• Dopamine Antagonists
• Serotonin Antagonists (5HT3 Receptor Antagonists)
• Neurokinin Antagonists
• Antihistamines
• Corticosteroids
• Benzodiazepines
• Cannabinoids

1. What Are Dopamine Antagonists?

Dopamine antagonists are drugs that block the D₂ dopamine receptor in the brain and gastrointestinal neurons by preventing dopamine binding and activation of the receptor D₂ to induce the excitation of neurons.

Dopamine is an organic chemical involved in the transmission of instructions between neurons to control movement and reward-motivated behavior [2].

Dopamine performs its action by binding to dopamine-specific receptors found on the cell surface of neurons in the nervous system.

There are 6 types of dopamine receptors known as D₁, D₂, D_3, D₄, and D₅.

The activation of D₁ and D₅ through dopamine biding can induce the excitation or inhibition of the function of target neurons, while the activation of D₂, D_3, and D₄ by dopamine results in the inhibition of target neurons.

Dopamine antagonists include the following antiemetic drugs:

• Metoclopramide (Antiemetic class: Benzamides) also known as Primperan and Reglan
• Domperidone (Antiemetic class: Benzimidazoles) also known as Motilium
• Prochlorperazine (Antiemetic class: Phenothiazines) also known as Compazine and Stemetil
• Chlorpromazine (Antiemetic class: Phenothiazines) also known as Thorazine and Largactil
• Droperidol (Antiemetic class: Butyrophenones) also known as Inapsine, Droleptan, and Dridol
• Haloperidol (Antiemetic class: Butyrophenones) also known as Haldol and Serenace
• Olanzapine (Antiemetic class: Atypical Antipsychotics) also known as Zyprexa

In addition to blocking the dopamine receptor D₂, Prochlorperazine, Droperidol, Haloperidol, and Olanzapine also block serotonin, histamine, adrenergic, and muscarinic receptors [1].

2. What Are Serotonin Antagonists (5HT3 Receptor Antagonists)?

Serotonin antagonists or 5HT3 Receptor Antagonists are drugs that block 5HT3 receptors in the brain and gastrointestinal neurons by preventing serotonin binding and activation of the 5HT3 receptor to induce the excitation of neurons [3].

Serotonin is a chemical messenger involved in the neurotransmission of information related to mood, reward, learning, memory, and cognition.

Serotonin antagonists include the following antiemetic drugs:

• Ondansetron (Zofran)
• Granisetron (Kytril, Sancuso)
• Palonosetron (Aloxi)
• Tropisetron (Navoban)
• Dolasetron (Anzemet)

3. What Are Neurokinin Antagonists?

Neurokinin antagonists are drugs that block neurokinin receptor type 1 (NK₁) on neurons of the brain and peripheral nervous system by preventing substance P binding and activation of neurokinin receptor type 1 (NK₁) to induce the excitation of neurons [4].

Neurokinin receptor type 1 (NK₁) expression on cells is not limited to neurons but is also found on other non-neuronal cell types.

Substance P is a neuropeptide that functions as a neurotransmitter or neuromodulator and is involved in inflammation, vasodilatation (dilatation of vessels), pain, vomiting, mood, anxiety, and learning.

Neurokinin antagonists include the following antiemetic drugs:

• Aprepitant (Emend for oral use)
• Fosaprepitant (Emend used IV)
• Netupitant
• Netupitant/Palonosetron combination (Akynzeo)

4. What Are Antihistamines?

Antihistamines are drugs that block the H1 receptor on neurons of the brain and peripheral nervous system by preventing histamine binding and activation of the H1 receptor to induce the excitation of neurons.

The H1 receptor is also expressed on the surface of vascular endothelial cells, smooth muscles, and the heart.

Histamine is a well know actor in local immune responses, and is produced by mast cells and basophils; however, it is also an important neurotransmitter involved in itching following inflammation, and in the regulation of sleep-wakefulness cycle [5].

Antihistamines include the following antiemetic drugs:

• Doxylamine (Unisom)
• Cyclizine (Marezine, Valoid, Nausicalm)
• Pheniramine (Avil)
• Promethazine (Phenergan)

Doxylamine, Cyclizine, and Pheniramine also block muscarinic receptors, while Promethazine blocks dopamine D₂ receptors [1].

5. What Are Anticholinergics?

Anticholinergics block muscarinic receptors on neurons of the vestibular nuclei, and the vomiting and chemoreceptor center in the medulla of the brain by preventing acetylcholine binding and activation of the muscarinic receptors to induce the excitation of neurons.

Acetylcholine is an organic chemical involved in the transmission of instructions between neurons and muscles known as neuromotor or neuromuscular transmission, and between neurons that transmit information for brain organs and glands that are involved in attention, wakefulness, learning, memory (short-term memory), motivation, mood and emotion [6].

Hyoscine is an antihistamine used as an antiemetic and is also known as Transdemscop and Kwells.

6. What Are Benzodiazepines?

Benzodiazepines prevent the excitation of neurons by enhancing the effect of GABA on GABA_A receptors.

GABA (Gamma-Aminobutyric acid) is a chemical messenger and the major inhibitor of neurotransmission by reducing nerve impulses (action potential) [7].

Lorazepam is a benzodiazepine used as an antiemetic and is also known as Ativan.

7. What Are Corticosteroids?

Corticosteroids are anti-inflammatory drugs that inhibit the synthesis and release of the proinflammatory mediators, prostaglandins, by the brain.

Prostaglandins are produced and released by almost all types of cells and act on the uterus, platelets, vessels, and mast cells [8].

Dexamethasone is the anti-inflammatory drug used as an antiemetic and known by the trade names, Dextenza, Ozurdex, Cortidex, and Neofordex.

8. What Are Cannabinoids?

Cannabinoids are substances found in cannabis that activate the CB1 cannabinoid receptors in the brain and peripheral nervous system resulting in the modulation of the release of neurotransmitters [9].

Cannabinoids include the following antiemetic drugs:

• Tetrahydrocannabinol (Marinol, Syndros)
• Nabilone (Cesamet, Canemes)
• Nabiximols (Sativex)

9. When do you need an antiemetic drug?

Antiemetics are used for the treatment of nausea and vomiting associated with the following conditions:

• Gastroenteritis
• Chemotherapy-Induced Nausea and Vomiting
• Migraine-Related Nausea and Vomiting
• Vertigo
• Opioid-Induced Nausea and Vomiting
• Radiation-Induced Nausea and Vomiting
• Post-Surgery Nausea and Vomiting

9.1. Gastroenteritis

Gastroenteritis is an inflammation of the gastrointestinal tract due to viral, bacterial, or parasitic infections. It manifests with symptoms including abdominal pain, nausea, and vomiting.

Nausea and vomiting resulting from gastroenteritis can be treated using serotonin antagonists such as ondansetron and dopamine antagonists such as metoclopramide or prochlorperazine [10].

9.2. Chemotherapy-Induced Nausea and Vomiting

Chemotherapy compounds such as Paclitaxel can induce nausea and vomiting which can be blocked using the 5HT3 receptor antagonists (serotonin antagonists).

Induced nausea and vomiting by cisplatin chemotherapy require a combination of neurokinin antagonists, serotonin antagonists, and dexamethasone [11].

Some studies suggested the use of cannabinoids to reduce Chemotherapy-Induced Nausea and Vomiting [12].

9.3. Migraine-Related Nausea and Vomiting

A migraine is a severe form of headache that manifests as an excruciating pain on one side of the head accompanied by a feeling of sickness and an increased sensitivity to light and sound.

Migraine-related nausea and vomiting are treated using Metoclopramide (Primperan, Reglan) [13]. Dopamine antagonists such as prochlorperazine or chlorpromazine have also shown efficacity [14].

9.4. Vertigo

The treatment of vertigo– and motion sickness-induced nausea and vomiting, involves the use of antihistamines such as promethazine, dopamine antagonists such as prochlorperazine, and anticholinergics such as hyoscine [15].

9.5. Opioid-Induced Nausea and Vomiting

Treatment of opioid-induced nausea and vomiting is not well-defined; however, some studies showed the efficacy of some antiemetics such as the serotonin antagonist, Ondansetron (Zofran) [16].

9.6. Radiation-Induced Nausea and Vomiting

Radiation-Induced Nausea and Vomiting such as after radiotherapy, are treated with a serotonin antagonist and dexamethasone [17].

9.7. Post-Surgery Nausea and Vomiting

The treatment of post-surgery nausea and vomiting was suggested to use the serotonin antagonists, dexamethasone, the dopamine antagonist, droperidol, and the antihistamine, cyclizine [1].

Conclusion

Antiemetics are drugs used to treat nausea and vomiting associated with gastroenteritis, vertigo, migraine, surgery, opioids, radiation, and chemotherapy. Some of the antiemetics are more efficient for the treatment of a specific condition, while others have a larger effect range.

The post What Are the Common Antiemetics? appeared first on .

RLS is a common disease that affects about 10% of the general population [1].

1. What Is the Main Cause of Restless Leg Syndrome?

Although the cause is unknown, it is thought that the main cause of restless leg syndrome (RLS) is associated with an imbalance in the function of the neurotransmitter dopamine due to low levels of iron in the brain and body [1].

Dopamine is an organic chemical involved in the transmission of instructions between neurons to control muscle movements and reward-motivated behavior [2].

Other potential causes involve heredity, pregnancy, attention deficit hyperactivity disorder (ADHD), and medications.

1.1. What Is the Relation Between Restless Leg Syndrome and Heredity?

A role of heredity in RLS is associated with the high frequency of family history of RLS in patients diagnosed with this disease [3].

Monozygotic and dizygotic twin studies confirmed heredity involvement in RLS by showing the existence of a high concordance of RLS in monozygotic twins compared with that in dizygotic twins.

1.2. What Is the Relation Between Restless Leg Syndrome and Pregnancy?

Due to hormonal changes during the third semester of pregnancy, some women may experience RLS which disappears after delivery [4].

These changes involve an increase in the production of hormones, including estrogens, prolactin, progesterone, and thyroid hormone.

A reduction of iron and folate levels during pregnancy also appears to contribute to RLS due to their involvement in the synthesis of dopamine which further highlights the role of dopamine as the main cause of restless leg syndrome.

The prevalence of RLS during pregnancy was estimated to be in the range of 2.9-32% which is about 2-3 times higher than that in non-pregnant women.

1.3. What Is the Relation Between Restless Leg Syndrome and ADHD?

A relation Between Restless Leg Syndrome and ADHD was proposed by a study that showed that 44% of individuals with ADHD also had RLS.

Another important piece of information to add is that both ADHD and RLS have alterations related to dopamine levels in the brain [5].

1.4. What Is the Relation Between Restless Leg Syndrome and Medications?

Certain medications have been associated with restless leg syndrome, such as antidepressants (e.g., SSRIs, Tricyclics), withdrawal from sedative-hypnotic drugs (e.g., benzodiazepines), antiemetics (e.g., anticholinergics), antipsychotics, anticonvulsants, and antihistamines (e.g., diphenhydramine) [6].

Furthermore, alcohol and opioid withdrawal have also been associated with RLS.

2. Who Is Prone to Restless Leg Syndrome?

Restless leg syndrome (RLS) can develop at any age but is more common in women than men. There are also some factors that can increase the risk of RLS:

• Low Iron Levels
• Kidney Failure
• Neuropathy
• Rheumatoid Arthritis
• Diabetes Mellitus
• Celiac Disease
• Alcohol
• Iron Deficiency Anemia
• Parkinson’s Disease

2.1. Low Iron Levels

Iron is an essential cofactor in the production of dopamine and its deficiency can trigger RLS. Low iron levels can be due to blood loss through internal hemorrhage (e.g., gastrointestinal bleeding), excessive menstrual bleeding, frequent blood donations, or malabsorption.

2.2. Kidney Failure

Patients with chronic kidney disease on dialysis have decreased levels of iron due to the depletion of its storage in the blood.

2.3. Neuropathy

Increased levels of glucose in the blood such as during diabetes can lead to damage of nerves resulting in RLS.

2.4. Rheumatoid Arthritis

There is an elevated prevalence of RLS in patients with rheumatoid arthritis reaching between 27.7-31% [7].

2.5. Alcohol

Excessive consumption of alcohol (alcoholism) can lead to damage of nerves leading to RLS.

2.6. Celiac Disease

Celiac disease is an intestinal chronic disease characterized by a loss of appetite, malabsorption, and diarrhea due to gluten intolerance.

Celiac disease can also lead to iron deficiency which may lead to RLS. In fact, a study showed that 40% of studied patients with celiac disease had an iron deficiency [8].

2.7. Parkinson’s Disease

The characteristic dysfunction of dopamine in Parkinson’s Disease may explain why RLS is observed in some PD patients [9].

2.8. Iron Deficiency Anemia

Iron deficiency anemia is caused by a lack of iron in the body resulting in a reduction of the number of red blood cells leading to anemia. This lack of iron can also affect dopamine production.

3. What Symptoms Come with Restless Leg Syndrome?

Restless leg syndrome manifests with the following symptoms:

• An urge to move the legs due unpleasant sensations in the legs.
• An urge to move the legs during periods of rest or inactivity.
• The urge to move the legs may partially or totally be relieved by movement, such as walking or stretching.
• The urge to move the legs is increased in the evening or night than during the day.

4. Is Restless Leg Syndrome Psychological?

Although restless leg syndrome (RLS) is considered a neurological disease, a study that included 38 patients with RLS and 42 non-RLS controls, showed that patients with RLS have a lower internal locus of control (ability to impact its own health) and negative sleep-related personality traits compared to the non-RLS controls [10].

A negative sleep-related personality trait is associated with lower self-confidence, depression, higher mental arousal, and poorer quality of life.

5. How do you get rid of restless legs syndrome?

The treatment of RLS is aimed at relieving the associated symptoms that are caused by underlying physical conditions such as diabetes, celiac disease, or iron deficiency.

Medications to relieve the symptoms of RLS involve the use of dopaminergic drugs to improve dopamine effects, opioids to relieve the symptoms of severe RLS, and benzodiazepines for restful sleep.

Changes in lifestyle such as stopping alcohol, exercising (e.g., aerobics, stretching), taking iron supplements, respecting a regular sleep pattern, can help relieve some of the moderate symptoms.

Conclusion

Restless leg syndrome (RLS) can cause uncomfortable sensations that can affect sleep and the quality of life of the affected individual. The cause is unknown, but many studies highlighted the potential involvement of dopamine as the main cause.

RLS is also associated with several diseases which share with RLS the deficiency in iron which is an essential cofactor in the production of dopamine. However, other diseases and conditions such as diabetes or alcoholism can lead to nerve damage due to high blood levels of glucose or alcohol, respectively.

Although there is no specific treatment for RLS, dealing with this disease involves symptomatic treatments that aim at alleviating or reducing the undesirable and overwhelming manifestations of RLS.

The post What Is Restless Leg Syndrome (Willis-Ekbom Disease)? appeared first on .

• AMPA Receptor Antagonists
• Barbiturate antiepileptics
• Benzodiazepine antiepileptics
• Carbamate antiepileptics
• Carbonic Anhydrase Inhibitor antiepileptics
• Dibenzazepine antiepileptics
• Fatty Acid Derivative antiepileptics
• Gamma-Aminobutyric Acid Analogs
• Gamma-Aminobutyric Acid Reuptake Inhibitors
• Hydantoin antiepileptics
• Neuronal Potassium Channel Openers
• Oxazolidinedione antiepileptics
• Pyrrolidine antiepileptics
• Succinimide antiepileptics
• Triazine antiepileptics

1. What Is Epileptic Seizure?

An epileptic seizure is a neurological disorder due to an abnormally excessive, and repetitive neuronal activity in the brain resulting in seizures [1].

It is characterized by uncontrolled shakings caused by convulsions where the muscles of the body contract and relax rapidly and frequently, and loss of consciousness.

The seizures can be focal (only parts of the body) at the beginning and then become generalized to the whole body.

It was estimated that 50 million people worldwide have epilepsy [2]. In the United States, it was estimated that 1.2% of people have active epilepsy including 3 million adults and 470,000 children [3].

2. What Causes a Person to Have Epileptic Seizures?

Epileptic seizures are caused by excessive neuronal activity (hyperexcitation) that is not blocked by the inhibitory mechanisms in the brain.

In physiological conditions, there is always a balance between neuronal excitation and inhibition.

The inhibition of neuron excitation is controlled by a mechanism known as hyperpolarization which involves GABAergic neurons, gamma-aminobutyric acid (GABA) receptors, and potassium channels.

Hyperpolarization results in the inhibition of action potential resulting in the inhibition of the excitation of neurons in the brain.

Therefore, anomalies affecting GABAergic neurons, gamma-aminobutyric acid (GABA) receptors, or potassium channels lead to hyperexcitation of neurons causing seizures.

Seizures can be caused by the following conditions or disorders:

• Metabolic conditions (e.g., low blood pressure, high concentration of sodium in the blood)
• Encephalitis
• Meningitis
• drug overdose (e.g., antidepressants, cocaine, antipsychotics)
• developmental disorders (e.g., venous malformation)
• Hematoma or abscess (due to brain trauma or infections)
• Brain tumors

3. What Are the Types of Antiepileptics drugs?

3.1. What Are AMPA Receptor Antagonists?

The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA) is a receptor for the neurotransmitter glutamate.

Neurotransmitters are messengers that transmit specific chemical instructions from a neuron to another neuron and from neurons to tissues and organs.

Glutamate is the most abundant chemical messenger that is involved in excitatory neurotransmission which increases nerves impulses (action potential) [4].

AMPA receptor antagonists prevent the binding of glutamate to AMPA receptors which prevents its excitation activity toward neurons.

The most known AMPA receptor antagonist is Perampanel sold under the brand name Fycompa.

3.2. What Are Barbiturate Antiepileptics?

Barbiturates exert their antiepileptics effect through their binding to GABA receptors which inhibit neuron excitation.

They also bind to AMPA receptors which prevent the binding of glutamate and the excitation of neurons.

Barbiturate antiepileptics include drugs such as primidone (Mysoline), phenobarbital (Luminal, Mebaral), and Alphenal (Efrodal, Prophenal).

3.3. What Are Benzodiazepine Antiepileptics?

Benzodiazepines prevent the excitation of neurons by enhancing the effect of GABA on GABA_A receptors.

GABA (Gamma-Aminobutyric acid) is a chemical messenger and the major inhibitor of neurotransmission by reducing nerve impulses (action potential).

Therefore, it has an opposite action to that of glutamate and ensures balanced neurotransmission [5].

Benzodiazepine antiepileptics include drugs such as diazepam (Valium), midazolam (Versed), clonazepam (Klonopin), clobazam (Onfi), lorazepam (Ativan), and clorazepate (Tranxene T-Tab).

3.4. What Are Carbamate Antiepileptics?

Although the mechanism of action of carbamate antiepileptics is not well-known, they may be involved in promoting the activation of GABA_A receptors and the inhibition of AMPA receptors [6][7].

Carbamate antiepileptics include drugs such as Felbamate (Felbatol) and cenobamate (Xcopri).

3.5. What Are Carbonic Anhydrase Inhibitor Antiepileptics?

Carbonic anhydrase inhibitors block the activity of the enzyme carbon anhydrase involved in the maintenance of intracellular (within the cells) homeostasis by catalyzing reversible hydration (adding water) of carbon dioxide (CO2).

Low levels of carbon dioxide have been shown to increase the excitation of neurons, and therefore, the inhibition of carbonic anhydrase block the hyperexcitability of neurons during epileptic seizures [8].

Carbonic anhydrase Inhibitors antiepileptics include drugs such as topiramate, acetazolamide, zonisamide, and topiramate.

3.6. What Are Dibenzazepine Antiepileptics?

Dibenzazepine antiepileptics are inhibitors of voltage-gated sodium channels involved in the action potential of neurons resulting in the blockage of their excitation [9].

Dibenzazepine antiepileptics include drugs such as carbamazepine (Tegretol), oxcarbazepine (Trileptal), and rufinamide (Bansel).

3.7. What Are Fatty Acid Derivative Antiepileptics?

Fatty acid derivative antiepileptics are drugs that inhibit voltage-gated sodium channels and enhance the activity of GABA, resulting in the blockage of neurons excitation [10].

Fatty acid derivative antiepileptics include drugs such as valproic acid (Depakene), and divalproex sodium (Depakote).

3.8. What Are Gamma-Aminobutyric Acid Analogs?

Gamma-aminobutyric acid analogs or GABA analogs share a similar structure to that of GABA, and therefore, are capable to induce the inhibition of neurons excitation [11].

GABA analogs include drugs such as acamprosate (Campral), pregabalin (Lyrica), gabapentin (Neurontin), and gabapentin encarbil (Horizant).

3.9. What Are Gamma-Aminobutyric Acid Reuptake Inhibitors?

GABA reuptake inhibitors block GABA reuptake by gamma-aminobutyric acid transporters which increase extracellular neuronal concentrations of GABA leading to increased inhibition of neurons excitation [12].

GABA reuptake inhibitors include drugs such as tiagabine (Gabitril), and stiripentol (Diacomit).

3.10. What Are Hydantoin Antiepileptics?

Hydantoin antiepileptics are drugs that block voltage-gated sodium channels which prevents action potentials resulting in the inhibition of neurotransmission [13].

Hydantoin antiepileptics include drugs such as phenytoin (Phenytek), ethotoin (Peganone), fosphenytoin (Sesquient), and mephenytoin (mesantoin).

3.11. What Are Neuronal Potassium Channel Openers?

Neuronal potassium channel openers are drugs that activate voltage-gated potassium channels of the Kv7 subfamily which results in the hyperpolarization neurons and the inhibition of their excitation [14].

Neuronal potassium channel openers include drugs such as ezogabine (Potiga).

3.12. What Are Oxazolidinedione Antiepileptics?

Although oxazolidinedione antiepileptics reduce neurons excitation, their mechanism of action is unknown. These drugs also appear to cause birth defects due to maternal exposure during pregnancy [15].

Oxazolidinedione antiepileptics include drugs such as trimethadione (Tridione).

3.13. What Are Pyrrolidine Antiepileptics?

Although the mechanism by which pyrrolidine antiepileptics inhibit neurons excitation is not well known, it was suggested that the mechanism may be associated with the inhibition of presynaptic calcium channels through which reduces neurotransmission [16].

Pyrrolidine antiepileptics include drugs such as levetiracetam (Keppra), and brivaracetam (Briviact).

3.14. What Are Succinimide Antiepileptics?

Succinimide antiepileptics are drugs that reduce neurons excitation by blocking low voltage calcium channels (T-type calcium channels) involved in action potentials [17].

Succinimide antiepileptics include drugs such as Ethosuximide (Zarontin) and methsuximide (Celontin).

3.15. Triazine Antiepileptics

Triazine antiepileptics are drugs that inhibit neurons excitation by blocking voltage-gated sodium channels involved in the action potentials [18].

Triazine antiepileptics include drugs such as lamotrigine (Lamictal).

Conclusion

Although these categories of drugs are used for the treatment of epileptic seizures, they have also other activities that were not discussed in this article and will be discussed in another article.

The post What Are Anticonvulsant Drugs Used For? appeared first on .

• Connective Tissue
• Epithelial Tissue
• Muscle Tissue
• Nervous Tissue

1. What Is a Connective Tissue?

Connective tissue provides structure, support, protection, and connection to other tissues and organs of the body [1].

1.1. What Are the 3 Types of Connective Tissue?

Connective tissue is made of fibers, gelatinous-like substances, and cells, and is divided into 3 types of tissues: loose connective tissue, dense connective tissue, and specialized connective tissue.

1.1.1. Where Is Loose Connective Tissue Found and What Is Its Function?

Loose connective tissue is found in almost every part of the body where it maintains organs in place.

It is made of an extracellular matrix and fibers of collagen, elastin, and reticulum.

• What Is Extracellular Matrix?

The extracellular matrix (ECM) is a complex network made of macromolecules and minerals, including collagen, elastin, glycoproteins, laminin, fibronectin, hydroxyapatite, and enzymes [2].

The extracellular matrix is found between the different cells of the body where it works as a structural scaffold and serves as membranous support where cells stand.

Glycoproteins are a type of protein involved in the interactions between and within cells.

Laminin is made of glycoproteins and collagen that form a membrane where the cells stand. This type of membrane is known as the basement membrane.

Fibronectin is a glycoprotein that works like a biological glue that connects the cells to the extracellular matrix through its interaction with proteins known as integrins found on the surface of cells.

Hydroxyapatite is also known as the bone mineral is made of calcium and phosphorus. It is mostly found in the bone and teeth connective tissues.

Enzymes are proteins that work as a catalyst through reactions that produce products necessary for the function of cells and tissues.

What Are Collagen Fibers?

Collagen is made by cells known as fibroblasts and is assembled into fibrils that make the collagen fibers.

Collagen fibers provide structural support for the cells of the extracellular matrix.

What Are Collagen Fibers?

What Are Elastin Fibers?

Elastin fibers are fibers that provide elasticity to the tissues.

What Are Reticular Fibers?

Reticular fibers are a type of collagen made by reticular cells. They form a supportive network for soft tissues such as the liver, bone marrow, and lymphatic system.

1.1.2. Where Is Dense Connective Tissue Found and What Is Its Function?

Dense Connective Tissue is what makes the tendons and ligaments. It also provides structure, support, protection, and connectivity.

Dense Connective Tissue is also made of extracellular matrix and fibers of collagen, elastin, and reticulum.

1.1.3. What Is Specialized Connective Tissue and What Is Its Function?

Specialized connective tissues include the blood, bone, cartilage, and adipose tissue.

Blood is a bodily fluid that provides oxygen and nutrients to tissues and organs of the body. It also collects metabolic waste away from the cells. It is made of red blood cells and plasma.

The bone is a hard connective tissue (support and connect tissues) that contains a honey-comb shaped structure made of a mineralized matrix and bone cells.

Cartilage is a gelatinous-like substance that is found in body parts such as joints, rib cage, ears, nose, intervertebral discs, and bronchial tubes.

The Adipose tissue is a specialized tissue that stores fat and insulates the body.

2. What Is Epithelial Tissue?

Epithelial tissue or epithelium is made of one or more sheets of interconnected cells, known as epithelial cells, that cover the surface of organs and vessels and internal cavities of the body [3].

The epithelium is also part of the endocrine and exocrine glands that produce hormones and other substances and is the main component of the skin epidermis.

The epithelial cells have no blood vessels, and therefore, oxygen and nutrients are provided by the conjunctive tissue through basement membranes.

2.1. Epithelial Tissue Types

There are 8 different types of epithelial tissues according to their functions, morphologies, and localization in the body:

• Simple Squamous Epithelium
• Simple Cuboidal Epithelium
• Simple Columnar Epithelium
• Pseudostratified Columnar Epithelium
• Stratified Squamous tissue
• Stratified Cuboidal Epithelium
• Stratified Columnar Epithelium
• Transitional Epithelium

2.1.1. Where Is Simple Squamous Epithelium Found in the Body?

The simple squamous epithelium is made of flat epithelial cells that are found in the lining of vessels, heart, lungs, and lymphatic vessels.

The simple squamous epithelium is permeable which allows the diffusion and filtration of small molecules.

2.1.1. Where Is Simple Cuboidal Epithelium Found in the Body?

The simple cuboidal epithelium is made of cuboidal (cube-like shape) epithelial cells found in the kidneys and small glands. It is involved in absorption and secretion.

2.1.1. Where Is Simple Columnar Epithelium Found in the Body?

The simple columnar epithelium is made of ciliated epithelial cells that are shaped like columns, and that is found in bronchi, digestive tissue, and uterus.

2.1.1. Where Is Pseudostratified Columnar Epithelium Found in the Body?

The pseudostratified columnar epithelium is also made of ciliated epithelial cells that are shaped like columns.

However, their nuclei are found in different areas within each cell which makes them different from the simple columnar epithelial cells that have the nucleus at the bottom of the cells.

The pseudostratified columnar epithelium is found in the upper respiratory tract where they secrete and move mucus along the tract through cilia.

2.1.1. Where Is Stratified Squamous Epithelium Found in the Body?

The stratified squamous epithelium is made of layers of flat epithelial cells found in the mouth, esophagus, and vagina where it protects against abrasion.

2.1.1. Where Is Stratified Cuboidal Epithelium Found in the Body?

The stratified cuboidal epithelium is made of layers of cuboid epithelial cells found in mammary glands, salivary glands, and sweat glands where it acts as a protective tissue.

2.1.1. Where Is Stratified Columnar Epithelium Found in the Body?

The stratified columnar epithelium is made of layers of non-ciliated column-shaped epithelial cells found in male urethra and ducts of some glands where they are involved in secretion and have a

2.1.1. Where Is Transitional Epithelium Found in the Body?

The transitional epithelium is made of layers of epithelial cells that have different shapes and that are found in the bladder, urethra, and ureters where they allow these organs to stretch.

3. What Is Muscle Tissue?

The muscle tissue is made of cells and contractile proteins that allow the contraction and relaxation of muscles.

There are 3 types of muscle tissues according to their functions and localization in the body:

• Skeletal Muscle Tissue
• Smooth Muscle Tissue
• Cardiac Muscle Tissue

3.1. What Is Skeletal Muscle Tissue?

The skeletal or striatal muscle is made of elongated cylindrical muscle cells known as muscle fibers (myofibers) that are attached to bones through tendons [4].

Examples of skeletal muscles are the muscles of the arms and legs.

Each muscle fiber is a bundle of fibers arranged in parallel, known as myofibrils, and that are surrounded by collagen.

Myofibrils can be made of thin filaments containing actin or thick filaments made of myosin.

The filaments are known as myofilaments which are arranged in such a way that it alternate light and dark bands, hence the striatal aspect of the muscle.

3.2. What Is Smooth Muscle Tissue?

The smooth muscle tissue is made of smooth muscle cells known as myocytes.

Myocytes are elongated cells with a wide middle and contain proteins such as actin and myosin responsible for their contraction and relaxation.

Smooth muscle tissue is found in organs such as the intestines, stomach, bladder, uterus, and blood vessels.

3.3. What Is Cardiac Muscle Tissue?

The cardiac muscle tissue is what makes the myocardium of the heart, a muscle that is found between the endocardium (inner layer) and the epicardium (outer layer).

The cardiac muscle tissue is made of cardiac cells known as cardiomyocytes that provide the contraction and relaxation of the heart.

Some of the cardiomyocytes, known as peacemaker cells, are responsible for maintaining heartbeats and are found in the atria of the heart.

4. What Is Nervous Tissue?

The nervous tissue is the tissue that makes the nervous system including the peripheral and central nervous systems [5].

The central nervous system (CNS) includes the brain and the spinal cord, while the peripheral nervous system (PNS) includes the branching nerves that are outside the brain and the spinal cord.

The nervous tissue is made of neurons that transmit nerves impulses and neuroglia cells that provide support to neurons.

4.1. What Are Neurons and Their Functions?

Neurons are highly specialized cells that transmit nerve impulses (action potentials).

They are made of a cell body, an axon, and an axon terminal.

The cell body contains cell projections known as dendrites.

The axon extends from the cell body and all the way to the axon terminals which are cell projections.

Axons are covered by a sheet made of a fatty substance known as myelin sheet that protects the axon and helps with the transmission of nerve impulses.

Neurons are interconnected through gaps, known as synapses, that are found between a dendrite of one neuron and an axon terminal of another neuron.

Nerve impulses are transmitted from one neuron to another using neurotransmitters that are released from one neuron axon terminal to a dendrite of the following neuron through the synapses.

A neurotransmitter that is released in the synapse by the axon terminal of a neuron is captured by receptors that are specific to the neurotransmitter and that are found on the dendrite of the following neuron.

Once the dendrite of a neuron receives the neurotransmitter, there is a start of a nerve impulse (action potential) that is transmitted along the axon and all the way to the axon terminal where it is transferred to the next neuron.

This process of nerve transmission is known as neurotransmission.

Based on their function, neurons are classified as sensory, motor, or interneurons.

• What Are Sensory Neurons?

Sensory neurons or afferent neurons are neurons that transmit information (e.g., tactile, gustatory, visual, or auditory) from the different organs of the body to the central nervous system.

• What Are Motor Neurons?

Motor neurons or efferent neurons are neurons that transmit information from the nervous central nervous to different organs of the body to initiate an action (e.g., muscle).

• What Are Interneurons?

As their name indicates, interneurons are neurons that serve as neuronal bridges between neurons, such as between sensory or motor neurons and the central nervous system.

4.2. What Are Neuroglia Cells and Their Functions?

Neuroglia cells are not neurons but different types of cells that provide support to neurons and include microglia, astrocytes, oligodendrocytes, Schwann cells, and enteric glia [6].

• What are Microglia Cells?

Macroglia cells are macrophages that contribute to the immunity of the central nervous system.

• What Are Astrocytes?

Astrocytes or astroglia are star-shaped cells that have many functions such as providing nutrients to the nervous tissue, repair, and scarification of the brain and spinal cord, support of endothelial cells involved in the blood-brain barrier.

• What Are Oligodendrocytes?

Oligodendrocytes are cells that make the myelin sheet and provide insulation and support for neurons.

• What Are Schwann Cells?

Schwann cells are cells that make the myelin sheet and provide insulation and support for neurons in the peripheral nervous system.

• What Are Enteric Glia Cells?

Enteric glial cells are cells found in the enteric nervous system (gut nervous system) where they may play a role in neurotransmission [7].

In the central nervous system, the brain tissue can also be classified as grey matter and white matter

• What Is Grey Matter?

The grey matter is made of the neurons’ cell bodies, neurons’ unmyelinated axons, neurons’ dendrites, astrocytes, oligodendrocytes, synapses, and blood capillaries.

• What Is White Matter?

The white matter is mostly made of myelinated axons of neurons is found in a brain structure known as the corpus callosum which is a tract of fibers located under the cerebral cortex.

Conclusion

Tissues are what make the body, and therefore, taking care of our tissues through a healthy diet, exercise, and a healthy environment can only improve their function and health which will increase the potential of a healthier and longer life.

The post What Are the Tissues of the Body? appeared first on .

In addition to its role in controlling touch, the somatosensory cortex is also involved in sensing temperature, pain, and body position and movement.

The somatosensory cortex is divided into 4 regions known as Brodmann’s areas 3a, 3b, 1, and 2. Area 3b is also known as the primary somatosensory cortex or S1 [1].

• The neurons in area 3b and 1 are involved processing tactile (touch) information.

• The neurons in the area 3a are involved in processing information associated with the stimulation of proprioceptors found in muscles, joints, and tendons.

Proprioceptors are receptors that detect the forces (in the form of sensations) that are exerted on muscles, tendons, and joints.

• The neurons in the area 2 are involved in sensing both tactile information and the stimulation of proprioceptors.

The somatosensory cortex receives tactile information from sensory neurons that are connected to sensory receptors found in the skin, muscle, tendons, and joints.

There are 3 types of sensory neurons that send tactile information to the somatosensory cortex:

• First-order neurons

These neurons have their cell body in the spinal cord with one axon extending to connect with proprioceptors (mechanoreceptors) and the other axon extending to connect with a second-order neuron through the synapse.

• Second-order neurons

These are generally sensory nerves such as cranial nerves or trigeminal ganglia (part of the trigeminal nerve) that have their cell body in the spinal cord or the brainstem.

• Third-order neurons

These neurons have their body in the ventral posterior nucleus of the thalamus and extend their axons to the somatosensory cortex.

The ventral posterior nucleus serves as a relay for the transmission of tactile information.

1. Where Does the Sense of Touch Takes Place?

The sense of touch takes place in the skin through sensory receptors found in the skin.

2. What Are the 4 Touch Receptors?

They are 4 types of touch receptors including Merkel’s Disks, Meissner’s Corpuscles, Ruffini Endings, and Pacinian Corpuscle [2].

Once activated by touch, the receptors convert the tactile information (mechanical stimuli) into action potential that is transmitted by neurotransmission through first-order, second-order, and third-order neurons

• Merkel’s Disks

Merkel’s Disks are receptors found in the basal layer of the epidermis of non-hairy skin (e.g., fingertips) and have the capacity to sense corners, curves, and edges.

• Meissner’s Corpuscles

These receptors are also known as Wagner-Meissner corpuscles or tactile corpuscles. They are found in the dermal papillae of the thick non-hairy skin (glabrous skin) such as the skin of the sole and palm.

They are neurons endings involved in sensing fine touch and low-frequency vibrations [3].

• Ruffini Endings

These receptors are found in hairy skin and are activated by the stretching of the skin.

• Pacinian Corpuscle

These receptors are also known as Vater-Pacini corpuscle and lamellar corpuscle. They are mechanoreceptors (mechanical sensations) found in hairy and non-hairy skins and involved in sensing vibrations.

Touch receptors are also classified based on their adaptability to dynamic changes in the skin.

Pacinian corpuscle receptors have very rapid adaptability, while Meissner’s Corpuscles have rapid adaptability and Ruffini corpuscle, Merkel disks have slow adaptability.

3. What Are the Different Types of Touch Senses?

The different types of touch senses are classified into light touch, pressure, pleasant touch, vibration, temperature, and pain.

This classification is based on the type of receptor involved and the intensity of their sensitivity

Light Touch

A light touch is also known as protective touch as it is immediately set something that brushes the skin such as tickling.

Pressure

These receptors are activated when there is pressure or squeeze of the skin.

Pleasant Touch

This type of touch differentiates between pleasant and unpleasant touch.

Vibration

This type of touch is associated with the sensing of low-frequency vibrations.

Temperature

This type of touch is associated with the sensing of cold, hot, or warm objects.

Pain

This is due to the stimulation of nerves ends by noxious stimuli such as prolonged pressure or chemicals.

4. Are There Disorders of the Sense of Touch?

Disorders of the sense of touch are associated with the loss of sensitivity, the intensity of the sensitivity, and the capacity of recognizing the objects being sensed by touch.

They are caused by lesions affecting the somatosensory pathways, neurological diseases such as dementia, and chronic diseases such as diabetes.

Below are some of the disorders associated with touch:

• Astereognosis

This disorder is characterized by the inability to identify objects by touch only. It is caused by lesions in the post-central gyrus [4].

• Hyperesthesia

Hyperesthesia is characterized by an increased sensitivity to stimuli associated with senses such as hearing, tasting, touch, smelling. It is caused by excessive stimulation of the nervous system such as overconsumption of caffeine.

• Allodynia

Allodynia is a pain that is caused by a stimulus that is not the one that initiated the pain, such as feeling pain after a gentle shake of hands or light touch on the back.

• Analgesia

Analgesia is characterized by the inability to feel the pain caused by a stimulus (cause) that should normally have caused pain.

• Paraesthesia

This disorder is characterized by an abnormal sensation of the skin such as numbness, tingling, burning, chilling.

• Hypoesthesia

This disorder is characterized by a decrease in the sensation of touch associated with nerve damage, ischemia (reduced blood supply to tissues).

• Hypoalgesia

Unlike analgesia that characterized by the inability to feel pain, hypoalgesia is associated with a reduced response to a painful stimulus.

• Hyperalgesia

Hyperalgesia is characterized by an abnormally increased sensitivity to pain due to the release of inflammatory hormone-like substances, known as prostaglandins, that increase the sensitivity of the nociceptors.

Hyperalgesia can be caused by fibromyalgia, diabetes, infection, trauma, postherpetic neuralgia, and complex regional pain syndrome.

Conclusion

The touch sensory system is very complex and sophisticated thanks to the presence of highly specialized touch receptors that have a wide range of sensitivity and intensity.

This system provides us with the capacity of sensing cold, warm, and hot objects but also shapes and curves, and vibrations’ frequencies.

The post What Part of the Brain Controls Touch? appeared first on .

The auditory cortex is located in the temporal lobe of the brain.

The transmission of the auditory information through neurons to the auditory cortex is known as neurotransmission.

Sounds are that are received by the ear are transmitted by the vestibulocochlear nerve (8^th cranial nerve) and processed by the auditory sensory system.

The auditory sensory system includes the cochlear nuclei, the superior olivary complex, the inferior colliculus, the medial geniculate nucleus, and the auditory cortex

1. What Are the Steps of Hearing?

Sound processing is ensured by the auditory system that includes the ears and the sensory system and follows the following steps:

• Step 1: The sound enters the ear, travels through the ear canal, and reaches the eardrum.

• Step 2: The sound waves are amplified by the eardrum and the ossicles.

• Step 3: The amplified sound waves is received by the cochlea where it is transformed into nerve impulses by the hair cells (stereocilia) found in the organ of Corti.

Stereocilia are connected to sensory neurons through synapses where the auditory information is transferred through neurotransmission.

• Step 4: The nerves impulses are transmitted to the sensory cortex for processing by the auditory cortex.

1.1. What Is Ear and Its Function?

The ear is the first organ of hearing and is composed of the outer ear, middle ear, and inner ear [1].

• What Is Outer Ear?

The outer ear is composed of the visible part of the ear (Pinna or auricle), and the ear canal.

• What Is Middle Ear?

The middle of the ear contains the eardrum and 3 small bones known as ossicles and which are also involved in amplifying the sound waves before reaching the cochlea in the inner ear.

The eardrum is the membrane involved in the amplification of the sound waves that travel through the ear canal. It separates between the outer ear and the inner ear.

• What Is Inner Ear?

The inner ear contains the utricle, saccule, and the bony labyrinth which includes the semicircular canals, and the cochlea.

The utricle and saccule are involved in displacement and linear accelerations such as tilting the head and orientation.

The semicircular canals are filled with fluids and are involved in maintaining balance and coordination.

The cochlea is a cavity that is shaped like a spiral filled with fluids. It contains the organ of Corti where the hair cells (stereocilia) are found. The hair cells are responsible for transforming sound waves into impulses in coordination with sensory neurons in proximity.

1.2. What Is the Auditory Sensory System Function?

The auditory sensory system includes the vestibulocochlear nerve (8^th cranial nerve), the cochlear nuclei, the superior olivary complex, the inferior colliculus, the medial geniculate nucleus, and the auditory cortex.

• What Does the 8^th Cranial Nerve Do?

The 8^th cranial nerve is known as the vestibulocochlear nerve (cranial nerve VIII) or auditory nerve. It has two nerve branches, the cochlear nerve, and the vestibular nerve [2].

The cochlear nerve is involved in transmitting auditory information to the cochlear nucleus in the medulla oblongata found in the brainstem.

The vestibular nerve transmits information to the brain for the processing of body balance.

• What Is the Cochlear Nucleus?

The cochlear nucleus or cochlear nuclei are located in the brainstem and receive auditory information from the cochlear nerve. They work like a distribution center through the processing of different acoustic waves.

• What Does the Superior Olivary Nuclei do?

The superior olivary nuclei are also known as superior olive or superior olivary complex. It is located in the pons of the brain where it is involved in measuring the difference in sound intensity and azimuth.

The superior olivary complex receives auditory information from the cochlear nuclei.

• What Does the Inferior Colliculus in the Brain?

The inferior colliculus is located in the midbrain and plays a role as a relay for auditory information coming from the two ears and its integration. It is also involved in distinguishing between a pitch and a rhythm [2].

The inferior colliculus receives auditory information from the superior olivary complex and the auditory cortex.

• What is the medial geniculate nucleus?

The medial geniculate nucleus is located in the part of the brain known as the thalamus and is involved in the detection of sound intensity and duration.

The median geniculate nucleus receives auditory information from the medial geniculate nucleus.

• What is the Role of the Auditory Cortex?

The auditory cortex is part of the temporal lobe involved in transforming acoustics into perceptual representation such as recognizing the sound and its identification. It is also involved in language switching [3].

2. What Are Hearing Disorders?

Hearing disorders can affect both the ear and the auditory sensory system.

2.1. What Are the Most Common Ear Disorders?

What Are disorders of the Outer Ear?

There are several disorders of the outer ear that are due to the following causes:

• Absence of the outer ear (Anotia)
• Malformation of the outer ear (Microtia)
• Infection (Otitis externa)
• Wax build-up
• Bony tumor (Osteoma)
• Absence of ear canal (Atresia)
• Narrowing of the ear canal (stenosis)
• Fungal infection (Otomycosis)
• Disorders of the eardrum (perforation, thickening (tympanosclerosis), and inflammation (Myringitis).

What Are disorders of the Middle Ear?

• Otitis media (infection of the middle ear)
• Otosclerosis (bony growth in the middle ear)
• Eustachian tube dysfunction
• Ossicular chain discontinuity (loss of connectivity between the ossicles)
• Cholesteatoma (Tumor)

What Are disorders of the Inner Ear?

• Ménière’s disease (increased build-up of fluids in the inner ear) characterized by symptoms such as vertigo, ringing in the ear, and loss of hearing.
• Nose-induced hearing loss (NIHL)
• Presbycusis (age related degeneration of the cochlea)
• Perilymph fistula (fistula causing a leak of the inner ear fluid into the middle ear)

2.2. What Are the Most Common Disorders of the Auditory Sensory System?

What Are the Disorders of the Auditory Nerve?

• Acoustic Neuroma (tumor growing on the auditory nerve) causing hearing loss, dizziness, and ringing in the ear (tinnitus)
• Auditory Neuropathy Spectrum Disorder (auditory neuropathy) is due to alterations in the transmission of auditory information between the cochlea and the cochlear nuclei in the brainstem.

What Are the Disorders of the Cochlear Nuclei?

• These disorders are due to alterations in the transmission of the auditory information within the cochlear nuclei that can be caused by diseases (e.g., syphilis, multiple sclerosis, congenital malformation), stroke, or aging.

What Are the Disorders of the Higher Auditory Pathways?

• Minimal Auditory Deficiency Syndrome is due to language deprivation in children which may be caused by undiagnosed otitis media
• Central Deafness is rare and can be caused by a vascular lesion in the brain hemispheres.
• Auditory Processing Disorder is cause by a deficit of transmission of auditory information between the ear and the brain.

Conclusion

The auditory system is very complex and fascinating and involves both the ears and the brain processing sounds that are extremely diverse. Meanwhile, I am certainly going to enjoy listening to a nice piece of music while I still can.

The post How Does the Brain Processes Sound? appeared first on .

However, there are several steps before taste information reaches the gustatory cortex for processing:

• When a food is consumed, its breakdown in the mouth liberates chemical substances that interact with the tongue surface that contains raised bumps known as papillae.

The papillae contain taste buds that are specialized in detecting the types of taste through receptors known as gustatory receptors.

The gustatory receptors release neurotransmitters that activate sensory neurons (neurons involved in sensation) in proximity.

• The activation of the sensory neurons transmits (neurotransmission) the taste information (gustatory information) to facial and glossopharyngeal cranial nerves.

• Upon reception of the taste information, the nerves transmit it to a part of the brain known as the gustatory nucleus found in the medulla oblongata located in the lower part of the brainstem.

The medulla oblongata is responsible for several functions in the autonomous nervous system (involuntary nervous system), including swallowing, vomiting, sneezing, and coughing, ventilation, heartbeat, blood pressure.

• The gustatory nucleus in the medulla oblongata will then transmit the taste information to the thalamus which relays the information to the gustatory cortex for processing.

The thalamus is a part of the forebrain involved in the regulation of alertness, sleep, and consciousness.

It is also important to add that gustation (taste) is strongly linked to olfaction (smell) as the flavor of any type of food requires a combination of the two senses.

1. What Are the 5 Types of Taste?

The chemical substances that are generated during the breakdown can be classified as sweet, salty, sour, bitter, and umami [2]. However, some foods may have a mixture of more than 2 types of taste.

Sweet

A sweet taste is due to the presence of sugars such as glucose, fructose, or artificial sweeteners including aspartame, sucralose, or saccharine.

Salty

A salty taste is due to the presence of sodium chloride and other salts.

Sour

A sour taste is due to the presence of acids such as citric acid (orange juice)

Bitter

A bitter taste is the opposite taste to the acidic taste and is due to the presence of alkaloids that are mostly found in plants such as tea, coffee, aspirin, and tannins.

Umami

Umami taste is due to the presence of amino acids that form proteins found in meaty products.

Fatty taste is another type that has been proposed as a specific receptor for the omega 3 fatty acid, linoleic acid, was identified. Linoleic acid is mainly found in plant oils.

In addition, hot or spicy are not considered as tastes as they are pain signals associated with touch and temperature.

Taste qualities are also associated with the ability to distinguish between pleasant and unpleasant tastes but also between poison from food.

For example, most people tend to prefer sweet and umami tastes, while sour and bitter tastes are less preferred.

2. How Many Taste Buds Do Humans Have?

Humans have between 2000 to 4000 buds in total and are found in the papillae of the tongue but also in the back of the throat, nasal cavity, epiglottis, and the upper part of the esophagus. They are renewed every week [1].

Each taste bud contains between 10-40 gustatory receptors (sensory cells).

Papillae are divided into fungiform papillae (200-400 papillae), circumvallate papillae (7-12 papillae), and foliate papillae (about 20 papillae).

3. What Is a Flavor?

A flavor is a perception of food that combines taste and smell. It is mediated by the trigeminal nerve responsible for facial sensations, biting, and chewing.

4. What Are the Main Components of Flavor?

The main components of flavor include:

• Tastes (Sweet, bitter, acid, umami, and salty)
• Aroma (Pleasant smell from consumed food)
• Trigeminal Sensations (Facial sensations mediated by the trigeminal nerve)

6. What Part of the Brain Controls the Tongue?

The muscles monitoring the movement of the tongue are controlled by the medulla oblongata through the hypoglossal nerve.

7. What Causes a Person to Lose Taste?

The loss of taste is known as ageusia that can be due to several causes [3]:

• Head injury
• Middle ears or upper respiratory infections
• Dental problems or inadequate oral hygiene
• Environmental exposure to chemicals
• Medications
• Head and neck cancer radiotherapy
• Some surgical procedures involving the nose, ear, or the throat.

Disorders of taste can manifest in the following forms:

• Ageusia is disorder characterized by the complete absence of taste.
• Hypogeusia is adiminished taste.
• Hypergeusia is characterized by an enhanced perception of taste.
• Dysgeusia or parageusia is a distortion of tastemainly associated with an unpleasant perception of taste.

8- What are the symptoms of Taste Disorders?

• Changes in the taste of food and beverages that are usually consumed
• Changes in the intensity of taste of consumed food and beverages
• Absence or loss of taste
• Loss of weight associated with a loss of appetite

8- How are Taste Disorders Diagnosed

The otolaryngologist can assess the taste disorder by measuring the capacity of the affected individual to taste different types of tastes [3].

As taste disorders can be associated with middle ear and upper respiratory infections, the otolaryngologist will also examine potential problems with the ears and the throat.

For potential causes associated with poor dental hygiene, a dental examination is also performed.

8. How Can I Improve My Sense of Taste?

Treatment and improvement of the sense of taste depend on the cause of the taste disorder.

 however, some of these disorders can be prevented by ensuring good oral hygiene, consuming a variety of foods with different flavors, and staying patient when affected by cold.

Conclusion

Taste is very important for our everyday life. Not being able to taste a good dish of food or a beverage can be extremely stressful, and in some cases, can lead to a loss of appetite, weight loss, and depression. Unfortunately, it is only when we are having issues with our taste that we remember how important it is in our everyday life.

The post How Does Taste Work in the Brain? appeared first on .

• Odour sensing by receptors of the olfactory sensory neurons in the nose.
• The olfactory sensory neurons in the nose transmit the odour information (olfactory information) to the olfactory nerves through a process known as neurotransmission.
• The olfactory nerves transmit the olfactory information to the olfactory bulb, a neural structure responsible of olfaction (Smell).
• The olfactory bulb transmits the olfactory information to specific areas of the brain for processing and identification of the smell.

1. What Part of the Brain Is Most Responsible for Smell?

There are several and important parts of the brain that are responsible for smell; however, the olfactory bulb is responsible for transmitting the olfactory (smell) information from the olfactory nerves to the brain for processing.

This olfactory information is chemically identified and coded by a part of the olfactory bulb known as the glomeruli. This process is known as the odor map [1].

2. What Happens in the Brain When You Smell?

When the olfactory information is transmitted from the olfactory bulb to the brain, there are parts of the brain responsible for the processing of this information including the amygdala, the piriform cortex, and the entorhinal cortex [2].

• The Amygdala and Olfaction

The amygdala is the central hub for the management of fear within a network that involves other brain organs including the thalamus, the neocortex, the hypothalamus, the pituitary gland, the hippocampus, and the adrenal glands located on the top of the kidneys.

When the amygdala receives the olfactory information for processing it interrogates the memory siege, the hippocampus, for previous similar stimuli (e.g., olfactory stimuli).

Once the information is received from the hippocampus, the amygdala triggers the hypothalamus-pituitary-adrenal axis to initiate an adaptative reaction [3].

Depending on the nature of the smell which can be pleasant or unpleasant, associated or not with potential danger, a reaction such as robust approach (pleasant olfaction) or withdrawal if unpleasant or linked with potential danger (e.g., the smell of smoke due to fire) [4].

• The Olfactory Tubercle and Olfaction

The olfactory tubercle is part of the olfactory cortex found in the frontal lobe of the brain where is connected to the amygdala and the hippocampus.

It is involved in recognizing one’s body odor from the environment odors (sensory integration), motivated behaviors in response to odor (attractiveness or repulsion), and reward recognition [1].

• The Piriform Cortex and Olfaction

The piriform cortex is part of the brain known as the rhinencephalon located in the cerebrum. It is involved in odor perception and its differentiation from other odors and from a mixture of odors, and in odor memory [5].

• The Entorhinal Cortex and Olfaction

The Entorhinal cortex is part of the cerebral cortex where it plays a role as an interface between the hippocampus that is involved in memory and the neocortex involved in sensory perception (e.g., olfaction) spatial reasoning, and navigation, and cognition [6].

4. Can Smells Trigger Emotions?

There are common brain areas that are involved in both olfaction and emotion such as the amygdala, the hippocampus, the orbitofrontal cortex, the insula, and the cingulate cortex.

When the amygdala receives the olfactory information for processing it interrogates the memory siege, the hippocampus, for previous similar stimuli (e.g., olfactory stimuli).

Depending on the nature of the smell which can be pleasant or unpleasant, associated or not with potential danger, a reaction such as robust approach (pleasant olfaction) or withdrawal if unpleasant or linked with potential danger (e.g., the smell of smoke due to fire) [7].

The orbitofrontal cortex is involved in the reward value of taste but also in the reward value of odors which initiate an emotion [8].

The insula is a part of the cerebral cortex involved in emotion and in the processing of unpleasant odors [9].

The cingulate cortex is also part of the cerebral cortex that is involved in the formation and processing of emotions related to pleasant and unpleasant odors [10].

5. Does Smell Affect Memory?

Olfaction requires the involvement of the hippocampus, the brain part that controls memory. The amygdala processing of the olfactory information involves interrogating the hippocampus about previous experiences with the olfactory information.

6. What Is It Called When a Smell Triggers a Memory?

This effect is known as the Proustian effect based on the name of the novelist Marcel Proust.

7. Why Do Smells Make Me Angry?

The smell can trigger anger if that smell was associated with a past situation that caused anger to an individual.

The amygdala processing of the olfactory information involves interrogating the hippocampus about previous experiences with the olfactory information.

The olfactory information can also trigger emotions of anger through parts of the brain such as the amygdala, the hippocampus, the orbitofrontal cortex, the insula, and the cingulate cortex.

8. What Causes Loss of Smell?

The loss of smell can be complete and is known as anosmia or diminished and is known as hyposmia. These alterations in olfaction are due to physical or mental health disorders, viral infections, inflammation, environmental exposure, or aging [2].

Disorders or conditions such as Alzheimer’s disease, Parkinson’s disease, meningiomas, facial trauma or schizophrenia, may affect the function of the olfactory system leading to a loss of smell.

Upper respiratory viral infections and neurotropic viruses can also cause a loss of smell.

Neurotoxins found in some industrial workplaces such as solvents, metals, and particulate matter can cause a loss of smell [11].

9. What Is Aromatherapy and Its Benefits?

Aromatherapy is the use of plant essential oils through skin application or olfaction for the management of chronic pain, anxiety, some cognitive disorders, depression, insomnia, and stress-related disorders [12].

However, the clinical evidence is limited, and further research and clinical trials are required.

These are some of the essential plant oils that were used in different studies:

• Bergamot
• Chamomile-Roman
• Geranium
• Jasmine
• Juniper
• Lavender
• Lemon
• Mandarin
• Marjoram
• Melissa
• Neroli
• Patchouli
• Rose
• Rosemary
• Sage
• Spearmint
• Ylang-Ylang
• Vetiver

Conclusion

Olfaction is a complex process that involves the transmission of the olfactory information (smell) by specialized sensory neurons in the nose, the olfactory nerves, the olfactory bulb, and its processing by several regions of the brain.

Meanwhile, let’s enjoy the smell of a nice dish of food and a delicate perfume.

The post How Does Smell Get from the Nose to the Brain? appeared first on .

• Persecutory Delusions
• Grandiose Delusions
• Jealous Delusions
• Erotomanic Delusions
• Somatic Delusions
• Mixed Delusions
• Unspecified Delusions

The risk of delusional disorder in the general population is estimated between 0.05% to 0.1% and affects individuals from the age of 18 years to 90 years [1].

The persecutory and jealous delusions are common in males, while the erotomanic delusions are more common in females.

1- What Is a Persecutory Delusion?

A persecutory delusion or paranoia delusion is a fixed belief of being persecuted, potentially harmed, or conspired against resulting in emotional and behavioral actions that can be extreme.

2- What Is a Grandiose Delusion?

A grandiose delusion is a fixed belief of being famous or having prominence, talent, and great achievements (Megalomania).

3- What Is a Jealous Delusion?

A jealous delusion or Othello syndrome is a fixed belief of being betrayed by the partner (unfaithful) and having evidence to support the delusion. This type of delusion can lead to extreme violence such as suicide and homicide.

4- What Is a Erotomanic Delusion?

An erotomanic delusion is a fixed belief of being secretly loved by an individual who may be known, or famous and outside the circle of the delusional individual.

This type of delusion is associated with intense expressions of love that can lead to stalking and assaultive behavior.

5- What Is a Somatic Delusion?

A somatic delusion is a fixed belief of individuals in having something wrong with their bodies, such as having an ugly body, an unknown disease, or being infected with parasites and insects, leading them to visit many doctors to determine their delusional illness.

6- What Is a Mixed Delusion?

A mixed delusion is when the affected individual has a combination of several types of delusions.

7- What Is an Unspecified Delusion?

This type of delusion cannot be classified according to the different types of delusions.

8- What Are the Signs of Delusions?

A delusional individual may manifest the following signs:

• Fixed and non-changeable belief in the delusion
• The individual is emotionally invested in the delusion
• The delusional individual is suspicious when questioned about the delusion
• Irritability and hostility if contradicted about the delusion
• Impact of the delusion on everyday life of the delusional individual

9- What Medical Conditions Can Cause Delusions?

Although the mechanisms are not known, they are several biological causes that may contribute to the development of a delusional disorder:

• Head injury
• Seizures
• Dementia
• Basal ganglia disorder (rare disease affecting the brain and other parts of the nervous system)
• Temporal lobe Disease (resulting in seizures)
• Unbalance in neurotransmission due to anomalies in the function of tyrosine hydroxylase involved in the synthesis of dopamine, epinephrine, and norepinephrine [2].

10- What Genetic Factors Cause Delusions?

Delusions appear to be more common in individuals with family members diagnosed with a delusion disorder or paranoid personality characteristics [3].

11-What Environmental Factors Cause Delusions?

Stress, drug, and alcohol abuse, and individuals’ social isolation, such as immigrants, appear to be contributing factors of delusions.

12- What Psychological Conditions Cause Delusions?

Although delusions have fewer symptoms and functional disability, they have been classified on the same spectrum as schizophrenia, and therefore, the neuropsychological models that are applied to schizophrenia are also applied to delusions [4].

• A cognitive bias model measures emotional and affective states of an individual in response to the individual perception and response to received information.
• A cognitive deficit model evaluates the impact of cognitive impairments on the formation of a delusion.

13- How Are Delusions Diagnosed?

The diagnosis of delusion may involve the use of the Peters et al. Delusions Inventory (PDI) that measures the delusional disorder of the individual through evaluating the ideas and concepts (ideation) behind the delusion using the Present State Examination [5].

Other tools that are used for the diagnosis of delusions involve questionnaires and interviews of the patient and immediate family about the everyday life of the patients and the potential existence of a history of mental health disorders, such as schizophrenia or mood disorders [6].

The assessment of the potential existence of physical disorders such as dementia, metabolic disorders, infections, and endocrine disorders (e.g., hormonal unbalance) is also performed through checking the patient medical record.

The questionnaires, interviews, and medical history records can help in eliminating potential psychological and physical disorders that might be involved in the etiology (cause) of the delusions.

14- How Are Delusions Treated?

The treatment of delusions may involve pharmacotherapy, cognitive-behavioral therapy (CBT), psychosocial interventions, and supportive psychotherapy. However, building a good doctor-patient relationship is the key to the success of the treatment [1].

• Pharmacotherapy

This treatment involves the use of psychotic medications, and antidepressants are used for somatic delusions.

• Cognitive Behavioral therapy (CBT)

Cognitive-behavioral therapy (CBT) focuses on identifying biases, worries, interpersonal sensitivity, reasoning style, and any factor that may have influenced the formation of the delusion (ideation) and what the delusional individual consider as evidence for the delusion.

The discussion and analysis that are performed during CBT therapeutic can help deconstruct the ideation that is at the heart of the delusional disorder [7].

• Supportive Therapy

Supportive Therapy aims at reducing the discomfort of the delusional individual through gaining insights about the individual experiences with the delusion and providing suggestions.

This therapeutic approach can also help the acceptance of the treatment process through educating the delusional individual about the illness [8].

Conclusion

Psychotic disorders are associated with individuals that have different perceptions of reality than those of most people around them. Delusions are also psychotic disorders characterized by a fixed and non-changeable interpretation of the reality which other people around them do not perceive.

The delusion is also a process that relies on building fixed ideas and concepts which explain the difficulty in treating delusional individuals. Therefore, achieving a successful treatment of a particular delusion would involve deconstructing those exact same ideas and concepts that make the delusion. However, building a good doctor-patient relationship is the key to the success of the treatment.

The post What Are the Most Common Delusions? appeared first on .

1- What Are Omega 3 Fatty Acids?

Lipids or fats are made from saturated and unsaturated fatty acids. Omega 3 fatty acids are a type of fatty acids known as polyunsaturated fatty acids.

Omega 3 Fatty Acids are also divided into docosahexaenoic acid (DHA), linolenic acid (ALA), and eicosapentaenoic acid (EPA).

Docosahexaenoic Acid (DHA) is the principal constituent of the plasma membrane of neurons found in the brain and cerebral cortex. It is also found in the retina and skin.

Eicosapentaenoic Acid (EPA) is essential for the synthesis of the vasodilator, anticoagulant, and inflammatory hormone, Prostaglandin (PG). It is also essential critical for the synthesis of the pro-coagulation and thrombosis factor, thromboxane, and the inflammation mediators, leukotrienes.

Linolenic Acid (ALA) is involved in the regulation of blood lipids and endothelial (Vessels) function. It has also significant anti-inflammatory and anti-thrombotic effects.

2- Which Types of Omega-3 Fatty Acids Are Found in Fish?

Docosahexaenoic Acid (DHA) and Eicosapentaenoic Acid (EPA) are found in fatty fish such as salmon, tuna, herring, mackerel, sardine, and fish oils,

Linolenic Acid (ALA) is found in fish but in flaxseed, chia, walnuts, hemp, and vegetable oils.

3- Omega 3 Benefits for the Brain

Omega 3 fatty acids are present in the membrane of brain cells (neurons) and are protecting factors of the nervous system [1]. These are some of the functions of omega 3 fatty acids in the brain:

• Omega 3 Fatty Acids and Neurotransmission

Neurotransmission is the process of transmission of information between the brain and the other parts of the body.

This transmission is carried out by neurotransmitters, such as dopamine, serotonin, glutamate, GABA, along the neurons.

Neurotransmitters travel from one neuron to another through synapses; however, to do so they must be transported by membranous vesicles that are made essentially made of omega 3 fatty acids [2].

• Omega 3 Fatty Acids and Neurogenesis

Neurogenesis is a process of making neurons and other types of brain cells that begins during embryonic life and that continue in certain parts of the adult brain such as the hippocampus and the subventricular zone of the cerebral cortex.

The hippocampus is the part of the brain that is involved in memory and the subventricular zone is implicated in olfaction (sensation of smell).

Omega 3 fatty acids are necessary for the production of new hippocampal neurons and olfactory neurons as they are essential for the formation of the membranes of the new neurons.

• Omega 3 Fatty Acids and Membrane Receptor Function

Omega 3 fatty acids have been shown to regulate the activity of the adenosine A_2A and dopamine D₂ receptors that are found on neurons, and which modulate the function of the neurotransmitters, glutamate, and dopamine [3].

• Omega 3 Fatty Acids and Synaptic Plasticity

Neurotransmission is performed through the transfer of neurotransmitters from one neuron to another through synapses.

The changes in strength or weakness of the synapses are known as synaptic plasticity. These changes can regulate the number of neurotransmitter receptors that bind neurotransmitters, and therefore, control the excitation of neurons.

Omega 3 fatty acids are involved in changing the strength or efficacy of synaptic plasticity and inducing the growth of new synaptic connections [4].

• Omega 3 Fatty Acids and Neuroinflammation

Neuroinflammation is an inflammation that happens within the central nervous system (brain and spinal cord) following injury.

Omega 3 fatty acids have been shown to have anti-inflammatory properties through their involvement in the synthesis of pre-resolving mediators, such as resolvins, protectins, and maresins. These mediators are involved in the resolution of inflammation [5].

4- Omega-3 Fatty Acids and Neuropsychiatric Disorders

• Omega-3 Fatty Acids and Schizophrenia

A study found that the blood levels of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are significantly lower in schizophrenia patients compared to healthy control individuals.

It also found that schizophrenia patients who consume more omega 3 fatty acids have an improvement in schizophrenia symptoms [6].

• Omega-3 Fatty Acids and Mood Disorders

Mood disorders have been associated with abnormalities in the composition and concentration of omega 3 fatty acids.

Patients with major depression have significantly lower omega 3 fatty acids in the blood cells and the severity of the depression correlated with the concentration of 3 fatty acids [7] [8].

5- Omega-3 Fatty Acids and Alzheimer’s Disease (AD)

Several studies have shown a correlation between Alzheimer’s disease (AD) and the decrease in the levels of omega 3 fatty acids in the hippocampus and cortex [9][10].

However, further clinical trials are required to confirm the beneficial role of omega 3 fatty acids for patients with Alzheimer’s disease.

6- Omega-3 Fatty Acids and Attention Deficit Hyperactivity Disorder (ADHD)

Although the effect was modest, a study reported that supplementation with omega 3 fatty acids improved the symptoms of attention deficit hyperactivity disorder (ADHD) [11].

7- Omega-3 Fatty Acids and Acute Neuronal Injury

Excess or chronic neuroinflammation can cause damage and death of nerve cells. Through their neuroprotective and anti-inflammatory properties, Omega 3 fatty acids can prevent the induction of acute neuronal injury that is can be caused by neuroinflammation [12].

8- Omega-3 Fatty Acids and Traumatic Brain Injury

Traumatic brain injury can result in sensory and motor disabilities and post-traumatic inflammation that limit the regeneration of neuronal axons.

An experimental study showed a significant increase in locomotor performance and survival neurons following the administration of Omega 3 fatty acids [13].

Conclusion

Fish is rich in omega 3 fatty acids and specifically in docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). Omega 3 fatty acids have many roles in brain function, cognition, the generation of new neurons in the hippocampus and the cerebral cortex, and in neuroinflammation.

Omega 3 fatty acids also have neuroprotective properties that can help with the treatment of mental health disorders such as schizophrenia and major depression, Alzheimer’s disease, brain injury, ADHD, neuronal injury, and protection against neuroinflammation.

Therefore, to the question “Is It True That Fish Is Brain Food?”, the answer is an absolute, yes, and I will always have fish as part of my diet.

The post Is It True That Fish Is Brain Food? appeared first on .