threshold , so in a way strength of the stimulus matters. However, what is important to remember is that once the threshold has been exceeded, the strength of the stimulus has no importance or effect on the strength of the action potential whatsoever.

Properties of Action Potential 

The membrane of a neuron at rest is around -65mV or -65 milli-volts with the regard to the outside. Volts is a good indicator that we are dealing with electrical current. During action potential, however, the membrane potential becomes briefly positive. This change from a negative to positive membrane potential is depolarization. Depolarization, a very rapid process, will continue until the membrane potential reaches 40 mV. To give you an idea how rapid the entire process of action potential including reaching back to -65mV it takes 2 milliseconds.

An action potential will only ever travel in one direction because of the refractory period. When the action potential travels away from the soma or cell body towards the axon terminals it is called orthodromic conduction. When the action potential travels towards the soma, the action potential is called antidromic conduction. Regardless of the direction it is traveling, action potential conductance rate varies, but the typical rate is 10m/s. The average length of an axon is about 2cm.

The Process 

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1. Resting Potential: As stated before, the resting membrane potential is around -65 mV but it ranges depending on the neuron. Different textbooks will tell you different resting membrane potentials, but it’s not something you need to worry too much about. It is also important to note than Vm or the membrane action potential is equal to 0. Vm=0.

Threshold: The membrane potential at which there stimulus is strong enough to open the sodium channels. The opening of the voltage-gated sodium channels changes the ionic permeability of the membrane in favour of sodium.

2. Depolarisation

3. Rising Phase: As the membrane potential is negative at the resting phase, the opening of the sodium channels creates a great pull. This is because the sodium ions (Na+) are positive. The result is sodium ions rushing into the cell causing rapid depolarisation. This changes the membrane action potential towards the equilibrium value of sodium or ENa.

Overshoot

4. Falling Phase: The voltage-gated sodium channels become inactivated, and in turn the voltage-gated potassium channels open. This time around, there is a great pull on the potassium ions (K+, also positive) outside the cell as the sodium ions have made the membrane potential very positive. Potassium ions rush outside the cell, resulting in a negative membrane potential once more, close to  Eor the equilibrium value of potassium.

Undershoot: The membrane potential is more negative than -65 mV.

Absolute Refractory Period: The cell cannot fire during this period as there is a gradual restoration of the membrane potential back to -65mV and the Vm to 0. During this time, even if the stimulus is strong enough to exceed the threshold, the membrane will not fire. It lasts about 1ms.

Relative Refractory Period: The membrane potential stays hyper-polarised or at the undershoot until the potassium channels close. It can be difficult to initiate another action potential even after the absolute refractory period, longer than 1 ms.

Factors Influencing the Conduction Velocity 

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The rate of the action potential depends on the strength of the depolarising current; specifically, it is reflected in firing frequency of the action potential. The maximum frequency, however, is 1000 Hz. Generally, axon potential conduction velocity increases diameter of the axon as well as the size of the axon itself and the number of ion channels. Smaller axons tend to require a much greater stimulus to reach the threshold necessary for depolarisation, as such as they are more sensitive to local anaesthetics.

The Cranial Nerves

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The majority of the cranial nerves emerge from the brain stem on the ventral surface of the brain. Cranial nerves I and II emerge from the forebrain and cranial nerve XI from the brain stem as well as the spinal cord. As they are nerves they are classified as part of the peripheral nervous system; however, two of the cranial nerves are also considered part of the central nervous system, I and II. Each nerve often has fibers performing many different functions. Also they have associated cranial nerve nuclei in the midbrain, pons and medulla of the brainstem.

I. Olfactory: a special sensory cranial nerve responsible for our sensation of smell.

II. Optic: a special sensory cranial nerve responsible for our sensation of vision.

III. Oculomotor: a somatic and visceral motor cranial nerve responsible for the movement of the eye and eyelid as well as the parasympathetic control of pupil size.

IV. Trochlear: a somatic motor cranial nerve responsible for the movements of the eye.

V. Trigeminal: a somatic sensory and motor cranial nerve responsible for the sensation of touch on the face and the muscles of mastication.

VI. Abducens: a somatic motor cranial neuron responsible for the movements of eye.

VII. Facial: a somatic and special sensory cranial neuron responsible for the movement of muscles of facial expressions as well as the sensation of taste in the anterior 2/3 of the tongue.

VIII. Auditory-vestibular: a special sensory motor neuron responsible for the sensation of hearing and balance.

IX. Glossopharyngeal: a somatic and visceral motor cranial neuron as well as a visceral and special sensory cranial neuron responsible for the movement of muscles in the throat and the parasympathetic control of salivary glands in addition to the detection of blood pressure changes in aorta and the sensation of taste in posterior one third of tongue.

X. Vagus: a visceral motor and sensory cranial neuron as well as a somatic motor neuron responsible for the parasympathetic control of heart, lungs and abdominal organs as well as the sensation of pain associated with the viscera and movement of muscles in the throat.

XI. Spinal accessory: somatic motor neuron responsible for the movement of muscles in the throat and neck.

XII. Hypoglossal: a somatic motor cranial neuron responsible for the movement of the tongue.

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Citation:

Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. Neuroscience: Exploring the Brain. Philadelphia, PA: Lippincott Williams & Wilkins, 2007. Print.

Cocaine and the Brain

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As part of a new series on drugs that affect the nervous system, I thought I would begin with cocaine. Unlike many other drugs for some reason cocaine is associated with the rich, famous and successful rather than with troubled teenagers and the homeless. Despite its allure cocaine is a highly additive and highly deadly substance. As a powerful stimulant the powerful high can last anywhere from 15-30  minutes up to an hour. Surprisingly, at least to me, approximately 14% of the American population has tried cocaine (WedMD, 2013) with the largest demographic being males between the age of 18 to 25.

Introduction 

Cocaine like most other recreational drugs affects the brain; if it didn’t there would not be much allure to them really. Most people are after all drawn to drugs because of the escape they offer. Unfortunately, no drugs that play with the mind are to be trusted. As a class A drug, the side effects more than out weighs the highs. Cocaine affects the the neurochemical pathways by blocking the re-uptake of neurotransmitters such as norepinephrine, serotonin, and dopamine.

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As it blocks these three common neurotransmitters it is called a triple re-uptake inhibitor. Drugs that increase the concentration of these specific neurotransmitters are said to be positively reinforcing meaning they create a pleasurably feeling that can become addicting. Addictions such as sex, gambling, eating, etc. can become addictive because they also produce pleasurable feelings that can be self-reinforcing.

The High 

In cocaine users these highs are described as euphoric with accompanying feelings of supremacy, positive mood and also an increase in energy and alertness. You can see why famous detective Sherlock Holmes may have been drawn to such a drug. However, sometimes the high can result in increased levels of anxiety, restlessness, paranoia and irritability. Such symptoms illustrate the dangers of playing with our neurochemical balance; we cannot be certain the pathways we affect are going to result in positive feelings. People with a family history of mental illness are increasingly vulnerable to the effects of cocaine use because such a major flux in their brain chemistry can trigger the onset of disorders ranging from bipolar disorder to schizophrenia.

Physiological Symptoms 

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The dangers of cocaine abuse are not just limited to the brain. Travelling through the blood, cocaine can have devastating effects of the heart, the kidneys, the respiratory system, the gastrointestinal tract and even sexual function. You can read more about these effects on WedMD.

Pharmacology 

Extracted from the coca leaf, cocaine or benzoylmethylecgonine is a crystalline tropane alkaloid (-ine suffix) meaning that it has a crystal-like and nitrogen-based structure that occurs naturally. The coca leaf is mostly found and cultivated in the Andes of South America. From the coca extract the two major forms of cocaine are crack cocaine and powdered cocaine.

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Crack cocaine is the free-base from of the drug meaning it still in its crystalline structure making it possible to be melted down to be smoked.  Powdered cocaine can be dissolved into water or inhaled.

A major danger with cocaine is that it contains a lipophilic group, a hydrophilic group, and an aliphatic group. Meaning it can pass through polar and non-polar membranes, specifically the blood-brain barrier.

Cocaine Addiction 

Over time the reward-system established by frequent cocaine abuse causes damage to the dopamine pathway. This damage means that the pleasure experienced becomes diminished and for the person to experience the same high they must now increase their dosage. Increased cocaine dosage obviously increases the physiological and psychological effects of cocaine addiction.

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Physiological and psychological effects of addiction:

  1. Mood swings
  2. High blood pressure
  3. Panic attacks
  4. Cognitive impairment
  5. Changes in personality
  6. Psychosis: including tactile hallucinations (“coke bugs” or formication)
  7. Paranoia
  8. Insomnia
  9. Tachycardia (increased heart rate)

Symptoms of cocaine withdrawal include:

  1. Depression
  2. Paranoia
  3. Exhaustion
  4. Mood swings
  5. Itching
  6. Anxiety
  7. Insomnia
  8. Craving

Cocaine Overdose and Treatment 

Due to the serious nature of the effects of cocaine abuse, cocaine overdose is common amongst users. The most common cause of death due to overdose is tachycardia, and is a result of the body weakening due to the drug rather than an a lethal dosage. As such, cocaine related deaths are frequently accidental. The increased heart rate elevates blood pressure to the point of  respiratory failure, stroke, cerebral hemorrhage, or heart-failure.

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Unfortunately, even when a person overdosing is brought to an emergency room not much can be done except treat the symptoms. As of right now there is no antidote for cocaine. However, it is still important that these symptoms are treated as it may be able to prevent the above listed causes of cocaine-related deaths.

The symptoms to look for include:

  1. Nausea
  2. Chest pain
  3. Increased heart rate
  4. Fever
  5. Tremors
  6. Vomiting
  7. Seizures
  8. Paranoia
  9. Hallucinations
  10. Delirium

 

Thank you for reading! Please comment with any drug you would like to learn about next.

Citations:

“Cocaine Overdose Symptoms and Treatment.” Cocaine Overdose Symptoms, Signs, and Treatment. Project Know, 2013. Web. 16 Aug. 2013. <http://www.projectknow.com/research/cocaine-overdose/&gt;.

“Cocaine Use and Its Effects.” WebMD. WebMD, n.d. Web. 16 Aug. 2013. <http://www.webmd.com/mental-health/cocaine-use-and-its-effects&gt;.

“DrugFacts: Cocaine.” National Institute on Drug Abuse. NIH…Turning Discovery Into Health®, Apr. 2013. Web. 16 Aug. 2013. <http://www.drugabuse.gov/publications/drugfacts/cocaine&gt;