• Redness
• Swelling
• Heat
• Pain
• Loss of Function

1. What Is the Main Cause of Inflammation in the Body?

There are many causes of inflammation that is triggered by the body’s immune system:

• Injury such as a splinter, scrapes, trauma, or any damage caused by a foreign object.
• Pathogens, including viruses, bacteria, parasites, or fungi
• Chemicals such as glucose, fatty acids, chemical irritants (e.g., acids), toxins, and alcohol
• Radiation such as sunburns
• Biological such as damaged cells in the body

2. What Happens During Inflammation?

Inflammation involves the contribution of different immune cells which release substances known as inflammatory mediators, including hormones such as histamine and bradykinin [1].

These inflammatory mediators induce vasodilation (dilatation of the vessels) which promotes the blood flow in the injured tissue and the recruitment of inflammatory cells (neutrophils, monocytes, and endothelial cells) to the site of injury.

The vasodilatation and the blood rush into the injured tissue result in redness and heat which are 2 signs of acute inflammation.

The pain associated with inflammation is caused by the irritation of local nerves by the inflammatory mediators.

These inflammatory cells have specific roles during acute inflammation:

• Neutrophils initiate the phagocytosis and killing of pathogens to decontaminate the wound, while also promoting cell proliferation and angiogenesis.
• Monocytes also contribute to the phagocytosis and killing of pathogens, and become macrophages, which remove dead cells, and support cell proliferation and tissue restoration following injury.
• Endothelial cells are the building blocks for vessels, and during wound healing, these cells generate new vessels (angiogenesis) to satisfy the metabolic demands of the highly proliferative healing tissue. 

Depending on the site of injury, a transitory loss of function can be observed due to tissue damage, swelling, or pain during inflammation.

3. How long Does Inflammation Last For?

Inflammation can be acute lasting for a few days (2-3 days) or chronic which lasts for a longer time until the insult is resolved.

What Are the Outcomes of Inflammation?

The resolution of acute inflammation (initial inflammation) depends on the causes and the extent of tissue damage. It is characterized by the following outcomes:

• Complete repair of the injured tissue and without scars
• Resolution of the inflammation with the formation of a scar or fibrosis
• Formation of an abscess
• Chronic inflammation if the initial inflammation persists and remains unresolved

The complete repair of the injured tissue or the formation of scars is mediated by a process known as wound healing.

Wound healing is a natural reaction of our body to tissue damage and involves crosstalk between different cells, cytokines, inflammatory mediators, and the vascular system to repair the damaged tissue.

4. What Are the Most Common Inflammatory Diseases?

The most common inflammatory diseases are associated with chronic mediated inflammation which includes the following diseases [2]:

• Rheumatoid Arthritis
• Cardiovascular diseases
• Inflammatory Bowel Disease (IBD) 
• Allergic Asthma
• Chronic obstructive pulmonary disease (COPD)
• Diabetes
• Chronic Kidney Disease
• Cancer

4.1. Rheumatoid Arthritis

Rheumatoid arthritis is due to a local chronic inflammation that results in the infiltration of immune cells into the joints and the release of inflammatory mediators such as cytokines.

4.2. Cardiovascular diseases

Atherosclerosis is associated with a chronic inflammation that leads to heart diseases such as stroke, and myocardial infarction.

4.3. Inflammatory Bowel Disease (IBD)

Inflammatory Bowel Disease (IBD) is a group of chronic inflammatory disorders affecting the bowels that are caused by ulcerative colitis (inflammation of the colon due to ulcer) or Crohn’s disease.

4.4. Allergic Asthma

Allergic asthma is due to the inflammation of the airways caused by the inhalation of an allergen which results in their swelling and tightening affecting breathing.

4.5. Chronic obstructive pulmonary disease (COPD)

COPD is a chronic inflammatory lung disease due to the exposure of the airways to harmful particles or gases causing inflammation that obstruct airflow in the lung leading to breathing difficulties.

4.6. Diabetes

One of the characteristics of diabetes is the infiltration of immune cells, such as macrophages, into pancreatic tissue, and their release of pro-inflammatory molecules responsible for inflammation.

4.7. Chronic Kidney Disease (CDK)

Chronic kidney disease or chronic kidney failure is a progressive loss of the function of the kidney resulting from the accumulation of body wastes and fluids in the blood.

One of the causes of chronic kidney disease is the inflammation of the glomeruli that filter blood for the elimination of waste and fluids in urine.

4.8. Cancer

Chronic inflammation is one of the characteristics of different types of cancer from various origins (Prostate, hepatic, colorectal, ovarian, pancreatic, and lung cancers).

4.9. Neurodegenerative diseases

Neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease are associated with the production of proinflammatory molecules by the brain resident immune cells and microglia which cause brain damage.

5. What Is the Difference Between Inflammation and Infection?

Infections cause inflammation which is a natural process by which the body’s immune system fights against pathogens, including bacteria, viruses, fungi, or parasites.

6. How Do You Get Rid of Inflammation in the Body?

Unlike acute inflammation, chronic inflammation can last for a longer period, and therefore, requires management and treatment through lifestyle changes or medications [3].

6.1. Lifestyle changes

6.1.1. Diet

A diet rich in glucose and processed food rich in saturated fat and trans fats promotes inflammation leading to cardiovascular diseases and type 2 diabetes. Hence, a low glucose diet and avoiding processed food can prevent inflammation.

A diet rich in vegetables and fish oils, nuts, mung bean, green and black teas, and certain species (e.g., ginger, turmeric) can prevent or reduce inflammation as they contain antioxidants and polyphenols which have anti-inflammatory properties.

6.1.2. Physical Activity

In addition to weight loss associated with exercising, physical activity also results in energy consumption with reduces the levels of proinflammatory molecules in the body.

6.2. Medications

The most used anti-inflammatory medications include nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids. 

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as naproxen, ibuprofen, and aspirin, alleviate pain by inhibiting the function of the enzyme cyclooxygenase (Cox) involved in the synthesis of the proinflammatory molecules, prostaglandins.

Corticosteroids are prescribed for some inflammatory conditions such as arthritis, asthma, systemic lupus, and sarcoidosis.

Conclusion

Acute inflammation is a natural process by which the body’s immune system responds to injuries and infections. Acute inflammation takes a few days to resolve, leading to a complete repair of damaged tissues, fibrosis (scars), formation of an abscess, or chronic inflammation.

Chronic inflammation can be associated with several inflammatory diseases such as rheumatoid arthritis, allergic asthma, cancer, diabetes, cardiovascular diseases, chronic kidney disease, COPD, inflammatory bowel disease, and neurodegenerative diseases.

The treatment of chronic inflammation includes lifestyle changes, physical activity, and medications using anti-inflammatory drugs such as NSAIDs and corticosteroids.

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• Osteoarthritis
• Rheumatoid Arthritis
• Bursitis
• Gout

Joint diseases or arthropathies can be due to joint trauma, autoimmunity, infections, metabolic, or heredity.

1. What is joint Made of?

Joints or articulations connect the bones of the body and their composition depends on the type of joint that can be fibrous, cartilaginous, synovial, or facet [1].

1.1. What Is Fibrous Joint?

Fibrous Joints are fixed joints that do not move or have very restricted mobility. They are made of collagen fibers and are further divided into sutures, syndesmoses, and gomphoses.

• What Is Suture Joint?

Suture joints are the non-moving joints of the skull (cranium) in adults and which at birth had the mobility to allow the brain to develop further.

Once the brain developed, sutures lose their mobility and are held together with fibers known as Sharpey’s fibers that ossify and lead to the formation of one bone, the skull.

• What Is Syndesmosis?

Syndesmoses (plural for syndesmosis) are slightly moving joints that are together through interosseous membranes such as the one connecting the tibia bone with the fibula bone.

• What is Gomphosis joint?

Gomphoses (plural for gomphosis) are non-moving joints that connect the teeth to their sockets in the upper jawbone or mandible.

1.2. What Is Cartilaginous Joint?

This type of joint bones connections involves hyaline cartilage and/or fibrocartilage. Bones with hyaline cartilage are associated with joints of long bones, while bones with hyaline and fibrocartilage are associated with bones such as the pubic symphysis.

1.3. What Is Synovial Joint?

Synovial joints are the main joints of the body that can freely move. The type of joint is made of the synovial cavity which contains the synovial liquid secreted by the synovial membrane (synovium) and that fills the gap between the articular hyaline cartilage covering the ends of two bones.

The synovial cavity and the articular cartilages laterally surround the bursa, ligaments, and tendons. Examples of this type of joint are the knees and the wrists.

1.4. What Is Facet Joint?

Facet joints are joints that connect two vertebrates through their processes.

2. What Is Osteoarthritis?

Osteoarthritis is a degenerative joint disease characterized by an abrasive wearing of the cartilage of the joint and the underlying bone tissues resulting in the generation of abnormal bone growth from the margin of the affected joint [2].

Osteoarthritis mostly affects the fingers, hips, lower back, and neck. It affects 10% of men and 18% of women over 60 years of age, worldwide.

2.1. What Causes Osteoarthritis?

The causes of osteoarthritis can be primary or secondary.

2.1.1. What Is Primary Osteoarthritis?

Primary osteoarthritis is osteoarthritis which cause is not known (Idiopathic).

2.1.2. What Is Secondary Osteoarthritis?

Secondary osteoarthritis is osteoarthritis caused by a secondary condition or disease such as:

• Trauma

Injuries causing damages to the joints can result in secondary osteoarthritis.

• Congenital Joint Abnormalities

These abnormalities are acquired during embryonic life or at birth such as arthrogryposis multiplex congenital (crooked joints), or spondylolysis.

• Metabolic Diseases

The accumulation of minerals in the body including the joints is associated with diseases such as Wilson’s disease (accumulation of copper), hemochromatosis (accumulation of iron), or chondrocalcinosis (accumulation of calcium).

• Join Infections

Join infection by a pathogen can result in the inflammation of joints that can lead to osteoarthritis.

• Disorders of the Hyaline Cartilage

These disorders include diseases such as osteochondritis dissecans (non-traumatic loose body in the joints).

• Endocrine Diseases

Endocrine diseases, such as acromegaly, result in the enlargement of the joints that can cause osteoarthritis.

• Neurogenic Arthropathy

Neurogenic Arthropathy or Charcot Joint is a degenerative disease of weight-bearing joints.

• Aseptic Necrosis

This disorder is associated with the lack of blood supply to the joints causing necrosis (type of cell death).

2.2. What Are the Symptoms of Osteoarthritis?

Osteoarthritis is characterized by the following symptoms:

• Pain
• Stiffness
• Crepitus (crackling sound of the affected joint)
• Calcic spurs on the fingers and toes (outgrowth of new bones)

3. What Is Rheumatoid Arthritis?

Rheumatoid Arthritis is an autoimmune disease that affects primarily the joints but also organs of the body.

It is due to the attack of the joints by the body’s own immune system by cytokines, chemokines, and metalloproteases (tissue ingesting enzymes) causing inflammation of the synovial membrane (synovium), and the destruction of the cartilage and bone tissue of the affected joint [3].

3.1. What Causes Rheumatoid Arthritis?

The cause of rheumatoid arthritis is unknown; however, several risk factors have been proposed:

• Genetic Factors

There is an increase of rheumatoid arthritis in individuals with a family history of this disease which may involve genes involved in major histocompatibility complex (MHC) that plays an essential role in adaptive immune response [4].

• Environmental Factors

Environmental Factors including smoking and viral infections may contribute to the inflammation.

3.2. What Are the Symptoms of Rheumatoid Arthritis?

Rheumatoid arthritis is characterized by the following symptoms:

• Pain
• Swelling
• Stiffness
• Fixed deformities
• Fatigue
• Anorexia

4. What Is Bursitis?

Bursitis is an acute or chronic inflammation of the bursa affecting joints of the knee, hip, elbow, Achilles tendons, and Ischia.

4.1. What Causes Bursitis?

Bursitis is due to the following causes:

• Injury
• Inflammation (rheumatoid arthritis, gout, spondylitis, and psoriatic arthritis)
• Infection (e.g., Staphylococcus aureus)

4.2. What Are the Symptoms of Bursitis?

Symptoms of bursitis are mainly associated with pain, swelling, and limited motion of the joint.

5. What Is Gout?

Gout is characterized by the deposition of monosodium urate around and in the joints due to hyperuricemia (a high level of uric acid in the blood) [5].

The most common affected joints are those of the toe, knee, wrist, ankle, and elbow.

5.1. What Causes Gout?

Hyperuricemia is due to decreased renal or intestinal excretion of urate, increased production of urate, or increased intake of purine-rich foods such as liver, sardines, mussels, herring, anchovies, asparagus, and mushrooms.

5.2. What Are the Symptoms of Gout?

Gout is characterized by the following symptoms:

• Sudden onset of pain
• Severe pain
• Swelling
• Redness
• Warmth
• Tenderness

Conclusion

Joints are extremely important in our everyday life as it allows us to sit, walk, pick a book to read, or exercise. However, alterations in any component of the joint can make all these simple body movements difficult to execute, particularly, when these alterations affect the body-bearing joints.

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• Osteoporosis
• Paget’s Disease
• Rickets and Osteomalacia
• Osteogenesis Imperfecta
• Bone Tumors

1. What is Bone Made of?

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 [1].

1.1. What Are the Bone Cells and Their Functions?

There are 4 types of bone cells: osteoblasts, osteocytes, osteoclasts, and bone lining cells.

• What Are Osteoblasts?

Osteoblasts are cells that have a cuboidal shape (resembling a cube) found on the surface of bones where they produce components of the mineralized matrix including a specific type of collagen known as ossein, proteoglycans, and cell attachment proteins.

Osteoblasts are also involved in the mineralization of the bone by promoting the deposition of calcium and phosphorus to form the bone mineral hydroxyapatite crystals (bone minerals).

• What Are osteoclasts?

Osteoclasts are a type of phagocytes (engulfing cells) involved in the resorption of the bone that allows its remodeling during growth or mechanical stress.

The resorption of bone is a mechanism by which the bone tissue is broken down into minerals and their transfer to the blood.

• What Are Osteocytes?

Osteocytes are oblate-shaped cells that are widely distributed within the bone where they mainly act as mechanical stress sensors (mechanoreceptors).

They also contribute to the resorption of the bone tissue through a mechanism similar to the one of osteoclast known as osteocytic osteolysis and which involves the secretion of a protein known as sclerostin.

• What Are Bone Lining Cells?

Bone Lining Cells are elongated cells found on the surface of the bone where the protect the bone tissue from resorption.

1.2. What Is the Mineralized Matrix of the Bone?

The mineralized matrix of the bone is made up of deposited hydroxyapatite crystals, ossein, proteoglycans (glycosylated proteins), and cell attachment proteins. This matrix is what makes the bonne hard [2].

2. What Is Osteoporosis?

This disease is characterized by bone fragility and an increased risk of fractures due to the weakening of the bone structure and a low bone mass [3].

2.1. What Is the Difference Between Type 1 and Type 2 Osteoporosis?

Type 1 osteoporosis is called primary osteoporosis that is due to the loss of bone structure and mass associated with age, while secondary osteoporosis (Type 2 Osteoporosis) is associated with specific diseases and medications.

2.2. What Causes Osteoporosis?

The causes of osteoporosis depend on the type of osteoporosis, primary or secondary.

Primary osteoporosis is due to an age-related imbalance between the production of new bone and bone tissue resorption.

At an old age, our body capacity to form new bone is significantly reduced, while the resorption of bone tissue continues.

Secondary osteoporosis is associated with the following diseases and medications:

• Genetic Diseases such as cystic fibrosis and idiopathic hypercalciuria.

Osteoporosis associated with cystic fibrosis is due to the malabsorption of calcium and vitamin D, while Osteoporosis related to idiopathic hypercalciuria is due to the reduction in renal retention of calcium caused by renal failure.

• Hyperparathyroidism

This disorder is characterized by an increased secretion of the parathyroid hormone (Parathyrin) which regulates calcium concentration in the serum through its action on the bone, intestine, and kidneys.

• Intestinal Disorders such as celiac disease, biliary cirrhosis, Chron’s disease, or ulcerative colitis or alcoholic cirrhosis. Intestinal disorders are associated with malabsorption of calcium and phosphorus.

• Anorexia Nervosa

• Hormonal Imbalance such as estrogens or testosterone deficiency during adolescence associated with disorders that affect the onset of puberty (e.g., Turner syndrome or Kallmann syndrome)

• Tumors such as tumors of the pituitary gland or adrenal glands can increase the resorption of bone tissue that is mediated by increased glucocorticoids production.

• Autoimmune and Allergic Disorders such as lupus and rheumatoid arthritis.

• Medications such as glucocorticoids for the treatment of chronic inflammation, antiepileptic drugs, and cyclosporine, or tacrolimus for the prevention of organ transplant rejection.

2.3. What Are the First Signs of Osteoporosis?

The first signs of osteoporosis are a broken bone and a stooped posture (forward bending) due to fracture in the spine leading to difficulties in supporting own weight.

3. Paget’s Disease of Bone

This disease is characterized by alterations in the formation of new bones particularly the spine, skull, and leg bones associated with increased activity of osteoclasts involved in the resorption of bone tissue [4].

3.1. What Causes Paget’s Disease?

Although there is a strong familial predisposition, no genetic alterations have been associated with Paget’s disease.

The causes for this disease are unknown and potential involvement of a viral infection with measles has been proposed [5].

3.2. What Are the Symptoms of Paget’s Disease of Bone?

Although in most cases no symptoms are observed with this disease, symptoms are associated with deformities, fractures, and pain due to the production of bones with disorganized structures.

4. Rickets and Osteomalacia

Both rickets and osteomalacia are due to a deficiency in vitamin D in children (rickets) or in adults (osteomalacia) [6].

Vitamin D is essential in facilitating the mineralization of the bone by ensuring that sufficient concentrations of calcium and phosphorus are available.

Symptoms of rickets manifest with bone deformities such as bowed legs, pain, and large forehead while osteomalacia manifests with pain, bone fragility, and muscle weakness.

5. Osteogenesis Imperfecta

This genetic disease is also known as brittle bone disease characterized by bones that break easily. It is caused by mutations in the genes that encode collagen type I necessary for the formation of the bone tissue [7].

Depending on the severity of the disease, the symptoms manifest as follows:

• Short stature
• Bone malformations (long bones)
• Curved spine, blue color of the eye whites (sclerae)
• Loose joints
• Misshapen or brittle teeth
• Compression of the spine vertebrates
• Hearing loss
• Deformed hip
• Muscle weakness.

6. Bone Tumors

Bone tumors can be benign (noncancerous) such as osteochondroma or malignant such as osteosarcoma and Ewing’s sarcoma

• Osteochondroma

This benign tumor is characterized by an overgrowth of cartilage or bone near the growth plate.

Most osteochondromas do not manifest with symptoms; however, complications such as fractures, mechanical joint issues, and bone deformity can be caused by the tumor.

• Osteosarcoma

Osteosarcoma is a bone cancer mostly found in children and young adults and is caused by the malignant transformation of bone cells and supportive cells in the bone tissue.

It develops in the bones around the knee, the thigh, the tibia, and near the shoulder.  It manifests with pain, swelling, and fractures [7].

• Ewing’s sarcoma

Ewing’s sarcoma is an aggressive tumor of the bone or soft tissue also associated with malignant transformation of bone cells and supportive cells in the bone tissue [8]. It is mainly associated with adolescents and young adults.

This tumor develops in the bones of the leg, feet, arms, hands, spine, chest, pelvis, and skull but can also be found in other parts of the body in a form of soft tissue. It manifests with symptoms such as swelling, fever, pain, and fractures.

Conclusion

Most bone diseases are due to alterations of the balance between bone formation and bone tissue resorption associated with bone cells, and with calcium, phosphorus, and vitamin D deficiencies.

In certain cases, the cause of the bone disease is associated with benign or cancerous tumors that arise from the bone cells or the soft tissue.

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The hypothalamus works like a thermostat for the body and maintains the temperature in the range of 97.7-99.5 °F (36.5-37.5 °C) [1].

• What Is Hypothermia?

Hypothermia is when the body temperature is lower than 95 °F (35.5 °C).

• What Is Fever?

Hyperthermia is when the body temperature is higher than 99.5 °F (37.5 °C).

• What Is Hyperpyrexia?

Hyperpyrexia is when the temperature is higher than 104 °F (40 °C).

1. How Does the Hypothalamus Regulate Body Temperature?

The Hypothalamus regulates body temperature (Thermoregulation) through 3 mechanisms: Afferent sensing, central sensing, and efferent responses [2].

• Afferent Sensing

Afferent sensing is associated with temperature sensors known as thermoreceptors that are distributed throughout the body.

Thermoreceptors are sensory nerve endings that are part of the nervous system. They are categorized into receptors for warmth detection and receptors for cold detection [3].

Receptors for warmth detection are known as C fibers, while receptors for cold are known as Aδ fibers.

• Central Control

This part is controlled by the hypothalamus which receives information about the body temperature from the thermoreceptors.

• Efferent Responses

Efferent responses are automatic responses to changes in the temperature such as sweating, vasoconstriction (narrowing of the vessels), vasodilatation (dilatation of the vessels), and shivering [4].

2. What Hormone Controls Body Temperature?

The hypothalamus is the part of the brain that controls body temperature; however, heat is internally generated by the metabolisms (energy production) of the different organs of the body where thyroid hormones such as thyroxine (T4), and triiodothyronine (T3) play an essential role.

3. Does Low Body Temperature Indicate Thyroid Problems?

A low body temperature is not necessarily due to problems with the thyroid; however, increased sensitivity to cold is one of the symptoms of hypothyroidism [5].

4. What Time of Day Is Body Temperature the Highest?

The highest body temperature was reported to be an early evening at 6 pm [6].

5. What Factors Affect Body Temperature?

Temperature fluctuations can be associated with the following factors:

• Age

Older individuals (more than 60 years old) have a lower temperature mean (average) compared to those individuals less than 60 years old [1] [7].

• Sex

Women have a slightly lower temperature than men [1]. However, during pregnancy and ovulation, this temperature increases, while it is lower at the start of the menstrual cycle.

• Circadian Rhythms

The body temperature is highest at 6 pm in the evening and lowest at 3 am in the morning [6].

• Physical activity

During physical activity and exercise the body generates a significant amount of heat due to the intense energy consumption.

• Meals

There is an increase in the body s metabolism meals which leads to an increase in the temperature of the body.

• Fever

Fever is due to infections such as a virus or bacteria, heat exhaustion, and inflammation (e.g., rheumatoid arthritis).

• Medications

Antibiotics and blood pressure or seizures can increase the body temperature.

6. What Vitamins Help with Body Temperature?

Vitamins B1, B2, B3, B5, and B7 (Biotin) are directly involved in the metabolic conversion of food into energy necessary for the maintenance of body temperature.

7. Can Mental Stress Cause Fever?

Some individuals, especially young women, develop a high fever when they are exposed to emotional events which cause stress. This type of fever is known as psychogenic fever [8].

8. What Are the Disorders of Body Temperature?

Disorders of the body temperature include any disorders that can cause a fever or hypothermia.

8.1. What Causes Fever?

Fever is mainly caused by sepsis, however, inflammation, and medications can also contribute to fever.

8.1.1. What is Sepsis?

During sepsis, fever is caused by exogenous pyrogens (e.g., pathogens) or endogenous pyrogens such as cytokines that interact with an area of the brain known as the organum vasculosum of the lamina terminalis (OVLT) or supraoptic crest.

The activation of the OVLT results in the increase in the synthesis of molecules known as prostanoids which are involved in inflammation (e.g., prostaglandins and prostacyclins) and in vasoconstriction (thromboxanes).

Prostanoids act by slowing down the activity of the warm sensitive neurons of the hypothalamus leading to an increase in the temperature [9].

8.1.2. Is Fever Associated with Inflammation?

Inflammation is a natural event that occurs following tissue damage or infections that results in swelling, redness, heat, and pain.

During inflammation, several inflammatory mediators are released by the cells involved in wound healing or in fighting infections.

These mediators are also pyrogenic (causing fever) and may act in a similar way to that of the sepsis pyrogenic mediators.

In some cancer patients fever also appears to be mediated by the same mechanism as that of sepsis [10].

8.1.3. Which Drugs Induce fever?

Some pharmacological drugs can cause heat loss from the peripheries, directly damage tissues, interfere with the hypothalamus central temperature regulation, stimulate an immune response, or have pyrogenic properties [9].

• Antimicrobial agents such as beta-lactam antibodies and sulphonamides.
• Volatile anesthesic agents
• Anti-depressants such as SSRI
• Opioids such as fentanyl
• Central nervous system stimulants such as amphetamines and cocaine
• Psychedelics such as lysergide
• Anticholinergic agents such as bronchodilators and ephedrine
• Anti-emetics such as cyclizine
• Synthetic cathinones such as bupropion

8.1.4. What Is Endocrine fever?

Hyperthyroidism is associated with the increase in body temperature due to the increase in the secretion of the thyroid hormones, thyroxine (T4), and triiodothyronine (T3) that play an essential role in the metabolisms (energy production) of the different organs of the body [10].

8.2. What Causes Hypothermia?

There are several disorders and medications that cause hypothermia:

8.2.1. What Disorders Cause Hypothermia?

Some disorders can affect the body capacity to regulate core temperature:

• Hypothyroidism
• Diabetes
• Anorexia Nervosa
• Poor Nutrition
• Spinal Cord Injuries
• Severe Arthritis
• Stroke
• Parkinson Disease

8.2.2. What Medications Cause Hypothermia?

Changes in body temperature can be caused by the following drugs:

• Sedatives
• Antipsychotics
• Narcotic Pain Medications
• Antidepressants

8.3. Heart-Related Illness

In chronic heart failure, there is an alteration in the balance between heat production and heat loss but also an increased risk of ischemia or stroke that can damage the brain and also affect the metabolism [11].

Conclusion

The body temperature is controlled by the hypothalamus through mechanisms that involve afferent sensing, central control, and efferent responses. Any factors that disturb the normal functioning of these mechanisms lead to a change in the body’s temperature.

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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 .

1- What Are cytokines?

Cytokines are small proteins that are produced by white blood cells, such as lymphocytes T and lymphocytes B, and endothelial cells, mast cells, fibroblasts, and mesenchymal cells.

In the nervous system, cytokines are produced by microglia, astrocytes, endothelial cells, and macrophages [1].

• Lymphocytes T

Lymphocytes T are immune cells involved in the killing of viruses and cancer cells.

• Lymphocytes B

Lymphocytes B are immune cells that produce antibodies against viruses, bacteria, and cancer cells. Anomalies in the recognition of the body’s own antigens lead to autoimmune diseases.

• Endothelial Cells

Endothelial cells are the building block of vessels.

• Mesenchymal Cells

Mesenchymal Cells are cells that generate connective tissues.

• Fibroblasts

Fibroblasts are cells found in connective tissues where they produce collagen and are also involved in wound healing.

• Mast Cells

Mast cells are found in connective tissues where they produce histamine (neurotransmitter) and heparin (anticoagulant).

• Macrophages

Macrophages are a type of white cells that are responsible for engulfing and digesting viruses, microbes, cancer cells, debris of cells, and foreign substances.

• Microglia

Microglia are non-neuronal cells that are specifically found in the brain and the spinal cord where they play an essential role in the immune response.

• Astrocytes

Astrocytes are also non-neuronal cells responsible for providing nutrients to the nervous system and support the activity of the nervous system endothelial cells in forming the blood-brain barrier.

2- What Are Chemokines?

Chemokines are also cytokines that control the movement of lymphocytes in response to inflammation, infection, or cancer.

3- What Are Secondary Messengers?

When a ligand such as a growth factor, binds to a receptor on the surface of cells in the body there is a transmission of information within the cells by small molecules and ions that promote the expression of proteins necessary for the function of the cell.

4- What Are Reactive Oxygen Species (ROS)?

Reactive oxygen species (ROS) are produced by the metabolism of oxygen (O2) in the body’s cells. An excess of ROS (e.g., free radicals) can damage the DNA of the cells causing their death or mutations that can lead to cancer.

5- What Causes Neuroinflammation?

• Traumatic Brain Injury

A traumatic brain injury can be mechanical such as a blow to the brain or spinal cord leading to tissue damage, or pathological due to tissue damage caused by excitotoxicity (excessive excitation of neurotransmitters), ischemic injury, or alterations in mitochondria function [2].

• Spinal Cord Injury

A spinal injury is due to an acute or localized (focal) trauma, a reduced blood supply (ischemia), or excitotoxicity.

• Infection

The most known infection of the central nervous system (CNS) is due to Mycobacterium tuberculosis (tuberculosis), but there are other infections such as Plasmodium falciparum (malaria), Rickettsia conorii (Boutonneuse fever), Trypanosoma cruzi (Chagas disease) [3].

These infections cause inflammation by altering the function of the CNS vessels.

• Autoimmunity

Autoimmunity is due to the production of antibodies by lymphocytes B against antigens that are expressed by normal cells, including cells of the brain and spinal cord.

These antibodies are known as autoantibodies and attack the body’s cells and tissues causing their damage and inflammation.

• Toxic Metabolites

Alterations in CNS metabolites (Neurometabolites) such as N-acethylaspartate (NAA), creatine, and glutamine can cause injuries or death of neurons in the central nervous system leading to inflammation.

• Aging

Although the mechanisms are not known, there is an increase in proinflammatory cytokines and a decrease in anti-inflammatory cytokines in the aged central nervous system.

6- What Are the Symptoms of Neuroinflammation?

The symptoms of neuroinflammation depend on the injured part of the central nervous and the type of injury; however, some of the common symptoms are pain, depression, and fatigue.

7- What Mechanisms Mediate Inflammation in the Brain?

The immune response and inflammation in the brain and spinal cord are mainly mediated by microglia and astrocytes but also endothelial cells, and macrophages.

The brain and spinal cord are closed environments due to the presence of the blood-brain barrier (BBB), therefore, not all the cells of the immune system can enter [4].

Following the damage of the brain or spinal cord, microglia are activated and secrete cytokines and chemokines that recruit other cell types such as astrocytes, endothelial cells, and macrophages to repair the damage.

However, during the early stage of spinal injury, there is an infiltration of other immune cells, such as neutrophils, and monocytes. Lymphocytes also contribute to inflammation at a later stage of the injury [1].

9- How Does Neuroinflammation Contribute to Neurodegeneration?

Although the mechanisms are not well known, neuroinflammation has been implicated in the pathogenesis of dementia through its role in cerebral small vessel disease (SVD)-vascular dementia [5].

Neuroinflammation contributes to multiple sclerosis through the disruption of the blood-brain barrier resulting in the recruitment of immune cells and the secretion of proinflammatory factors and antibodies against the myelin sheath.

It was suggested that neuroinflammation also contributes to Alzheimer’s disease through the incapacity of microglia to eliminate amyloid-beta plaques [6].

10- How Is Neuroinflammation Treated?

For multiple sclerosis, a monoclonal antibody (rituximab) has been successfully used to target lymphocytes B responsible for the production of antibodies against the myelin sheet.

However, this treatment has also a potential risk of inducing a rare disease known as progressive multifocal leukoencephalopathy that causes damage to the white matter in multiple parts of the brain [7].

For Alzheimer’s disease and Parkinson’s disease, there are several ongoing clinical trials using inhibitors that regulate the function of microglia and astrocytes which are involved in the pathogenesis of AD and PD [7].

Conclusion

Neuroinflammation is a natural response of the brain and spinal cord to injuries, autoimmunity, infection, toxic metabolites, and aging.

Although its role is to promote the repair of tissues’ damage, proinflammatory cytokines can also result in the recruitment of other types of cells, such as immune cells, fibroblasts, and lymphocytes that can lead to additional and indirect tissue damage resulting in neurodegenerative diseases such as dementia, multiple sclerosis, Alzheimer’s disease, and Parkinson’s disease.

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However, pain is not only physical because a sensory experience can also be due to mental health conditions such as depression, anxiety, or anger.

Therefore, a difference exists between pain and the cause of the pain. The link between the two is mediated by our nervous system through a process known as nociception.

It was estimated that 20.4% of adult individuals had chronic pain and that 7.4% of adult individuals had chronic pain which limited their activities, such as working, in the past 3 months [2].

1- What is emotional pain?

Emotional pain can be defined by the heartache we feel when losing someone or something that was important to us.

2- Is pain an emotion or feeling?

A Feeling is the outcome or expression of our interpretation of an emotion that was caused by pain (physical or psychological).

3- What is the worst mental pain?

They are several mental conditions that are characterized by unbearable psychological and emotional pain that is characterized by suicidal thoughts (suicidal ideation).

These include Emotionally unstable personality disorder (borderline personality disorder) and seasonal affective disorder.

4- What are Nociceptors?

Nociceptors are sensory neurons that respond to damage or potential damage through alerting communications to the brain and spine [3].

Nociceptors can be mechanical, thermal, mechano-thermal, polymodal, or silent.

Mechanical nociceptors respond to mechanical damage or pressure, while thermal nociceptors respond to cold or hot temperatures.

Mechano-thermal nociceptors respond to both mechanical and thermal stimuli, while silent nociceptors respond to inflammatory mediators.

5- What Are the Types of Pain?

• Acute Pain

Acute pain is caused by spasms of skeletal muscles and the activation of the sympathetic nervous system that is due to an injury or a trauma. The duration of the pain is short and disappears with the healing of the injury.

• Chronic Pain

Chronic pain is also caused by an injury or a disease, but the pain would continue even after the healing period.

• Nociceptive Pain

Nociceptive pain is caused by an injury, trauma, chemicals, or surgery that results in the activation and release of inflammatory mediators by nociceptor neurons (sensory neurons) which activate inflammation in the injured area [4].

• Neuropathic Pain

Neuropathic pain is due to direct damages or compression of the sensory nerves associated with sciatica, neuropathies such as phantom limb pain, Wallerian degeneration, segmental demyelination, or diabetic neuropathies.

5- Are There Other Classifications of Pain?

• 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.

• Hyperpathia

Hyperpathia is a neuropathic pain characterized by an abnormal, repetitive, and elevated pain reaction to the stimulus (cause).

• Causalgia

Causalgia is neuropathic pain that combines a sensation of burning pain, hyperpathia, and allodynia.

• Dysesthesia

Dysesthesia is an unpleasant and abnormal sensation such as cold sensation, tingling, burning, numbness, tickling, or pain that is caused by nerve trauma or irritation.

• 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.

• Hyperesthesia

Hyperesthesia is characterized by an increased sensitivity to stimuli associated with senses such as hearing, tasting, touch, smelling,

Hyperesthesia is caused by excessive stimulation of the nervous system such as overconsumption of caffeine.

• Hypoalgesia

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

6- What Are the Symptoms of Pain?

The symptoms of pain are categorized corresponding to the pain intensity, duration, and pain-related disability [5]. These categories allow the classification of pain into mild, moderate, or severe using assessment methods:

• Visual Analogue Scale

This method consists in drawing a line between two points. The first point is the “no pain” and the second point is the “as bad as it could be”.

The individual in pain is requested to mark the level of pain within the two endpoints.

• Graphic Rating Scale (GRS)

This method represents a drawing of a line with levels from 1 to ten representing the intensity of pain. No pain is represented by the number 0 and “as bad as it could be” is represented by the number 10.

The individual in pain is requested to indicate the number from 0 to 10 which represents the level of pain experienced by the individual.

• Verbal Rating Scale

This method evaluates the pain experienced by the patient using adjectives to describe the level of pain.

• Pain Drawing

In this method, the patient is requested to indicate the location of the pain on a drawn human body.

• McGill Pain Questionnaire (MPQ)

This questionnaire assesses the pain-rating index, the number of words describing the pain, and the level of pain on a scale of 1-5.

8- What Is the Treatment of Pain?

Pain is mainly managed.

• Non-pharmacological Management

Non-pharmacological management involves:

– Exercise such as swimming, walking, yoga, Pilates, and exercise bike.

– Physical therapy through physiotherapists and occupational therapists who will help with stretching and pain-relieving exercises.

– Psychological management through social support, psychologists, and psychotherapists.

• Pharmacological Management

For mild and moderate pain, non-opioid analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are used.

Although there is a high risk of dependency, opioid analgesics (e.g., morphine) are used for the treatment of severe pain.

Conclusion

Although the risk factors in the progression from acute to chronic pain are well known, identifying patients who are predisposed to this progression through assessing the status of the acute pain, the physiological and reactivity of the patients to pain, should help better manage this switch from acute to chronic pain.

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• Direct Sciatic Nerve Compression
• Inflammation

It is estimated that the annual incidence in the general population is between 1% to 5% and the lifetime incidence is between 10% and 40% [1].

1- How Long Will Sciatica Take to Heal?

Sciatica can lasts 4-6 weeks, however, it can last longer depending on the causes.

2- What is the Sciatic Nerve?

The sciatic nerve is responsible for sensations in the feet and legs.

It is hosted and protected by the spine and starts at the base of the brain and travels all the way to the lumbar region of the spine where it branches into right and left.

Each branch will continue its enervation route all the way to the feet (right or left).

2- What Triggers Sciatica?

• Direct Sciatic Nerve Compression

Our spine or vertebral column is made of 24 vertebrates, the sacrum, and the coccyx.

We have 7 vertebrates of the neck (cervical vertebrates), 12 of the midback (thoracic vertebrates), and 5 of the lower back (lumbar vertebrates).

Each vertebrate is joined to another vertebrate by a disc (intervertebral disk).

• Lumbar Herniated Disc

When a lumbar intervertebral disc bulges or herniates, it can compress the sciatic nerve resulting in pain.

Lumbar Herniated Disc causes 90% of the direct sciatic nerve compressions [2].

• Degeneration

The degeneration of the tissues of vertebrates in the lumbar part of the spine can result in the compression of the sciatic nerve.

• Spondylolisthesis

When a vertebrate slips out of position due to a stress fracture it can compress the sciatic nerve.

• Lumbar Spinal Stenosis

The spine canal through with passes the sciatic nerve may decrease in size due to factors, such as age, resulting in the compression of the sciatic nerve.

• Lumbar or Pelvic Muscular Spasm

Spasm in muscles such as the piriformis muscle can irritate or compress the sciatic nerve.

• Hematoma or abscess

Hematoma or abscesses around the sciatic nerve can cause compression of the sciatic nerve.

• Tumors

Spinal tumors that originate from the vertebra, spinal cord, or nerves can also compress the sciatic nerve.

• Inflammation

Within the spine, there is an acid substance known as hyaluronic acid. When the spine is damaged, this substance leaks into the surrounding tissues of the sciatic nerve causing its irritation, inflammation, or compression.

3- What Are the Risk Factors of Sciatic Nerve Pain (Sciatica)?

• Occupation and Sciatica

There is a predisposition for sciatica in workers including truck drivers, carpenters, and machine operators due to long hours in uncomfortable positions.

• Lack of Physical Activity and Sciatica

Lack of physical activity can weaken lower back muscles (lack of flexibility, tone, and movement) resulting in less support for the lumbar spine and potential compression of the sciatic nerve.

• Smoking and Sciatica

Although the mechanism is not well known, smoking appears to be a modest risk of sciatica [3].

• Mental Health and Sciatic

Depression and anxiety disorders have been associated with sciatica due to the release of inflammation factors (inflammatory mediators) in the lower back region which can irritate the sciatic nerve [4].

• Tall height in older age groups (50 to 60 years)

A study that included 13680 participants found a correlation between tall height and lower back pain or related surgery [5].

• Obesity and excess weight

Weight being carried in the front can be a weight on the spine and related muscles which may cause muscle strain that can potentially lead to sciatica.

• Genetic susceptibility

A study reported a higher incidence of sciatica or prolapsed disc in first-degree relatives of patients hospitalized for herniated lumbar disc or surgery [6].  

Another study of 9365 pairs of adult twins found a correlation between genetics and the incidence of sciatica [7].

• Previous injury

Previous injuries in athletes or workers can result in lumbar intervertebral disc bulges or herniation.

• Diabetes

Diabetes is a metabolic disorder that can cause damages to the sciatic nerve.

• Pregnancy

The growing baby during pregnancy can generate extra weight resulting in a weight that is applied on the spine and related muscles which may cause muscle strain.

• Recreational Activities

In a study that involved 2077 workers, regular walking and jogging have been shown to increase the incidence of sciatica [8].

5- What Are the Symptoms of Sciatica?

• Pain in the lower back, buttock, and leg which can be intermittent or persistent.
• Reduced movement and mobility together with moderate or severe pain.
• Weakness in the lower back and leg.
• Numbness or pins-and-needles sensations along the leg and foot.

6- When Should I Worry About Sciatica?

Sciatica can be due to severe or chronic conditions such as tumors, bilateral sciatica, scarred tissues, hematoma, cysts or abscesses, spinal tuberculosis, medications non-responsive infections, or fracture in the vertebrates of the lumbar spine.

These conditions may require surgery to restore the function of the lower spine and surrounding tissues.

5- Sciatica Treatment

Sciatica treatment may involve non-surgical or surgical therapies.

• Non-surgical therapies

Exercises for Sciatica

Physical therapy aims at restoring strength to the spine and lower-back muscles, buttocks, hip, and abdomen which may involve swimming, walking, and specific stretching movements with a help of a physical therapist.

Lifestyle Changes

Losing weight through a healthy diet can significantly reduce chronic sciatica by decreasing the weight being carried in the front, and therefore, reducing the weight on the spine and related muscles.

This effort can be complemented with exercise to strengthen the spine and lower back muscles, buttocks, hip, and abdomen.

For workers with a predisposition for sciatica, preventing certain positions or intermittent stretching while working can prevent or reduce the risk of sciatica.

Alternative therapies

Acupuncture, yoga, and massages can relieve muscle spasms at the lower back and leg, and therefore, pain associated with sciatica.

Medication

Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, and spinal injections of steroids (corticosteroids) are used to temporarily reduce pain associated with inflammation and swelling.

Myorelaxants are also used to relax the muscles and relieve the spasms.

• Surgery

Surgery is required to remove the tumors, abscesses, hematomas that compress the spine and the sciatic nerve.

When the sciatica is due to a hernia of a disc or multiple discs or to lumbar spinal stenosis, surgery is necessary to restore their function.

Conclusion

Sciatica is a very painful experience that can be due to lifestyle or working conditions but also to severely debilitating conditions that require several surgical procedures to restore the function of the lower spine and reduce the irritation or compression of the sciatic nerve.

The post What Causes Sciatic Nerve Pain? appeared first on .

It can also be caused by environmental factors such as sleeping habits, the safety of the place where you sleep, and the comfort of the bedding and the room where you sleep.

Corresponding to the statistics of the American Sleep Association (ASA), approximately 30% of adults experience short-term insomnia, while 10% of adults suffer chronic insomnia [1]. In the United Kingdom, approximately 50% of adults complain of short-term insomnia, while 10-15% suffer from chronic insomnia [2].

Why Do We Need Sleep?

Sleep is essential to our biological metabolism and for the proper functioning of our nervous system. For instance, insomnia can significantly affect protein metabolism necessary for the function of cells, tissue, and organs. It can also lead to cognitive disorders (e.g., effect on learning and memory), and mood swings.

How Is Sleep Controlled?

Sleep is controlled by the brain through the suprachiasmatic nucleus of the hypothalamus. The sleep pattern occurs through repetition of a cycle that comprises 5 phases measured by electroencephalography (ECG) [3]:

• Phase 1: light sleep phase characterized by slow eyes’ movement and muscle relaxation.

• Phase 2: this phase is characterized by the cessation of eyes’ movement and the slowdown of the brain waves such as the electrical pulses associated with wakefulness.

• Phase 3: beginning of deep sleep delta waves. At this stage, the delta waves are interrupted by faster and smaller waves.

• Phase 4: characterized uninterrupted delta waves leading to deep sleep.

• Rapid Eye Movement (REM): this phase is characterized by rapid eye movements, rise in heart and blood pressure, and dreaming.

Most adults require 7-9 hours’ sleep, while teenagers need 9 hours’ sleep and infants typically sleep for about 16 hours. However, biological, and environmental factors can alter the length and quality of sleep leading to insomnia.

What Are the Biological Causes of Insomnia?

1- Chronic Disease Conditions

Any chronic condition that causes pain can have dramatic effects on sleep. For instance, Rheumatoid arthritis can lead to shorter sleep times and fragmented sleep, resulting in a poor sleep quality that feeds back into a heightening sensitivity to pain, creating a vicious cycle [4].

2- Genetic Factors

Using the genome-wide association study (GWAS) and a genome-wide gene-based association study (GWGAS) in 113,006 individuals, a study identified 3 loci (location of genes on chromosomes) and 7 genes that are associated with insomnia. Among these, a strong association between the developmental gene MEIS1 and insomnia was reported for both males and females [5].

3- Breathing-Associated Conditions

Conditions that prevent proper breathing such as sleep apnoea, asthma, congestive heart failure, and chronic obstructive pulmonary diseases, can all lead to insomnia. Breathing difficulties result in frequent wakening, shorter sleep times, and fragmented sleep, which lead to poor sleep quality.

4- Urinary Conditions

Conditions such as an enlarged prostate and urinary tract infection result in frequent urination at night (Nocturia) that affects sleep quality.

5- Mental Health Disorders

• Anxiety and Depression:

Anxiety and Depression are mental states characterized by psychological symptoms such as low mood and self-esteem, irritability and intolerance to others, difficulty in making decisions, and suicidal thoughts.

A study that analyzed the link between depression and insomnia in 7954 respondents who were questioned about sleep complaints and psychiatric symptoms, found that the risk of developing new major depression was much higher in those who had insomnia at both interviews compared with those without insomnia [6]

• Post-Traumatic Stress Disorder (PTSD)

One of the main characteristics of PTSD is nightmares that relate to previous traumatic events. Nightmares can disrupt sleep, and their repetitive frequency can create a fear of falling asleep [7].

• Chronic Fatigue Syndrome

Insomnia can be caused by chronic fatigue syndrome, an illness characterized by profound disabling tiredness, a diminished capacity to perform routine tasks and sleep disruption that lasts for more than 6 months.

• Headaches and Migraines

A Headache is a symptom of continuous pain in the head, face, or neck that can last from 30 minutes to several hours, while a migraine is a severe form of headache that manifest as an excruciating pain on one side of the head accompanied by a feeling of sickness and an increased sensitivity to light and sound. Pain from headaches and migraines can significantly affect the quality of sleep.

6- Medication

Medications such as diuretics, some steroids (e.g., prednisone), decongestants, beta-blockers, asthma medications (e.g., theophylline) can lead to short-term or long-term insomnia depending on the duration of the treatments. For instance, diuretics can increase the frequency of urination, while prednisone can cause headaches, stomach pain, and sleep disruptions.

7- Stimulants

Caffeine, nicotine, and other central nervous system stimulants increase alertness which prevents the willingness of going to sleep.

8- Restless Legs Syndrome

Restless Legs Syndrome is the urge to move legs due to unpleasant sensations, such as tingling and aching, and that is relieved by movement. This condition can result in sleepless nights, and therefore, contributes to insomnia.

10- Dementia

The sleep hormone melatonin is essential in the synchronization of the circadian rhythms, and in ensuring the quality of sleep. In dementia individuals, melatonin secretion is low or dysregulated which affects sleep and leads to insomnia [8].

What Are the Environmental Causes?

Environmental factors such as the comfort of the bedding and the room where you sleep, are essential for quality sleep. For instance, if the bed is uncomfortable or if your partner is snoring, or your surrounding is noisy, the quality of your sleep will be affected.

What Is the Treatment for Insomnia?

Depending on the causes of insomnia, treatment can include lifestyles changes that promote quality of sleep or cognitive behavioral therapy (OBT). Lifestyle changes can involve improving the quality of the bedding, the room where you sleep, consuming less coffee and nicotine-associated products, and exercising.

Cognitive-behavioral therapy can help improve sleep patterns through the introduction of changes in behaviors and thoughts that interfere with sleep such as maintaining a consistent sleep schedule. For insomnia that is caused by anxiety, depression, and chronic fatigue syndrome, cognitive behavioral therapy can help improve cognitive disorders, behaviors, and develop coping strategies that can also help with sleep.

Conclusion

Insomnia is a serious condition that can have severe repercussions on daily life. If untreated insomnia can lead to mental health problems such as anxiety and depression. Although most of the causes can be prevented through changing lifestyle and environmental factors, some are associated with genetics, aging, and neurodegenerative diseases that require more advanced medical treatments.

References

[1] https://www.sleepassociation.org/about-sleep/sleep-statistics/

[2] Morphy, H., Dunn, K.M., Lewis, M., Boardman, H.F. and Croft, P.R., 2007. Epidemiology of insomnia: a longitudinal study in a UK population. Sleep, 30(3), pp.274-280.

[3] Brown, R.E., Basheer, R., McKenna, J.T., Strecker, R.E. and McCarley, R.W., 2012. Control of sleep and wakefulness. Physiological reviews.

[4] Ohayon, M.M., 2005. Relationship between chronic painful physical condition and insomnia. Journal of psychiatric research, 39(2), pp.151-159.

[5] Hammerschlag, A.R., Stringer, S., De Leeuw, C.A., Sniekers, S., Taskesen, E., Watanabe, K., Blanken, T.F., Dekker, K., Te Lindert, B.H., Wassing, R. and Jonsdottir, I., 2017. Genome-wide association analysis of insomnia complaints identifies risk genes and genetic overlap with psychiatric and metabolic traits. Nature genetics, 49(11), pp.1584-1592.

[6] Ford, D.E. and Kamerow, D.B., 1989. Epidemiologic study of sleep disturbances and psychiatric disorders: an opportunity for prevention?. Jama, 262(11), pp.1479-1484.

[7] Maher, M.J., Rego, S.A. and Asnis, G.M., 2006. Sleep disturbances in patients with post-traumatic stress disorder: epidemiology, impact and approaches to management. CNS drugs, 20(7), pp.567-591.

[8] Liu, R.Y., Zhou, J.N., van Heerikhuize, J., Hofman, M.A. and Swaab, D.F., 1999. Decreased melatonin levels in postmortem cerebrospinal fluid in relation to aging, Alzheimer’s disease, and apolipoprotein E-ε4/4 genotype. The Journal of clinical endocrinology & metabolism, 84(1), pp.323-327.

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1. Epidemiology of Chronic Fatigue Syndrome

Based on prevalence estimates from the Institute of Medicine, chronic fatigue syndrome affects around 0.2-2.6% of the global population. It mainly affects adults between 40 and 60 years, with a female predominance [1][2]. It also occurs in children and adolescents; however, it appears to be at a lower rate [3].

2. What Causes Chronic Fatigue Syndrome?

There are several causes of chronic fatigue syndrome including genetic, neurological, immunological, infectious, sleep-related, and psychiatric [2].

A. Is Chronic Fatigue Syndrome a Genetic Condition?

Several studies investigated the association between chronic fatigue syndrome and family genetic history. One of the studies compared the rate of chronic fatigue syndrome (CFS) between 25 individuals with CFS and 36 control subjects and found significantly higher rates of CFS in individuals with CFS relatives [4].

By analyzing data from a chronic fatigue twin registry, other studies found higher rates of chronic fatigue syndrome in monozygotic (identical) compared to dizygotic twins and that a genetic predisposition to chronic fatigue syndrome exists in female twins [5].

However, further investigations are required to confirm the involvement of family genetic history in the etiology of CFS [2].

B. Is Chronic Fatigue Syndrome a Neurological Condition?

Due to the presence of symptoms of fatigue, impaired concentration diminished attention and memory, and headache in cases of CFS, neuropsychological and neuroendocrine studies, were performed by several research groups.

Neuropsychological studies

Although studies tested the capacity of information processing, working memory, and poor learning in CFS individuals, the results showed that these individuals have normal cognitive and global intellectual abilities [6].

Neuroendocrine studies

Abnormalities in the hypothalamic-pituitary-adrenal axis and serotonin pathways were reported in patients with CFS. These individuals had an altered physiological response to stress associated with reduced levels of cortisol, a disorder of central neurotransmitters, and disturbance of the functional relationship between cortisol and central neurotransmitters [7].

C. Is Chronic Fatigue Syndrome an Immunological Condition?

Analysis of the immune system in CFS individuals demonstrated the presence of alterations affecting the function of natural killer (NK) cells and regulatory T and B cells, and higher frequencies of various autoantibodies [8] [9]. However, other studies showed the absence of changes in lymphocyte subsets in CFS individuals [10].

D. Is Chronic Fatigue Syndrome Due to Infections?

Although several studies reported potential associations between CSF and viral infections, such as Epstein–Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus (HHV) 6, HHV-7, HHV-8, human parvovirus B19 (B19V), enteroviruses, lentiviruses, the role of viral infections in CSF etiology have not been confirmed and remains inconclusive [11].

E. Is Chronic Fatigue Syndrome Due to Sleep Disruption?

Although many studies suggested an association between CSF and sleep disturbances using sleep parameters such as slow-wave sleep, apnea-hypopnea index, spectral activity, and multiple sleep latency testing, a recent study showed that the reported results are inconsistent due to subjects’ recruitment decisions, confounding factors, small sample sizes and unconfirmed findings [12].

F. Is Chronic Fatigue Syndrome a Psychiatric Condition?

Several studies suggested that CSF is a psychiatric disorder that originates in CSF individuals who have mood disorders, such as anxiety, and major depression, and somatization disorder which includes symptoms such as headaches, dizziness, generalized pain, bowel movement, and fatigue [13] [14].

H. Is Chronic Fatigue Syndrome Due to Lack of Exercise?

A study showed that CSF individuals have less physical activity than non-CSF individuals, suggesting that the lack of physical activity could aggravate fatigue in CSF patients [15]. Interestingly, another study showed that individuals with CSF who received a graded exercise program had improvements in physical activities and in some cognitive variables [16].

3. How Is Chronic Fatigue Syndrome Diagnosed?

Unfortunately, there is no specific test for CSF, and the diagnosis is based on the observation of symptoms including sleep disturbances, headaches, joint, and muscle pain, disabling tiredness, flu-like symptoms, dizziness, and heart palpitations.

4. How Is Chronic Fatigue Syndrome Treated?

The treatment of chronic fatigue syndrome is symptomatic and involves the use of a graded exercise program to improve physical activity, medications to control sleeping disruptions and pain, and cognitive behavioral therapy to improve cognitive disorders, and behaviors, and to develop coping strategies.

5. Frequently Asked Questions about What Is Chronic Fatigue Syndrome?

What is Chronic Fatigue Syndrome (CFS)?

Chronic Fatigue Syndrome, also known as myalgic encephalomyelitis (ME/CFS), is a complex disorder characterized by extreme fatigue that doesn’t improve with rest and may worsen with physical or mental activity.

What are the symptoms of CFS?

The main symptom of CFS is severe fatigue that lasts for at least six months and is not alleviated by rest. Other common symptoms include muscle pain, joint pain, headaches, unrefreshing sleep, memory problems, and difficulty concentrating.

What causes Chronic Fatigue Syndrome?

The exact cause of CFS is unknown, but it is believed to involve a combination of factors, including viral infections, immune system dysfunction, hormonal imbalances, and genetic predisposition. Psychological factors such as stress may also play a role.

How is Chronic Fatigue Syndrome diagnosed?

There is no specific test for CFS, so diagnosis is based on ruling out other possible causes of the symptoms. Doctors may perform a thorough medical history, physical examination, and various tests to rule out other conditions with similar symptoms.

Is there a cure for Chronic Fatigue Syndrome?

Currently, there is no cure for CFS. Treatment focuses on managing symptoms and improving quality of life. This may include medications to relieve pain and improve sleep, as well as lifestyle changes such as pacing activities and managing stress.

Can exercise help with Chronic Fatigue Syndrome?

While exercise is important for overall health, it can be challenging for people with CFS due to their extreme fatigue and other symptoms.

A carefully tailored exercise program, such as graded exercise therapy, may be beneficial for some individuals, but it should be approached cautiously and under the guidance of a healthcare professional.

Is Chronic Fatigue Syndrome a mental illness?

No, CFS is not a mental illness, although psychological factors such as stress may contribute to its development or exacerbation. CFS is recognized as a physical illness by major medical organizations, including the World Health Organization and the Centers for Disease Control and Prevention.

Can children get Chronic Fatigue Syndrome?

Yes, children and adolescents can develop Chronic Fatigue Syndrome. It may manifest differently in younger individuals compared to adults, with symptoms such as difficulty concentrating, school absences, and reduced participation in activities.

How common is Chronic Fatigue Syndrome?

CFS is estimated to affect between 0.1% and 0.4% of the population, though rates may vary depending on the criteria used for diagnosis and other factors. It can occur in people of all ages, genders, and ethnicities.

What should I do if I think I have Chronic Fatigue Syndrome?

If you are experiencing persistent, unexplained fatigue along with other symptoms of CFS, it’s important to consult with a healthcare professional. They can perform a thorough evaluation to determine the cause of your symptoms and develop an appropriate treatment plan.

Conclusion

Although chronic fatigue syndrome appears to be associated with psychiatric and neurological disorders, other factors such as viral infections, immunity, and hereditary, may also be involved. A better understanding of the etiology of this syndrome using studies that comprise larger cohorts of CSF patients would certainly lead to the development of more efficient therapies that are specific to chronic fatigue syndrome.

References

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