Smoking is the number one cause of Reinke's edema. Other factors include gastroesophageal reflux, hypothyroidism and chronic overuse of the voice. Smoking is the only risk factor that may lead to cancer. Additionally, the combination of several risk factors increase the likelihood of an individual developing Reinke's edema. For example, an individual who smokes and also has gastric reflux would have an increased susceptibility for developing Reinke's edema over time.

Reinke's edema is commonly diagnosed in middle-aged females with a history of smoking (aged 50 years or older). Because males have lower pitched voices than females, males are less likely to observe a significant changes in the voice, and are therefore less likely to seek treatment. Females also report more physical discomfort due to Reinke's edema. The risk of Reinke's edema increases with age and also with prolonged exposure to smoking. Additionally, individuals in professions that require constant use of the voice, such as singers, teachers, and radio hosts, may be at an increased risk for developing the disease.

Because the disease is heavily linked to smoking, there is no established way to screen for Reinke's edema. Similarly, the only way to prevent Reinke's edema is to avoid smoking. By adopting a non-smoking lifestyle after being diagnosed with Reinke's edema, it is possible to stop the disease's progression, although it is not possible to reverse it. Therefore, it is critical to maintain a non-smoking lifestyle even after surgery, because the fluid can re-emerge. In fact, in many cases surgeons will not perform surgery without the guarantee that the individual will stop smoking.

CES is often concurrent with congenital or degenerative diseases and represents a high cost of care to those admitted to the hospital for surgery. Hospital stays generally last 4 to 5 days, and cost an average of $100,000 to $150,000, unless the patient lives in a country where healthcare is free at the point of delivery.

No set risk factors have been clearly defined for CES at this point in time. Individuals most at risk for disc herniation are the most likely to develop CES. Race has little influence with the notable exception that African Americans appear slightly less likely to develop CES than other groups; similarly, men are slightly more likely to develop CES than women. Middle age also appears to be a notable risk factor, as those populations are more likely to develop a herniated disc; heavy lifting can also be inferred as a risk factor for CES.

In older patients, CCS most often occurs after acute hyperextension injury in an individual with long-standing cervical spondylosis. A slow, chronic cause in this age group is when the cord gets caught and squeezed between a posterior intervertebral disc herniation against the anterior cord and/or with posterior pressure on the cord from hypertrophy of the ligamentum flavum (Lhermitte's sign may be the experience that causes the patient to seek medical diagnosis). However, CCS is not exclusive to older patients as younger individuals can also sustain an injury leading to CCS. Typically, younger patients are more likely to get CCS as a result of a high-force trauma or a bony instability in the cervical spine. Historically, spinal cord damage was believed to originate from concussion or contusion of the cord with stasis of axoplasmic flow, causing edematous injury rather than destructive hematomyelia. More recently, autopsy studies have demonstrated that CCS may be caused by bleeding into the central part of the cord, portending less favorable prognosis. Studies also have shown from postmortem evaluation that CCS probably is associated with selective axonal disruption in the lateral columns at the level of the injury to the spinal cord with relative preservation of the grey matter.

Transverse myelitis is a neurological condition in which the spinal cord is inflamed. The inflammation damages nerve fibers, and causes them to lose their myelin coating leading to decreased electrical conductivity in the central nervous system. "Transverse" implies that the inflammation extends across the entire width of the spinal cord. Partial transverse myelitis and partial myelitis are terms used to define inflammation of the spinal cord that affects part of the width of the spinal cord.

Central cord syndrome (CCS) is the most common form of cervical spinal cord injury. It is characterized by loss of motion and sensation in arms and hands. It usually results from trauma which causes damage to the neck, leading to major injury to the central grey matter of the spinal cord. The syndrome is more common in people over the age of 50 because osteoarthritis in the neck region causes weakening of the vertebrae. CCS most frequently occurs among older persons with cervical spondylosis, however, it also may occur in younger individuals.

CCS is the most common incomplete spinal cord injury syndrome. It accounts for approximately 9% of traumatic SCIs. After an incomplete injury, the brain still has the capacity to send and receive some signals below the site of injury. Sending and receiving of signals to and from parts of the body is reduced, not entirely blocked. CCS gives a greater motor loss in the upper limbs than in the lower limbs, with variable sensory loss.

It was first described by Schneider in 1954. It is generally associated with favorable prognosis for some degree of neurological and functional recovery. However, factors such as age, preexisting conditions, and extent of injury will affect the recovery process.

Up to now, prevalence studies investigating rates of dysphonia on a large-scale level have been limited. According to a large sample of 55 million patients seeking health-care treatment in the United States, dysphonia can be found in approximately 1% of the population. Higher rates are reported in females and elderly adults, however, dysphonia can be found in both sexes and across age groups. It is proposed that higher rates in females are due to anatomical differences of the vocal mechanism.

Certain occupational groups may be more prone to developing voice disorders, namely dysphonia. Occupations that require extensive use of voice may be at a greater risk such as teachers and singers. However, the evidence is highly variable and must be interpreted carefully.

Vehicle-related SCI is prevented with measures including societal and individual efforts to reduce driving under the influence of drugs or alcohol, distracted driving, and drowsy driving. Other efforts include increasing road safety (such as marking hazards and adding lighting) and vehicle safety, both to prevent accidents (such as routine maintenance and antilock brakes) and to mitigate the damage of crashes (such as head restraints, air bags, seat belts, and child safety seats). Falls can be prevented by making changes to the environment, such as nonslip materials and grab bars in bathtubs and showers, railings for stairs, child and safety gates for windows. Gun-related injuries can be prevented with conflict resolution training, gun safety education campaigns, and changes to the technology of guns (such as trigger locks) to improve their safety. Sports injuries can be prevented with changes to sports rules and equipment to increase safety, and education campaigns to reduce risky practices such as diving into water of unknown depth or head-first tackling in association football.

Spinal cord injuries are most often caused by physical trauma. Forces involved can be hyperflexion (forward movement of the head); hyperextension (backward movement); lateral stress (sideways movement); rotation (twisting of the head); compression (force along the axis of the spine downward from the head or upward from the pelvis); or distraction (pulling apart of the vertebrae). Traumatic SCI can result in contusion, compression, or stretch injury. It is a major risk of many types of vertebral fracture. Pre-existing asymptomatic congenital anomalies can cause major neurological deficits, such as hemiparesis, to result from otherwise minor trauma.

In the US, Motor vehicle accidents are the most common cause of SCIs; second are falls, then violence such as gunshot wounds, then sports injuries. In some countries falls are more common, even surpassing vehicle crashes as the leading cause of SCI. The rates of violence-related SCI depend heavily on place and time. Of all sports-related SCIs, shallow water dives are the most common cause; winter sports and water sports have been increasing as causes while association football and trampoline injuries have been declining. Hanging can cause injury to the cervical spine, as may occur in attempted suicide. Military conflicts are another cause, and when they occur they are associated with increased rates of SCI. Another potential cause of SCI is iatrogenic injury, caused by an improperly done medical procedure such as an injection into the spinal column.

SCI can also be of a nontraumatic origin. Nontraumatic lesions cause anywhere from 30 to 80% of all SCI; the percentage varies by locale, influenced by efforts to prevent trauma. Developed countries have higher percentages of SCI due to degenerative conditions and tumors than developing countries. In developed countries, the most common cause of nontraumatic SCI is degenerative diseases, followed by tumors; in many developing countries the leading cause is infection such as HIV and tuberculosis. SCI may occur in intervertebral disc disease, and spinal cord vascular disease. Spontaneous bleeding can occur within or outside of the protective membranes that line the cord, and intervertebral disks can herniate. Damage can result from dysfunction of the blood vessels, as in arteriovenous malformation, or when a blood clot becomes lodged in a blood vessel and cuts off blood supply to the cord. When systemic blood pressure drops, blood flow to the spinal cord may be reduced, potentially causing a loss of sensation and voluntary movement in the areas supplied by the affected level of the spinal cord. Congenital conditions and tumors that compress the cord can also cause SCI, as can vertebral spondylosis and ischemia. Multiple sclerosis is a disease that can damage the spinal cord, as can infectious or inflammatory conditions such as tuberculosis, herpes zoster or herpes simplex, meningitis, myelitis, and syphilis.

The following increase an individual's chances for acquiring VCD:

- Upper airway inflammation (allergic or non-allergic rhinitis, chronic sinusitis, recurrent upper respiratory infections)

- Gastroesophageal reflux disease

- Past traumatic event that involved breathing (e.g. near-drowning, suffocation)

- Severe emotional trauma or distress

- Female gender

- Playing a wind instrument

- Playing a competitive or elite sport

Many health conditions can cause autonomic neuropathy. Some common causes of autonomic neuropathy include:

- Diabetes, which is the most common cause of autonomic neuropathy, can gradually cause nerve damage throughout the body.

- Injury to nerves caused by surgery or radiation to the neck.

- Treatment with certain medications, including some drugs used in cancer chemotherapy.

- Abnormal protein buildup in organs (amyloidosis), which affects the organs and the nervous system.

- Other chronic illnesses, such as Parkinson's disease, multiple sclerosis and some types of dementia.

- Autonomic neuropathy may also be caused by an abnormal attack by the immune system that occurs as a result of some cancers (paraneoplastic syndrome).

- Certain infectious diseases. Some viruses and bacteria, such as botulism, Lyme disease and HIV, can cause autonomic neuropathy.

- Inherited disorders. Certain hereditary disorders can cause autonomic neuropathy.

- Autoimmune diseases, in which the immune system attacks and damages parts of the body, including the nerves. Examples include Sjogren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and celiac disease. Guillain-Barre syndrome is an autoimmune disease that happens rapidly and can affect autonomic nerves.

The exact cause of VCD is not known, and it is unlikely that a single underlying cause exists. Several contributing factors have been identified, which vary widely among VCD patients with different medical histories. Physical exercise (including, but not limited to, competitive athletics) is one of the major triggers for VCD episodes, leading to its frequent misdiagnosis as exercise-induced asthma. Other triggers include airborne pollutants and irritants such as smoke, dust, gases, soldering fumes, cleaning chemicals such as ammonia, perfumes, and other odours. Gastroesophageal reflux disease (GERD) and rhinosinusitis (inflammation of the paranasal sinuses and nasal cavity) may also play a role in inflaming the airway and leading to symptoms of VCD as discussed below.

Laryngeal hyperresponsiveness is considered the most likely physiologic cause of VCD, brought on by a range of different triggers that cause inflammation and/or irritation of the larynx (voice box). The glottic closure reflex (or laryngeal adductor reflex) serves to protect the airway, and it is possible that this reflex becomes hyperactive in some individuals, resulting in the paradoxical vocal fold closure seen in VCD. Two major causes of laryngeal inflammation and hyperresponsiveness are gastroesophageal reflux disease (GERD) and postnasal drip (associated with rhinosinusitis, allergic or nonallergic rhinitis, or a viral upper respiratory tract infection (URI)). Rhinosinusitis is very common among patients with VCD and for many patients, VCD symptoms are ameliorated when the rhinosinusitis is treated. GERD is also common among VCD patients, but only some experience an improvement in VCD symptoms when GERD is treated. Other causes of laryngeal hyperresponsiveness include inhalation of toxins and irritants, cold and dry air, episodic croup and laryngopharyngeal reflux (LPR).

VCD has long been strongly associated with a variety of psychological or psychogenic factors, including conversion disorder, major depression, obsessive-compulsive disorder, anxiety (especially in adolescents), stress (particularly stress relating to competitive sports), physical and sexual abuse, post-traumatic stress disorder, panic attacks, factitious disorder and adjustment disorder. It is important to note that anxiety and depression may occur in certain patients as a "result" of having VCD, rather than being the cause of it. Psychological factors are important precipitating factors for many patients with VCD; although exercise is also a major trigger for episodes of VCD, some patients experience VCD co-occurring with anxiety regardless of whether or not they are physically active at the time of the VCD/anxiety episode. Experiencing or witnessing a traumatic event related to breathing (such as a near-drowning or life-threatening asthma attack, for example), has also been identified as a risk factor for VCD.

VCD has also been associated with certain neurologic diseases including Arnold-Chiari malformation, cerebral aqueduct stenosis, cortical or upper motor neuron injury (such as that resulting from stroke), amyotrophic lateral sclerosis (ALS), parkinsonism syndromes and other movement disorders. However, this association occurs only rarely.

Although HSP is a progressive condition, the prognosis for individuals with HSP varies greatly. It primarily affects the legs although there can be some upperbody involvement in some individuals. Some cases are seriously disabling while others are less disabling and are compatible with a productive and full life. The majority of individuals with HSP have a normal life expectancy.

There are disturbances in sensory nerves and motor nerves and dysfunction of the autonomic nervous system at the level of the lesion or below. Therefore, the signs and symptoms depend on the area of spine involved:

- Cervical: If the upper cervical cord is involved, all four limbs may be involved and there is risk of respiratory paralysis (cervical nerve segments C3, 4, 5 innervate the abdominal diaphragm). Lesions of the lower cervical (C5–T1) region will cause a combination of upper and lower motor neuron signs in the upper limbs, and exclusively upper motor neuron signs in the lower limbs. Cervical lesions account for about 20% of cases.

- Thoracic: A lesion of the thoracic spinal cord (T1–12) will produce upper motor neuron signs in the lower limbs, presenting as a spastic diplegia. This is the most common location of the lesion,

Reinke's edema is the swelling of the vocal cords due to fluid (edema) collected within the Reinke's space. First identified by the German anatomist Friedrich B. Reinke in 1895, the Reinke's space is a gelatinous layer of the vocal cord located underneath the outer cells of the vocal cord. When a person speaks, the Reinke's space vibrates to allow for sound to be produced (phonation). The Reinke's space is sometimes referred to as the superficial lamina propria.

Reinke's edema is characterized by the "sac-like" appearance of the fluid-filled vocal cords. The swelling of the vocal folds causes the voice to become deep and hoarse. Therefore, the major symptom of Reinke's edema is a hoarseness similar to laryngitis. The major cause associated with Reinke's edema is smoking. In fact, 97% of patient's diagnosed with Reinke's edema are habitual smokers. Other identified risk factors include overuse of the vocal cords, gastroesophageal reflux, and hypothyroidism. The disease is more often cited in women than in men, because lower voice changes are more noticeable in women.

The first cases of Reinke's edema were recorded in 1891 by M. Hajek, followed by F. Reinke in 1895. In his investigations, Reinke injected a stained glue into the superficial lamina propria (Reinke's space) to mimic edema. Reinke's edema is considered to be a benign (non-cancercous) polyp (protrusion) that represents 10% of all benign laryngeal pathologies. Treatment of Reinke’s edema starts with the elimination of associated risk factors, such as smoking, gastric reflux, and hypothyroidism. Advanced cases may undergo phonosurgery to remove the fluid from the vocal cords.

Although the exact cause of spasmodic dysphonia (i.e., laryngeal dystonia) is still unknown, epidemiological, genetic and neurological pathogenic factors have been proposed in recent research.

Risk factors include:

- Being female

- Being middle aged

- Having a family history of neurological diseases (e.g., tremor, dystonia, meningitis and other neurological diseases)

- Stressful events

- Upper respiratory tract infections

- Sinus and throat illnesses

- Heavy voice use

- Cervical dystonia

- Childhood measles or mumps

- Pregnancy and parturition

It has not been established whether these factors directly impact the development of spasmodic dysphonia (SD), however these factors could be used to identify possible and/or at-risk patients.

Researchers have also explored the possibility of a genetic component to SD. Three genes have been identified that may be related to the development of focal or segmental dystonia: TUBB4A, THAP1 and TOR1A genes. However, a recent study that examined the mutation of these three genes in 86 SD patients found that only 2.3% of the patients had novel/rare variants in THAP1 but none in TUBB4A and TOR1A. Evidence of a genetic contribution for dystonia involving the larynx is still weak and more research is needed in order to establish a causal relationship between SD and specific genes.

SD is a neurological disorder rather than a disorder of the larynx, and as in other forms of dystonia, interventions at the end organ (i.e., larynx) have not offered a definitive cure, only symptomatic relief. The pathophysiology underlying dystonia is becoming better understood as a result of discoveries about genetically based forms of the disorder, and this approach is the most promising avenue to a long-term solution.

SD is classified as a neurological disorder. However, because the voice can sound normal or near normal at times, some practitioners believe it to be psychogenic, that is, originating in the affected person's mind rather than from a physical cause. No medical organizations or groups take this position. A comparison of SD patients compared with vocal fold paralysis (VFP) patients found that 41.7% of the SD patients met the DSM-IV criteria for psychiatric comorbidity compared with 19.5% of the VFP group. However, another study found the opposite, with SD patients having significantly less psychiatric comorbidity compared to VFP patients: "The prevalence of major psychiatric cases varied considerably among the groups, from a low of seven percent (1/14) for spasmodic dysphonia, to 29.4 percent (5/17) for functional dysphonia, to a high of 63.6 percent (7/11) for vocal cord paralysis." A review in the journal Swiss Medicine Weekly states that "Psychogenic causes, a 'psychological disequilibrium', and an increased tension of the laryngeal muscles are presumed to be one end of the spectrum of possible factors leading to the development of the disorder". Alternatively, many investigators into the condition feel that the psychiatric comorbidity associated with voice disorders is a result of the social isolation and anxiety that patients with these conditions feel as a consequence of their difficulty with speech, as opposed to the cause of their dysphonia. The opinion that SD is psychogenic is not upheld by experts in the scientific community.

SD is formally classified as a movement disorder, one of the focal dystonias, and is also known as laryngeal dystonia.

Myelopathy describes any neurologic deficit related to the spinal cord. When due to trauma, it is known as (acute) spinal cord injury. When inflammatory, it is known as myelitis. Disease that is vascular in nature is known as vascular myelopathy. The most common form of myelopathy in human, "cervical spondylotic myelopathy (CSM)", is caused by arthritic changes (spondylosis) of the cervical spine, which result in narrowing of the spinal canal (spinal stenosis) ultimately causing compression of the spinal cord. In Asian populations, spinal cord compression often occurs due to a different, inflammatory process affecting the posterior longitudinal ligament.

Generally, there are two forms of syringomyelia: congenital and acquired. (In addition, one form of the disorder involves the brainstem. The brainstem controls many of our vital functions, such as respiration and heartbeat. When syrinxes affect the brainstem, the condition is called syringobulbia.)

The first major form relates to an abnormality of the brain called an Arnold–Chiari malformation or Chiari Malformation. This is the most common cause of syringomyelia, where the anatomic abnormality, which may be due to a small posterior fossa, causes the lower part of the cerebellum to protrude from its normal location in the back of the head into the cervical or neck portion of the spinal canal. A syrinx may then develop in the cervical region of the spinal cord. Here, symptoms usually begin between the ages of 25 and 40 and may worsen with straining, called a valsalva maneuver, or any activity that causes cerebrospinal fluid pressure to fluctuate suddenly. Some patients, however, may have long periods of stability. Some patients with this form of the disorder also have hydrocephalus, in which cerebrospinal fluid accumulates in the skull, or a condition called arachnoiditis, in which a covering of the spinal cord—the arachnoid membrane—is inflamed.

Some cases of syringomyelia are familial, although this is rare.

Familial dysautonomia is seen almost exclusively in Ashkenazi Jews and is inherited in an autosomal recessive fashion. Both parents must be carriers in order for a child to be affected. The carrier frequency in Jewish individuals of Eastern European (Ashkenazi) ancestry is about 1/30, while the carrier frequency in non-Jewish individuals is unknown. If both parents are carriers, there is a one in four, or 25%, chance with each pregnancy for an affected child. Genetic counseling and genetic testing is recommended for families who may be carriers of familial dysautonomia.

Worldwide, there have been approximately 600 diagnoses recorded since discovery of the disease, with approximately 350 of them still living.

HSP is a group of genetic disorders. It follows general inheritance rules and can be inherited in an autosomal dominant, autosomal recessive or X-linked recessive manner. The mode of inheritance involved has a direct impact on the chances of inheriting the disorder. Over 70 genotypes had been described, and over 50 genetic loci have been linked to this condition. Ten genes have been identified with autosomal dominant inheritance. One of these SPG4 accounts for ~50% of all genetically solved cases cases, or approximately 25% of all HSP cases. Twelve genes are known to be inherited in an autosomal recessive fashion. Collectively this latter group account for ~1/3 cases.

Most altered genes have known function, but for some the function haven’t been identified yet. All of them are listed in the gene list below, including their mode of inheritance. Some examples are spastin (SPG4) and paraplegin (SPG7) are both AAA ATPases.

Vestibulocochlear dysfunction progressive familial, known also as familial progressive vestibulocochlear dysfunction is an autosomal dominant disease that results in sensorineural hearing loss and vestibular areflexia. Patients report feelings of vague dissiness, blurred vision, dysequilibrium in the dark, and progressive hearing impairment.

There is currently no cure for FD and death occurs in 50% of the affected individuals by age 30. There are only two treatment centers, one at New York University Hospital and one at the Sheba Medical Center in Israel. One is being planned for the San Francisco area.

The survival rate and quality of life have increased since the mid-1980s mostly due to a greater understanding of the most dangerous symptoms. At present, FD patients can be expected to function independently if treatment is begun early and major disabilities avoided.

A major issue has been aspiration pneumonia, where food or regurgitated stomach content would be aspirated into the lungs causing infections. Fundoplications (by preventing regurgitation) and gastrostomy tubes (to provide nonoral nutrition) have reduced the frequency of hospitalization.

Other issues which can be treated include FD crises, scoliosis, and various eye conditions due to limited or no tears.

An FD crisis is the body's loss of control of various autonomic nervous system functions including blood pressure, heart rate, and body temperature. Both short-term and chronic periodic high or low blood pressure have consequences and medication is used to stabilize blood pressure.

The presbylarynx is a condition in which age-related atrophy of the soft tissues of the larynx results in weak voice and restricted vocal range and stamina. In other words, it is the loss of vocal fold tone and elasticity due to aging which affects voice quality.

Voice disorders are medical conditions involving abnormal pitch, loudness or quality of the sound produced by the larynx and thereby affecting speech production. These include:

- Puberphonia

- Chorditis

- Vocal fold nodules

- Vocal fold cysts

- Vocal cord paresis

- Reinke's edema

- Spasmodic dysphonia

- Foreign accent syndrome

- Bogart–Bacall syndrome

- Laryngeal papillomatosis

- Laryngitis