<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tachycardia and can you explain it in depth? [/INST] Tachycardia, also called tachyarrhythmia, is a heart rate that exceeds the normal resting rate. In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults. Heart rates above the resting rate may be normal (such as with exercise) or abnormal (such as with electrical problems within the heart).

Complications
Tachycardia can lead to fainting.When the rate of blood flow becomes too rapid, or fast  blood flow passes on damaged endothelium, it  increases the friction within vessels resulting in turbulence and other disturbances. According to the Virchows triad, this is one of the three conditions that can lead to thrombosis (i.e., blood clots within vessels).

Causes
Some causes of tachycardia include:

Diagnosis
The upper threshold of a normal human resting heart rate is based on age. Cutoff values for tachycardia in different age groups are fairly well standardized; typical cutoffs are listed below:
1–2 days: Tachycardia >159 beats per minute (bpm)
3–6 days: Tachycardia >166 bpm
1–3 weeks: Tachycardia >182 bpm
1–2 months: Tachycardia >179 bpm
3–5 months: Tachycardia >186 bpm
6–11 months: Tachycardia >169 bpm
1–2 years: Tachycardia >151 bpm
3–4 years: Tachycardia >137 bpm
5–7 years: Tachycardia >133 bpm
8–11 years: Tachycardia >130 bpm
12–15 years: Tachycardia >119 bpm
>15 years – adult: Tachycardia >100 bpmHeart rate is considered in the context of the prevailing clinical picture. When the heart beats excessively or rapidly, the heart pumps less efficiently and provides less blood flow to the rest of the body, including the heart itself. The increased heart rate also leads to increased work and oxygen demand by the heart, which can lead to rate related ischemia.

Differential diagnosis
An electrocardiogram (ECG) is used to classify the type of tachycardia. They may be classified into narrow and wide complex based on the QRS complex. Equal or less than 0.1s for narrow complex. Presented order of most to least common, they are:
Narrow complex
Sinus tachycardia, which originates from the sino-atrial (SA) node, near the base of the superior vena cava
Atrial fibrillation
Atrial flutter
AV nodal reentrant tachycardia
Accessory pathway mediated tachycardia
Atrial tachycardia
Multifocal atrial tachycardia
Cardiac Tamponade
Junctional tachycardia (rare in adults)
Wide complex
Ventricular tachycardia, any tachycardia that originates in the ventricles
Any narrow complex tachycardia combined with a problem with the conduction system of the heart, often termed "supraventricular tachycardia with aberrancy"
A narrow complex tachycardia with an accessory conduction pathway, often termed "supraventricular tachycardia with pre-excitation" (e.g. Wolff–Parkinson–White syndrome)
Pacemaker-tracked or pacemaker-mediated tachycardiaTachycardias may be classified as either narrow complex tachycardias (supraventricular tachycardias) or wide complex tachycardias. Narrow and wide refer to the width of the QRS complex on the ECG. Narrow complex tachycardias tend to originate in the atria, while wide complex tachycardias tend to originate in the ventricles. Tachycardias can be further classified as either regular or irregular.

Sinus
The body has several feedback mechanisms to maintain adequate blood flow and blood pressure.  If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia. This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow. The most common cause of the latter is orthostatic hypotension (also called postural hypotension).  Fever, hyperventilation, diarrhea and severe infections can also cause tachycardia, primarily due to increase in metabolic demands.An increase in sympathetic nervous system stimulation causes the heart rate to increase, both by the direct action of sympathetic nerve fibers on the heart and by causing the endocrine system to release hormones such as epinephrine (adrenaline), which have a similar effect.  Increased sympathetic stimulation is usually due to physical or psychological stress.  This is the basis for the so-called fight-or-flight response, but such stimulation can also be induced by stimulants such as ephedrine, amphetamines or cocaine.  Certain endocrine disorders such as pheochromocytoma can also cause epinephrine release and can result in tachycardia independent of nervous system stimulation. Hyperthyroidism can also cause tachycardia. The upper limit of normal rate for sinus tachycardia is thought to be 220 bpm minus age.

Inappropriate sinus tachycardia
Inappropriate sinus tachycardia (IST) is a rare but benign type of cardiac arrhythmia that may be caused by a structural abnormality in the sinus node. It can occur in seemingly healthy individuals with no history of cardiovascular disease.  Other causes may include Autonomic nervous system deficits, autoimmune response, or drug interactions. Although symptoms might be distressing, treatment is not generally needed.

Ventricular
Ventricular tachycardia (VT or V-tach) is a potentially life-threatening cardiac arrhythmia that originates in the ventricles. It is usually a regular, wide complex tachycardia with a rate between 120 and 250 beats per minute. A medically significant subvariant of ventricular tachycardia is called torsades de pointes (literally meaning "twisting of the points", due to its appearance on an EKG), which tends to result from a long QT interval.Both of these rhythms normally last for only a few seconds to minutes (paroxysmal tachycardia), but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.

Supraventricular
This is a type of tachycardia that originates from above the ventricles, such as the atria.  It is sometimes known as paroxysmal atrial tachycardia (PAT).  Several types of supraventricular tachycardia are known to exist.

Atrial fibrillation
Atrial fibrillation is one of the most common cardiac arrhythmias. In general, it is an irregular, narrow complex rhythm. However, it may show wide QRS complexes on the ECG if a bundle branch block is present. At high rates, the QRS complex may also become wide due to the Ashman phenomenon. It may be difficult to determine the rhythms regularity when the rate exceeds 150 beats per minute. Depending on the patients health and other variables such as medications taken for rate control, atrial fibrillation may cause heart rates that span from 50 to 250 beats per minute (or even higher if an accessory pathway is present). However, new-onset atrial fibrillation tends to present with rates between 100 and 150 beats per minute.

AV nodal reentrant tachycardia
AV nodal reentrant tachycardia (AVNRT) is the most common reentrant tachycardia. It is a regular narrow complex tachycardia that usually responds well to the Valsalva maneuver or the drug adenosine. However, unstable patients sometimes require synchronized cardioversion. Definitive care may include catheter ablation.

AV reentrant tachycardia
AV reentrant tachycardia (AVRT) requires an accessory pathway for its maintenance. AVRT may involve orthodromic conduction (where the impulse travels down the AV node to the ventricles and back up to the atria through the accessory pathway) or antidromic conduction (which the impulse travels down the accessory pathway and back up to the atria through the AV node). Orthodromic conduction usually results in a narrow complex tachycardia, and antidromic conduction usually results in a wide complex tachycardia that often mimics ventricular tachycardia. Most antiarrhythmics are contraindicated in the emergency treatment of AVRT, because they may paradoxically increase conduction across the accessory pathway.

Junctional tachycardia
Junctional tachycardia is an automatic tachycardia originating in the AV junction. It tends to be a regular, narrow complex tachycardia and may be a sign of digitalis toxicity.

Management
The management of tachycardia depends on its type (wide complex versus narrow complex), whether or not the person is stable or unstable, and whether the instability is due to the tachycardia. Unstable means that either important organ functions are affected or cardiac arrest is about to occur.

Unstable
In those that are unstable with a narrow complex tachycardia, intravenous adenosine may be attempted </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Respiratory alkalosis and can you explain it in depth? [/INST] Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide. This condition is one of the four primary disturbance of acid–base homeostasis.

Signs and symptoms
Signs and symptoms of respiratory alkalosis are as follows:
Palpitation
Tetany
Convulsion
Sweating

Causes
Respiratory alkalosis may be produced as a result of the following causes:

Mechanism
The mechanism of respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased breathing produces increased alveolar respiration, expelling CO2 from the circulation. This alters the dynamic chemical equilibrium of carbon dioxide in the circulatory system. Circulating hydrogen ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase according to the following reaction:

            H
            C

              O

                3

                −

            +

              H

                +

            →

              H

                2

            C

              O

                3

            →
            C

              O

                2

            +

              H

                2

            O

    {\displaystyle {\rm {HCO_{3}^{-}+H^{+}\rightarrow H_{2}CO_{3}\rightarrow CO_{2}+H_{2}O}}}
   This causes decreased circulating hydrogen ion concentration, and increased pH (alkalosis).

Diagnosis
The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual.The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentrations (and blood pH) after a respiratory or metabolic acid-base disturbance

Classification
There are two types of respiratory alkalosis: chronic and acute as a result of the 3–5 day delay in kidney compensation of the abnormality.
Acute respiratory alkalosis occurs rapidly, have a high pH because the response of the kidneys is slow.
Chronic respiratory alkalosis is a more long-standing condition, here one finds the kidneys have time to decrease the bicarbonate level.

pH
Alkalosis refers to the process due to which there is elevation of blood pH.
Alkalemia refers to an arterial blood pH of greater than 7.45.

Treatment
Respiratory alkalosis is very rarely life-threatening, though pH level should not be 7.5 or greater. The aim in treatment is to detect the underlying cause. When PaCO2 is adjusted rapidly in individuals with chronic respiratory alkalosis, metabolic acidosis may occur. If the individual is on a mechanical ventilator then preventing hyperventilation is done via monitoring ABG levels.

In popular culture
In The Andromeda Strain, one of the characters is exposed to contamination, but saves himself by increasing his respiratory rate to induce alkalosis.

See also
References
Further reading
Lang, Florian (2009-03-19). Encyclopedia of Molecular Mechanisms of Disease: With 213 Tables. Springer Science & Business Media. ISBN 9783540671367.
Unwin, R.; Stidwell, R.; Taylor, S.; Capasso, G. (1997-11-01). "The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo". American Journal of Physiology. Renal Physiology. 273 (5): F698–F705 </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Fundic gland polyp and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Testicular atrophy and can you explain it in depth? [/INST] Testicular atrophy is a medical condition in which one or both testicles (or "testes") diminish in size and may be accompanied by reduced testicular function. Testicular atrophy is not related to the temporary shrinkage of the surrounding scrotum, which might occur in response to cold temperature.As the testicles are involved in testosterone and sperm production, the signs and symptoms of testicular atrophy overlap with those related to infertility or low testosterone levels. In a prepubescent person with testicular atrophy, there may be underdevelopment of secondary sex characteristics (e.g. lack of penis growth). In sexually developed individuals, testicular atrophy may be accompanied with lower sex drive and increased breast tissue. Additional signs and symptoms vary and can depend on the specific cause of the testicle shrinkage. Some causes include age, alcohol use, hormone therapy, direct damage to the testicles, and infection.Diagnosis of testicular atrophy includes physical examination of the testicles as well as imaging to measure testicular volume. A testosterone blood level is also taken to assess function of the testicles. Additional tests may be ordered depending on the suspected cause(s) of the shrinkage. Treatment and potential reversibility of testicular atrophy are also dependent on the cause.

Signs and symptoms
There are different signs and symptoms associated with testicular atrophy depending on the persons age. Symptoms before puberty are centered more around the stunting of sexual characteristics associated with hormonal changes, while symptoms after puberty include a wider range of factors. Other signs and symptoms may stem from underlying conditions which cause testicular atrophy. The most perceptible sign of testicular atrophy is shrinkage of the testicle(s).Signs and symptoms before puberty include:

lack of development of pubic hair
lack of development of facial hair
lack of penis growth
lower testosteroneTestosterone is a hormone that is found primarily in a portion of the male-assigned reproductive system called the testes and is normally measured in nanograms per deciliter. Testosterone is in charge of the growth and production of many sexual attributes in people with testes, including facial hair, pubic hair, penis size, vocal and muscle mass changes, regulation of sex drive, and sperm production. Normal testosterone levels in people with testes who have not yet hit puberty are less than 20 nanograms per deciliter. Low testosterone can be defined as hypogonadism in people with testes. Hypogonadism in people with testes is established as the hormonal inhibition of testosterone that can either be inherited or acquired at a later stage in life. Under the circumstances of pre-pubescent hypogonadism, many sexual developmental characteristics may be altered. Testosterone affects hair growth by regulating the follicle itself, which in turn affects the specific growth phases of the hair follicle. As a person with testes hits puberty, androgen, a steroid sex hormone, is produced at an increased rate, which creates terminal hair follicles. Terminal hair follicles create thicker and more pigmented hair which is also regulated by testosterone production. Testosterone also impacts pre-pubescent penis size by providing penile tissue with girth and density. The drop in testosterone values is mainly due to significant impairment of Leydig cells brought upon by hypogonadism. Leydig cells are located in the testes and serve to create testosterone and androgen. Once they are damaged, the production of testosterone is stunted.Signs and symptoms after puberty include:

reduced sex drive
tender testicles
trouble conceiving
reduction of pubic or facial hair
decreased muscle mass
lower testosteroneTypical testosterone levels of people with testes after puberty range from 300 to 1,200 nanograms per deciliter. Low testosterone values in people with testes post-puberty would be considered any value under 300 nanograms per deciliter. Decreased testosterone values caused by testicular atrophy can lead to and explain many of the signs and symptoms listed above, including a reduced sex drive, infertility, soft testicles, reduction of hair, and lower muscle mass throughout the body. Testosterone plays an important role in physiologically stimulating sex drive in people with testes. If testosterone levels drop below normal values, libido (sexual drive) is reduced, which can lead to the development of erectile dysfunction (a condition in which the penis is not able to get or stay erect). This can indirectly affect fertility as well. In addition, testosterone is important in muscle mass formation. It increases the amount of lean muscle mass in the body. Testosterone encourages metabolic activity in the body, which in turn stimulates protein synthesis. Protein synthesis is highly important for the development and enlargement of muscle. Therefore, a lack of testosterone would alter this metabolic process, leading to a decrease in muscle mass.Signs and symptoms of testicular atrophy that are due to a secondary medical condition include:

inflammation
fever
sensitivity or pain of the testicle(s)
nauseaSecondary medical conditions that may cause the signs and symptoms listed above include testicular cancer, chronic alcohol use, sexually transmitted infections, COVID-19, orchitis, varicoceles, or torsion of the testes.

Causes
Age
Shrinkage of the testicles is common with advanced age, as overall reproductive function declines.

Alcohol use
High alcohol usage lowers testosterone levels by direct damage to the Leydig cells (which produce testosterone) and by affecting hormones involved in signaling to the Leydig cells to produce testosterone. As a result, testicular atrophy is a common feature among individuals with high alcohol use. Testicular malformations and low testosterone levels is also commonly found in people with alcoholic cirrhosis as the negative effect of alcohol use is worsened by the liver damage itself. Excessive alcohol intake can cause inflammation and the degradation of cells in the liver, which can then cause testicular abnormalities (including testicular atrophy).

Anabolic steroid use and hormone therapy
Anabolic steroid use and testosterone replacement therapy (TRT) have been found to cause testicular atrophy through similar mechanisms. Anabolic steroids and TRT are both used (either by prescription or illicitly) to mimic the effects of testosterone produced by the body, such as building muscle and maintaining sex drive. However, they also inhibit the bodys own production of sperm and testosterone, which can lead to shrinkage of the testicles.Testicular atrophy is also a side effect of estrogen therapy.

COVID-19
COVID-19 can lead to reduced testosterone production and testicular abnormalities due to changes in the secretion of gonadotropins, which are hormones involved in regulating testosterone production. These hormonal effects may be due to inflammation and oxidative stress caused by COVID-19. This might inform whether healthcare providers decide to monitor those who have survived COVID-19 for hormonal changes and potential fertility issues.

Orchitis
Orchitis, or inflammation of the testicles due to a bacterial or viral infection, can lead to testicular atrophy. Mumps has historically been significantly associated with orchitis and testicular atrophy, but has become rare in countries that have high mumps vaccination rates.

Varicoceles and testicular torsion
Varicoceles and testicular torsion are conditions in which direct damage to the testicles can potentially lead to testicular atrophy. Varicoceles are pooling of blood in the veins that deliver blood away from the testicles and are relatively common, occurring in approximately 15% of adolescent and adults with testicles. Currently, it is not clearly established how often varicoceles actually become a direct cause of issues related to fertility. Testicular torsion is the twisting of the testicle within the scrotum and can rapidly result in damage due to interruption in blood flow to the affected testicle. Unlike varicoceles, testicular torsion is considered a medical emergency.

Other health conditions
There is a possible correlation of cystic fibrosis and its impact to bilateral testicular atrophy. Cystic fibrosis is a disease which causes mucus buildup in various organs. Evidence has shown that cystic fibrosis affects multiple systems in the human body, including the reproductive system. Around 97-98% of people with cystic fibrosis who have testicles are infertile due to a missing vas deferens, the tube in the male-assigned reproductive system that carries sperm out of the testes. Additionally, cystic fibrosis can result in the atrophy of male-assigned reproductive organs by causing dehydrated secretions.

Diagnosis
Physical examination
A healthcare provider may initially assess size and shape as well as firmness and texture of the testicles.

Ultrasonography
Ultrasonography is used to detect testicular volume. Testicular volume measured to be less than 12 mL is a sign of testicular atrophy. In addition, testicular atrophy can be recognized as greater than 50% loss of testicular volume or a post-operative testicle with less than 25% of the volume of the opposite testicle.

Lab tests
Assessment of testicular function is also dependent on lab tests. Low testosterone is a potential cause of testicular atrophy, and laboratory values of blood samples can confirm low free or bioavailable testosterone.Due to the high levels of oxidative stress in the semen, there may also be higher levels of sperm DNA fragmentation for people with varicoceles. In some cases, people with testicular damage who do not undergo repair of the varicoceles will have testicular atrophy.

Treatment
Medication
Treatment with selective estrogen receptor modulators (SERMs) alone or in addition to self-administered injections of hCG aim to correct hormonal imbalances caused by anabolic steroid use and can help prevent or reverse testicular atrophy for some people.

Surgery
People who have testicular atrophy due to testicular torsion are immediately referred to surgery regardless of the ultrasound findings, since delays rapidly decrease the rate of recovery. The consequences of not treating will result in decreased fertility and may result in the need of an orchiectomy, a surgical procedure to remove one or both testicles </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hemiparesis and can you explain it in depth? [/INST] Hemiparesis, or unilateral paresis, is weakness of one entire side of the body (hemi- means "half"). Hemiplegia is, in its most severe form, complete paralysis of half of the body.  Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke.

Signs and symptoms
Depending on the type of hemiparesis diagnosed, different bodily functions can be affected.  Some effects are expected (e.g., partial paralysis of a limb on the affected side). Other impairments, though, can at first seem completely non-related to the limb weakness but are, in fact, a direct result of the damage to the affected side of the brain.

Loss of motor skills
People with hemiparesis often have difficulties maintaining their balance due to limb paralysis leading to an inability to properly shift body weight. This makes performing everyday activities such as dressing, eating, grabbing objects, or using the bathroom more difficult. Hemiparesis with origin in the lower section of the brain creates a condition known as ataxia, a loss of both gross and fine motor skills, often manifesting as staggering and stumbling. Pure Motor Hemiparesis, a form of hemiparesis characterized by sided weakness in the leg, arm, and face, is the most commonly diagnosed form of hemiparesis.

Pusher syndrome
Pusher syndrome is a clinical disorder following left or right brain damage in which patients actively push their weight away from the nonhemiparetic side to the hemiparetic side.  In contrast to most stroke patients, who typically prefer more weight-bearing on their nonhemiparetic side, this abnormal condition can vary in severity and leads to a loss of postural balance. The lesion involved in this syndrome is thought to be in the posterior thalamus on either side, or multiple areas of the right cerebral hemisphere.With a diagnosis of pusher behaviour, three important variables should be seen, the most obvious of which is spontaneous body posture of a longitudinal tilt of the torso toward the paretic side of the body occurring on a regular basis and not only on occasion.  The use of the nonparetic extremities to create the pathological lateral tilt of the body axis is another sign to be noted when diagnosing for pusher behaviour.  This includes abduction and extension of the extremities of the non-affected side, to help in the push toward the affected (paretic) side.  The third variable that is seen is that attempts of the therapist to correct the pusher posture by aiming to realign them to upright posture are resisted by the patient.In patients with acute stroke and hemiparesis, the disorder is present in 10.4% of patients. Rehabilitation may take longer in patients that display pusher behaviour. The Copenhagen Stroke Study found that patients that presented with ipsilateral pushing used 3.6 weeks more to reach the same functional outcome level on the Barthel Index, than did patients without ipsilateral pushing.Pushing behavior has shown that perception of body posture in relation to gravity is altered. Patients experience their body as oriented "upright" when the body is actually tilted to the side of the brain lesion.  In addition, patients seem to show no disturbed processing of visual and vestibular inputs when determining subjective visual vertical. In sitting, the push presents as a strong lateral lean toward the affected side and in standing, creates a highly unstable situation as the patient is unable to support their body weight on the weakened lower extremity. The increased risk of falls must be addressed with therapy to correct their altered perception of vertical.Pusher syndrome is sometimes confused with and used interchangeably as the term hemispatial neglect, and some previous theories suggest that neglect leads to pusher syndrome.  However, another study had observed that pusher syndrome is also present in patients with left hemisphere lesions, leading to aphasia, providing a stark contrast to what was previously believed regarding hemispatial neglect, which mostly occurs with a right hemisphere lesion.Karnath  summarizes these two conflicting views, as they conclude that both neglect and aphasia are highly correlated with pusher syndrome possibly due to the close proximity of relevant brain structures associated with these two respective syndromes. However, the article goes on to state that it is imperative to note that both neglect and aphasia are not the underlying causes of pusher syndrome.Physical therapists focus on motor learning strategies when treating these patients. Verbal cues, consistent feedback, practicing correct orientation and weight shifting are all effective strategies used to reduce the effects of this disorder. Having a patient sit with their stronger side next to a wall and instructing them to lean towards the wall is an example of a possible treatment for pusher behaviour.A new (2003) physical therapy approach for patients with pusher syndrome suggests that the visual control of vertical upright orientation, which is undisturbed in these patients, is the central element of intervention in treatment. In sequential order, treatment is designed for patients to realize their altered perception of vertical, use visual aids for feedback about body orientation, learn the movements necessary to reach proper vertical position, and maintain vertical body position while performing other activities.

Classification of pusher syndrome
Individuals who present with pusher syndrome or lateropulsion, as defined by Davies, vary in their degree and severity of this condition and therefore appropriate measures need to be implemented in order to evaluate the level of "pushing". There has been a shift towards early diagnosis and evaluation of functional status for individuals who have had a stroke and presenting with pusher syndrome in order to decrease the time spent as an in-patient at hospitals and promote the return to function as early as possible. Moreover, in order to assist therapists in the classification of pusher syndrome, specific scales have been developed with validity that coincides with the criteria set out by Davies definition of "pusher syndrome". In a study by Babyar et al., an examination of such scales helped determine the relevance, practical aspects and clinimetric properties of three specific scales existing today for lateropulsion. The three scales examined were the Clinical Scale of Contraversive Pushing, Modified Scale of Contraversive Pushing, and the Burke Lateropulsion Scale. The results of the study show that reliability for each scale is good; moreover, the Scale of Contraversive Pushing was determined to have acceptable clinimetric properties, and the other two scales addressed more functional positions that will help therapists with clinical decisions and research.

Causes
The most common cause of hemiparesis and hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. A permanent brain injury that occurs during the intrauterine life, during delivery or early in life can lead to hemiplegic cerebral palsy. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the upper motor neuron syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury. There is tentative evidence of an association with undiagnosed celiac disease and improvement after withdrawal of gluten from the diet.Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke.  Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

Common
Vascular: cerebral hemorrhage, stroke, cerebral palsy
Infective: encephalitis, meningitis, brain abscess, cerebral palsy, spinal epidural abscess
Neoplastic: glioma, meningioma, brain tumors, spinal cord tumors
Demyelination: multiple sclerosis, disseminated sclerosis, ADEM, neuromyelitis optica
Traumatic: cerebral lacerations, subdural hematoma, epidural hematoma, cerebral palsy, vertebral compression fracture
Iatrogenic: local anaesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
Ictal: seizure, Todds paralysis
Congenital: cerebral palsy, Neonatal-Onset Multisystem Inflammatory Disease (NOMID)
Degenerative: ALS, corticobasal degeneration
Parasomnia: sleep paralysis

Mechanism
Movement of the body is primarily controlled by the pyramidal (or corticospinal) tract, a pathway of neurons that begins in the motor areas of the brain, projects down through the internal capsule, continues through the brainstem, decussates (or cross midline) at the lower medulla, then travels down the spinal cord into the motor neurons that control each muscle. In addition to this main pathway, there are smaller contributing pathways (including the anterior corticospinal tract), some portions of which do not cross the midline.Because of this anatomy, injuries to the pyramidal tract above the medulla generally cause contralateral hemiparesis (weakness on the opposite side as the injury). Injuries at the lower medulla, spinal cord, and peripheral nerves result in ipsilateral hemiparesis.In a few cases, lesions above the medulla have resulted in ipsilateral hemiparesis:

In several reported cases, patients with hemiparesis from an old contralateral brain injury subsequently experienced worsening of their hemiparesis when hit with a second stroke in the ipsilateral brain. The authors hypothesize that brain reorganization after the initial injury led to more reliance on uncrossed motor pathways, and when these compensatory pathways were damaged by a second stroke, motor function worsened further.
A case report describes a patient with a congenitally uncrossed pyramidal tract, who developed right-sided hemiparesis after a hemorrhage in the right brain.

Diagnosis
Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.Hemiplegia patients usually show a characteristic gait.  The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward.  The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

Assessment tools
There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patients hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:
Prioritize treatment interventions based on specific identifiable motor and sensory deficits
Create appropriate short- and long-term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient
Evaluate the potential burden of care and monitor any changes based on either improving or declining scoresSome of the most commonly used scales in the assessment of hemiplegia are:

The Fugl-Meyer Assessment of sensorimotor function (FMA)The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident (CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance.   Administration of the FMA should be done after reviewing a training manual.

The Chedoke-McMaster Stroke Assessment (CMSA)This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning.  A training workshop is recommended if the measure is being utilized for the purpose of data collection.

The Stroke Rehabilitation Assessment of Movement (STREAM)The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score).  The higher the score, the better movement and mobility is available for the individual being scored.

Treatment
Treatment for hemiparesis is the same treatment given to those recovering from strokes or brain injuries. Health care professionals such as physical therapists and occupational therapists play a large role in assisting these patients in their recovery. Treatment is focused on improving sensation and motor abilities, allowing the patient to better manage their activities of daily living. Some strategies used for treatment include promoting the use of the hemiparetic limb during functional tasks, maintaining range of motion, and using neuromuscular electrical stimulation to decrease spasticity and increase awareness of the limb.At the more advanced level, using constraint-induced movement therapy will encourage overall function and use of the affected limb. Mirror Therapy (MT) has also been used early in stroke rehabilitation and involves using the unaffected limb to stimulate motor function of the hemiparetic limb. Results from a study on patients with severe hemiparesis concluded that MT was successful in improving motor and sensory function of the distal hemiparetic upper limb.  Active participation is critical to the motor learning and recovery process, therefore its important to keep these individuals motivated so they can make continual improvements.
Also speech pathologists work to increase function for people with hemiparesis.Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Medication
Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.
Intra-muscular injection of Botulinum toxin A is used to treat spasticity that is associated with hemiparesis both in cerebral palsy children and stroke in adults. It can be injected into a muscle or more commonly muscle groups of the upper or lower extremities. Botulinum toxin A induces temporary muscle paralysis or relaxation. The main goal of Botulinum toxin A is to maintain the range of motion of affected joints and to prevent the occurrence of fixed joint contractures or stiffness. A randomized trial pointed out that individualized homeopathic medication in addition to the standard physiotherapy might have some effect in post-stroke hemiparesis.

Surgery
Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.

Rehabilitation
Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical therapy
Physical therapy  (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques.  Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation.  Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation in the hopes to minimize disability and pain.  Although many individuals with stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living.

Occupational therapy
Occupational therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing.  Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your childs hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Orthotic Intervention
Orthotic devices are one type of intervention for relieving symptoms of hemiparesis. Commonly called braces, orthotics range from off the shelf to custom fabricated solutions, but their main goal is alike, to supplement diminished or missing muscle function and joint laxity </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Radiculopathy and can you explain it in depth? [/INST] Radiculopathy, also commonly referred to as pinched nerve, refers to a set of conditions in which one or more nerves are affected and do not work properly (a neuropathy). Radiculopathy can result in pain (radicular pain), weakness, altered sensation (paresthesia) or difficulty controlling specific muscles. Pinched nerves arise when surrounding bone or tissue, such as cartilage, muscles or tendons, put pressure on the nerve and disrupt its function.In a radiculopathy, the problem occurs at or near the root of the nerve, shortly after its exit from the spinal cord. However, the pain or other symptoms often radiate to the  part of the body served by that nerve. For example, a nerve root impingement in the neck can produce pain and weakness in the forearm. Likewise, an impingement in the lower back or lumbar-sacral spine can be manifested with symptoms in the foot.
The radicular pain that results from a radiculopathy should not be confused with referred pain, which is different both in mechanism and clinical features. Polyradiculopathy refers to the condition where more than one spinal nerve root is affected.

Causes
Radiculopathy most often is caused by mechanical compression of a nerve root usually at the exit foramen or lateral recess. It may be secondary to intervertebral disk herniation (most commonly at C7 and then the C6 level), degenerative disc disease, osteoarthritis, facet joint degeneration/hypertrophy, ligamentous hypertrophy, spondylolisthesis, or a combination of these factors. Other possible causes of radiculopathy include neoplastic disease, infections such as shingles, HIV, or Lyme disease, spinal epidural abscess, spinal epidural hematoma, proximal diabetic neuropathy, Tarlov cysts, or, more rarely, sarcoidosis, arachnoiditis,  tethered spinal cord syndrome, or transverse myelitis.Repeated, longer term exposure (5 years or more) to certain work-related activities may put people at risk of developing lumbosacral radiculopathy. These behaviours may include physically demanding work, bending over or twisting at the trunk, lifting and carrying, or a combination of these activities.Less common causes of radiculopathy include injury caused by tumor (which can compress nerve roots locally) and diabetes (which can effectively cause ischemia or lack of blood flow to nerves).

Diagnosis
Signs and Symptoms
Radiculopathy is a diagnosis commonly made by physicians in primary care specialties, orthopedics, physiatry, and neurology. The diagnosis may be suggested by symptoms of pain, numbness, paresthesia, and weakness in a pattern consistent with the distribution of a particular nerve root, such as sciatica. Neck pain or back pain may also be present. Physical examination may reveal motor and sensory deficits in the distribution of a nerve root. In the case of cervical radiculopathy, Spurlings test may elicit or reproduce symptoms radiating down the arm. Similarly, in the case of lumbosacral radiculopathy, a straight leg raise maneuver or a femoral nerve stretch test may demonstrate radiculopathic symptoms down the leg. Deep tendon reflexes (also known as a Stretch reflex) may be diminished or absent in areas innervated by a particular nerve root.Diagnosis typically involves electromyography and lumbar puncture. Shingles is more common among the elderly and immunocompromised; usually (but not always) pain is followed by appearance of a rash with small blisters along a single dermatome. It can be confirmed by quick laboratory tests. Acute Lyme radiculopathy follows a history of outdoor activities during warmer months in likely tick habitats in the previous 1–12 weeks. In the U.S., Lyme is most common in New England and Mid-Atlantic states and parts of Wisconsin and Minnesota, but it is expanding to other areas. The first manifestation is usually an expanding rash possibly accompanied by flu-like symptoms. Lyme radiculopathy is usually worse at night and accompanied by extreme sleep disturbance, lymphocytic meningitis with variable headache and no fever, and sometimes by facial palsy or Lyme carditis. Lyme can also cause a milder, chronic radiculopathy an average of 8 months after the acute illness. Lyme can be confirmed by blood antibody tests and possibly lumbar puncture. If present, the above conditions should be treated immediately.Although most cases of radiculopathy are compressive and resolve with conservative treatment within 4–6 weeks, guidelines for managing radiculopathy recommend first excluding possible causes that, although rare, require immediate attention, among them the following. Cauda equina syndrome should be investigated in case of saddle anesthesia, loss of bladder or bowel control, or leg weakness. Cancer should be suspected if there is previous history of cancer, unexplained weight loss, or low-back pain that does not decrease by lying down or is unremitting. Spinal epidural abscess is more common among those with diabetes mellitus or immunocompromised, who use intravenous drugs, or had spinal surgery, injection or catheter; it typically causes fever, leukocytosis and increased erythrocyte sedimentation rate. If any of the previous is suspected, urgent magnetic resonance imaging is recommended for confirmation. Proximal diabetic neuropathy typically affects middle aged and older people with well-controlled type-2 diabetes mellitus; onset is sudden causing pain usually in multiple dermatomes quickly followed by weakness.Investigations
If symptoms do not improve after 4–6 weeks of conservative treatment, or the person is more than 50 years old, further tests are recommended. The American College of Radiology recommends that projectional radiography is the most appropriate initial study in all patients with chronic neck pain. Two additional diagnostic tests that may be of use are magnetic resonance imaging and electrodiagnostic testing. Magnetic resonance imaging (MRI) of the portion of the spine where radiculopathy is suspected may reveal evidence of degenerative change, arthritic disease, or another explanatory lesion responsible for the patients symptoms. Electrodiagnostic testing, consisting of NCS (nerve conduction study) and EMG (electromyography), is also a powerful diagnostic tool that may show nerve root injury in suspected areas. On nerve conduction studies, the pattern of diminished Compound muscle action potential and normal sensory nerve action potential may be seen given that the lesion is proximal to the posterior root ganglion. Needle EMG is the more sensitive portion of the test, and may reveal active denervation in the distribution of the involved nerve root, and neurogenic-appearing voluntary motor units in more chronic radiculopathies. Given the key role of electrodiagnostic testing in the diagnosis of acute and chronic radiculopathies, the American Association of Neuromuscular & Electrodiagnostic Medicine has issued evidence-based practice guidelines, for the diagnosis of both cervical and lumbosacral radiculopathies. The American Association of Neuromuscular & Electrodiagnostic Medicine has also participated in the Choosing Wisely Campaign and several of their recommendations relate to what tests are unnecessary for neck and back pain.

Treatment
Ideally, effective treatment aims to resolve the underlying cause and restores the nerve root to normal function. Conservative treatment may include bed rest, physical therapy, or simply continuing to do usual activities; for pain, nonsteroidal anti-inflammatory drugs, nonopioid or, in some cases, narcotic analgesics may be prescribed. A systematic review found moderate quality evidence that spinal manipulation is effective for the treatment of acute lumbar radiculopathy and cervical radiculopathy. Only low level evidence was found to support spinal manipulation for the treatment of chronic lumbar radiculopathies, and no evidence was found to exist for treatment of thoracic radiculopathy. Evidence also supports consideration of epidural steroid injection with local anesthetic in improving both pain and function in cases of lumbosacral radiculopathy.

Rehabilitation
With a recent injury (e.g. one that occurred one week ago), a formal physical therapy referral is not yet indicated. Often mild to moderate injuries will resolve or greatly improve within the first few weeks. Additionally, patients with acute injuries are often too sore to participate effectively in physical therapy so soon after the insult. Waiting two to three weeks is generally recommended before starting formal physical therapy. In acute injury resulting in lumbosacral radiculopathy, conservative treatment such as acetaminophen and NSAIDs should be the first line of therapy.Therapeutic exercises are frequently used in combination with many of the previously mentioned modalities and with great results. A variety of exercise regimens are available in patient treatment. An exercise regimen should be modified according to the abilities and weaknesses of the patient. Stabilization of the cervicothoracic region is helpful in limiting pain and preventing re-injury. Cervical and lumbar support braces typically are not indicated for radiculopathy, and may lead to weakness of support musculature. The first part of the stabilization procedure is achieving a pain free full range of motion which can be accomplished through stretching exercises. Subsequently, a strengthening exercise program should be designed to restore the deconditioned cervical, shoulder girdle, and upper trunk musculature. As reliance on the neck brace diminishes, an isometric exercise regimen should be introduced. This is a preferred method of exercise during the sub-acute phase because it resists atrophy and is least likely to exacerbate the condition. Single plane resistance exercises against cervical flexion, extension, bending, and rotation are used.

Surgery
While conservative approaches for rehabilitation are ideal, some patients will not improve and surgery is still an option. Patients with large cervical disk bulges may be recommended for surgery; however, most often, conservative management will help the herniation regress naturally </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hypoproteinemia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Vertigo and can you explain it in depth? [/INST] Vertigo is a condition where a person has the sensation of movement or of surrounding objects moving when they are not. Often it feels like a spinning or swaying movement. This may be associated with nausea, vomiting, sweating, or difficulties walking. It is typically worse when the head is moved. Vertigo is the most common type of dizziness.The most common disorders that result in vertigo are benign paroxysmal positional vertigo (BPPV), Ménières disease, and labyrinthitis. Less common causes include stroke, brain tumors, brain injury, multiple sclerosis, migraines, trauma, and uneven pressures between the middle ears. Physiologic vertigo may occur following being exposed to motion for a prolonged period such as when on a ship or simply following spinning with the eyes closed. Other causes may include toxin exposures such as to carbon monoxide, alcohol, or aspirin. Vertigo typically indicates a problem in a part of the vestibular system. Other causes of dizziness include presyncope, disequilibrium, and non-specific dizziness.Benign paroxysmal positional vertigo is more likely in someone who gets repeated episodes of vertigo with movement and is otherwise normal between these episodes. The episodes of vertigo should last less than one minute. The Dix-Hallpike test typically produces a period of rapid eye movements known as nystagmus in this condition. In Ménières disease there is often ringing in the ears, hearing loss, and the attacks of vertigo last more than twenty minutes. In labyrinthitis the onset of vertigo is sudden and the nystagmus occurs without movement. In this condition vertigo can last for days. More severe causes should also be considered. This is especially true if other problems such as weakness, headache, double vision, or numbness occur.Dizziness affects approximately 20–40% of people at some point in time, while about 7.5–10% have vertigo. About 5% have vertigo in a given year. It becomes more common with age and affects women two to three times more often than men. Vertigo accounts for about 2–3% of emergency department visits in the developed world.

Classification
Vertigo is classified into either peripheral or central, depending on the location of the dysfunction of the vestibular pathway, although it can also be caused by psychological factors.Vertigo can also be classified into objective, subjective, and pseudovertigo. Objective vertigo describes when the person has the sensation that stationary objects in the environment are moving. Subjective vertigo refers to when the person feels as if they are moving. The third type is known as pseudovertigo, an intensive sensation of rotation inside the persons head. While this classification appears in textbooks, it is unclear what relation it has to the pathophysiology or treatment of vertigo.

Peripheral
Vertigo that is caused by problems with the inner ear or vestibular system, which is composed of the semicircular canals, the vestibule (utricle and saccule), and the vestibular nerve is called "peripheral", "otologic", or "vestibular" vertigo. The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32% of all peripheral vertigo. Other causes include Ménières disease (12%), superior canal dehiscence syndrome, labyrinthitis, and visual vertigo. Any cause of inflammation such as common cold, influenza, and bacterial infections may cause transient vertigo if it involves the inner ear, as may chemical insults (e.g., aminoglycosides) or physical trauma (e.g., skull fractures). Motion sickness is sometimes classified as a cause of peripheral vertigo.People with peripheral vertigo typically present with mild to moderate imbalance, nausea, vomiting, hearing loss, tinnitus, fullness, and pain in the ear. In addition, lesions of the internal auditory canal may be associated with facial weakness on the same side. Due to a rapid compensation process, acute vertigo as a result of a peripheral lesion tends to improve in a short period of time (days to weeks).

Central
Vertigo that arises from injury to the balance centers of the central nervous system (CNS), often from a lesion in the brainstem or cerebellum, is called "central" vertigo and is generally associated with less prominent movement illusion and nausea than vertigo of peripheral origin. Central vertigo may have accompanying neurologic deficits (such as slurred speech and double vision), and pathologic nystagmus (which is pure vertical/torsional). Central pathology can cause disequilibrium, which is the sensation of being off balance. The balance disorder associated with central lesions causing vertigo is often so severe that many people are unable to stand or walk.A number of conditions that involve the central nervous system may lead to vertigo including:  lesions caused by infarctions or hemorrhage, tumors present in the cerebellopontine angle such as a vestibular schwannoma or cerebellar tumors, epilepsy, cervical spine disorders such as cervical spondylosis, degenerative ataxia disorders, migraine headaches, lateral medullary syndrome, Chiari malformation, multiple sclerosis, parkinsonism, as well as cerebral dysfunction. Central vertigo may not improve or may do so more slowly than vertigo caused by disturbance to peripheral structures. Alcohol can result in positional alcohol nystagmus (PAN).

Signs and symptoms
Vertigo is a sensation of spinning while stationary. It is commonly associated with nausea or vomiting, unsteadiness (postural instability), falls, changes to a persons thoughts, and difficulties in walking. Recurrent episodes in those with vertigo are common and frequently impair the quality of life. Blurred vision, difficulty in speaking, a lowered level of consciousness, and hearing loss may also occur. The signs and symptoms of vertigo can present as a persistent (insidious) onset or an episodic (sudden) onset.Persistent onset vertigo is characterized by symptoms lasting for longer than one day and is caused by degenerative changes that affect balance as people age. Naturally, the nerve conduction slows with aging and a decreased vibratory sensation is common. Additionally, there is a degeneration of the ampulla and otolith organs with an increase in age. Persistent onset is commonly paired with central vertigo signs and symptoms.The characteristics of an episodic onset vertigo are indicated by symptoms lasting for a smaller, more memorable amount of time, typically lasting for only seconds to minutes.

Pathophysiology
The neurochemistry of vertigo includes six primary neurotransmitters that have been identified between the three-neuron arc that drives the vestibulo-ocular reflex (VOR). Glutamate maintains the resting discharge of the central vestibular neurons and may modulate synaptic transmission in all three neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. Gamma-Aminobutyric acid (GABA) is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections among the cerebellar Purkinje cells, the lateral vestibular nucleus, and the vertical VOR.
Three other neurotransmitters work centrally. Dopamine may accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. Dopamine, histamine, serotonin, and acetylcholine are neurotransmitters thought to produce vomiting. It is known that centrally acting antihistamines modulate the symptoms of acute symptomatic vertigo.

Diagnosis
Tests for vertigo often attempt to elicit nystagmus and to differentiate vertigo from other causes of dizziness such as presyncope, hyperventilation syndrome, disequilibrium, or psychiatric causes of lightheadedness. Tests of vestibular system (balance) function include electronystagmography (ENG), Dix-Hallpike maneuver, rotation tests, head-thrust test, caloric reflex test, and computerized dynamic posturography (CDP).The HINTS test, which is a combination of three physical examination tests that may be performed by physicians at the bedside, has been deemed helpful in differentiating between central and peripheral causes of vertigo. The HINTS test involves the horizontal head impulse test, observation of nystagmus on primary gaze, and the test of skew. CT scans or MRIs are sometimes used by physicians when diagnosing vertigo.Tests of auditory system (hearing) function include pure tone audiometry, speech audiometry, acoustic reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and the auditory brainstem response test.A number of specific conditions can cause vertigo. In the elderly, however, the condition is often multifactorial.A recent history of underwater diving can indicate a possibility of barotrauma or decompression sickness involvement, but does not exclude all other possibilities. The dive profile (which is frequently recorded by dive computer) can be useful to assess a probability for decompression sickness, which can be confirmed by therapeutic recompression.

Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder and occurs when loose calcium carbonate debris has broken off of the otoconial membrane and enters a semicircular canal thereby creating the sensation of motion. People with BPPV may experience brief periods of vertigo, usually under a minute, which occur with change in the position.This is the most common cause of vertigo. It occurs in 0.6% of the population yearly with 10% having an attack during their lifetime. It is believed to be due to a mechanical malfunction of the inner ear. BPPV may be diagnosed with the Dix-Hallpike test and can be effectively treated with repositioning movements such as the Epley maneuver.

Ménières disease
Ménières disease is an inner ear disorder of unknown origin, but is thought to be caused by an increase in the amount of endolymphatic fluid present in the inner ear (endolymphatic hydrops). However, this idea has not been directly confirmed with histopathologic studies, but electrophysiologic studies have been suggestive of this mechanism. Ménières disease frequently presents with recurrent, spontaneous attacks of severe vertigo in combination with ringing in the ears (tinnitus), a feeling of pressure or fullness in the ear (aural fullness), severe nausea or vomiting, imbalance, and hearing loss. As the disease worsens, hearing loss will progress.

Labyrinthitis
Labyrinthitis presents with severe vertigo with associated nausea, vomiting, and generalized imbalance and is believed to be caused by a viral infection of the inner ear, although several theories have been put forward and the cause remains uncertain. Individuals with vestibular neuritis do not typically have auditory symptoms, but may experience a sensation of aural fullness or tinnitus. Persisting balance problems may remain in 30% of people affected.

Vestibular migraine
Vestibular migraine is the association of vertigo and migraines and is one of the most common causes of recurrent, spontaneous episodes of vertigo. The cause of vestibular migraines is currently unclear; however, one hypothesized cause is that the stimulation of the trigeminal nerve leads to nystagmus in individuals with migraines. Approximately 40% of all migraine patients will have an accompanying vestibular syndrome, such as vertigo, dizziness, or disruption of the balance system.Other suggested causes of vestibular migraines include the following: unilateral neuronal instability of the vestibular nerve, idiopathic asymmetric activation of the vestibular nuclei in the brainstem, and vasospasm of the blood vessels supplying the labyrinth or central vestibular pathways resulting in ischemia to these structures. Vestibular migraines are estimated to affect 1–3% of the general population and may affect 10% of people with migraine . Additionally, vestibular migraines tend to occur more often in women and rarely affect individuals after the sixth decade of life.

Motion sickness
Motion sickness is common and is related to vestibular migraine. It is nausea and vomiting in response to motion and is typically worse if the journey is on a winding road or involves many stops and starts, or if the person is reading in a moving car. It is caused by a mismatch between visual input and vestibular sensation. For example, the person is reading a book that is stationary in relation to the body, but the vestibular system senses that the car, and thus the body, is moving.

Alternobaric vertigo
Alternobaric vertigo is caused by a pressure difference between the middle ear cavities, usually due to blockage or partial blockage of one eustachian tube, usually when flying or diving underwater. It is most pronounced when the diver is in the vertical position; the spinning is toward the ear with the higher pressure and tends to develop when the pressures differ by 60 cm of water or more.

Decompression sickness
Vertigo is recorded as a symptom of decompression sickness in 5.3% of cases by the U.S. Navy as reported by Powell, 2008 including isobaric decompression sickness.
Decompression sickness can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of different inert gases. This is known as isobaric counterdiffusion, and presents a problem for very deep dives. For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium, but is about 4.5 times more soluble </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Peripheral neuropathy and can you explain it in depth? [/INST] Peripheral neuropathy, often shortened to neuropathy, is a general term describing disease affecting the peripheral nerves, meaning nerves beyond the brain and spinal cord. Damage to peripheral nerves may impair sensation, movement, gland, or organ function depending on which nerves are affected; in other words, neuropathy affecting motor, sensory, or autonomic nerves result in different symptoms. More than one type of nerve may be affected simultaneously. Peripheral neuropathy may be acute (with sudden onset, rapid progress) or chronic (symptoms begin subtly and progress slowly), and may be reversible or permanent.
Common causes include systemic diseases (such as diabetes or leprosy), hyperglycemia-induced glycation, vitamin deficiency, medication (e.g., chemotherapy, or commonly prescribed antibiotics including metronidazole and the fluoroquinolone class of antibiotics (such as ciprofloxacin, levofloxacin, moxifloxacin)), traumatic injury, ischemia, radiation therapy, excessive alcohol consumption, immune system disease, celiac disease, non-celiac gluten sensitivity, or viral infection. It can also be genetic (present from birth) or idiopathic (no known cause). In conventional medical usage, the word neuropathy (neuro-, "nervous system" and -pathy, "disease of") without modifier usually means peripheral neuropathy.
Neuropathy affecting just one nerve is called "mononeuropathy" and neuropathy involving nerves in roughly the same areas on both sides of the body is called "symmetrical polyneuropathy" or simply "polyneuropathy". When two or more (typically just a few, but sometimes many) separate nerves in disparate areas of the body are affected it is called "mononeuritis multiplex", "multifocal mononeuropathy", or "multiple mononeuropathy".Neuropathy may cause painful cramps, fasciculations (fine muscle twitching), muscle loss, bone degeneration, and changes in the skin, hair, and nails. Additionally, motor neuropathy may cause impaired balance and coordination or, most commonly, muscle weakness; sensory neuropathy may cause numbness to touch and vibration, reduced position sense causing poorer coordination and balance, reduced sensitivity to temperature change and pain, spontaneous tingling or burning pain, or allodynia (pain from normally nonpainful stimuli, such as light touch); and autonomic neuropathy may produce diverse symptoms, depending on the affected glands and organs, but common symptoms are poor bladder control, abnormal blood pressure or heart rate, and reduced ability to sweat normally.

Classification
Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., inflammation (neuritis), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy). The affected nerves are found in an EMG (electromyography) / NCS (nerve conduction study) test and the classification is applied upon completion of the exam.

Mononeuropathy
Mononeuropathy is a type of neuropathy that only affects a single nerve. Diagnostically, it is important to distinguish it from polyneuropathy because when a single nerve is affected, it is more likely to be due to localized trauma or infection.The most common cause of mononeuropathy is physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples. Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may cause mononeuropathy.

Polyneuropathy
"Polyneuropathy" is a pattern of nerve damage that is quite different from mononeuropathy, often more serious and affecting more areas of the body. The term "peripheral neuropathy" sometimes is used loosely to refer to polyneuropathy. In cases of polyneuropathy, many nerve cells in various parts of the body are affected, without regard to the nerve through which they pass; not all nerve cells are affected in any particular case. In distal axonopathy, one common pattern is that the cell bodies of neurons remain intact, but the axons are affected in proportion to their length; the longest axons are the most affected. Diabetic neuropathy is the most common cause of this pattern. In demyelinating polyneuropathies, the myelin sheath around axons is damaged, which affects the ability of the axons to conduct electrical impulses. The third and least common pattern affects the cell bodies of neurons directly. This usually picks out either the motor neurons (known as motor neuron disease) or the sensory neurons (known as sensory neuronopathy or dorsal root ganglionopathy).The effect of this is to cause symptoms in more than one part of the body, often symmetrically on left and right sides. As for any neuropathy, the chief symptoms include motor symptoms such as weakness or clumsiness of movement; and sensory symptoms such as unusual or unpleasant sensations such as tingling or burning; reduced ability to feel sensations such as texture or temperature, and impaired balance when standing or walking. In many polyneuropathies, these symptoms occur first and most severely in the feet. Autonomic symptoms also may occur, such as dizziness on standing up, erectile dysfunction, and difficulty controlling urination.Polyneuropathies usually are caused by processes that affect the body as a whole. Diabetes and impaired glucose tolerance are the most common causes. Hyperglycemia-induced formation of advanced glycation end products (AGEs) is related to diabetic neuropathy. Other causes relate to the particular type of polyneuropathy, and there are many different causes of each type, including inflammatory diseases such as Lyme disease, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs).
Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. It is important to recognize that at one time it was thought that many of the cases of small fiber peripheral neuropathy with typical symptoms of tingling, pain, and loss of sensation in the feet and hands were due to glucose intolerance before a diagnosis of diabetes or pre-diabetes. However, in August 2015, the Mayo Clinic published a scientific study in the Journal of the Neurological Sciences showing "no significant increase in...symptoms...in the prediabetes group", and stated that "A search for alternate neuropathy causes is needed in patients with prediabetes."The treatment of polyneuropathies is aimed firstly at eliminating or controlling the cause, secondly at maintaining muscle strength and physical function, and thirdly at controlling symptoms such as neuropathic pain.

Mononeuritis multiplex
Mononeuritis multiplex, occasionally termed polyneuritis multiplex, is simultaneous or sequential involvement of individual noncontiguous nerve trunks, either partially or completely, evolving over days to years and typically presenting with acute or subacute loss of sensory and motor function of individual nerves. The pattern of involvement is asymmetric, however, as the disease progresses, deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy. Therefore, attention to the pattern of early symptoms is important.
Mononeuritis multiplex is sometimes associated with a deep, aching pain that is worse at night and frequently in the lower back, hip, or leg. In people with diabetes mellitus, mononeuritis multiplex typically is encountered as acute, unilateral, and severe thigh pain followed by anterior muscle weakness and loss of knee reflex.Electrodiagnostic medicine studies will show multifocal sensory motor axonal neuropathy.It is caused by, or associated with, several medical conditions:

Autonomic neuropathy
Autonomic neuropathy is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a persons conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.Autonomic neuropathy is one cause of malfunction of the autonomic nervous system, but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy.The signs and symptoms of autonomic neuropathy include the following:

Urinary bladder conditions: bladder incontinence or urine retention
Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhoea, constipation
Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion
Respiratory system: impairments in the signals associated with regulation of breathing and gas exchange (central sleep apnea, hypopnea, bradypnea).
Skin : thermal regulation, dryness through sweat disturbances
Other areas: hypoglycemia unawareness, genital impotence

Neuritis
Neuritis is a general term for inflammation of a nerve or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia (pins-and-needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.
Causes of neuritis include:

Signs and symptoms
Those with diseases or dysfunctions of their nerves may present with problems in any of the normal nerve functions. Symptoms vary depending on the types of nerve fiber involved. In terms of sensory function, symptoms commonly include loss of function ("negative") symptoms, including numbness, tremor, impairment of balance, and gait abnormality. Gain of function (positive) symptoms include tingling, pain, itching, crawling, and pins-and-needles. Motor symptoms include loss of function ("negative") symptoms of weakness, tiredness, muscle atrophy, and gait abnormalities; and gain of function ("positive") symptoms of cramps, and muscle twitch (fasciculations).In the most common form, length-dependent peripheral neuropathy, pain and parasthesia appears symmetrically and generally at the terminals of the longest nerves, which are in the lower legs and feet. Sensory symptoms generally develop before motor symptoms such as weakness. Length-dependent peripheral neuropathy symptoms make a slow ascent of the lower limbs, while symptoms may never appear in the upper limbs; if they do, it will be around the time that leg symptoms reach the knee. When the nerves of the autonomic nervous system are affected, symptoms may include constipation, dry mouth, difficulty urinating, and dizziness when standing.

CAP-PRI Scale for diagnosis
A user-friendly, disease-specific, quality-of-life scale can be used to monitor how someone is doing living with the burden of chronic, sensorimotor polyneuropathy. This scale, called the Chronic, Acquired Polyneuropathy - Patient-reported Index (CAP-PRI), contains only 15 items and is completed by the person affected by polyneuropathy. The total score and individual item scores can be followed over time, with item scoring used by the patient and care-provider to estimate clinical status of some of the more common life domains and symptoms impacted by polyneuropathy.

Causes
The causes are grouped broadly as follows:

Diagnosis
Peripheral neuropathy may first be considered when an individual reports symptoms of numbness, tingling, and pain in feet. After ruling out a lesion in the central nervous system as a cause, diagnosis may be made on the basis of symptoms, laboratory and additional testing, clinical history, and a detailed examination.
During physical examination, specifically a neurological examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, although those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies, such as Guillain–Barré syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Classically, ankle jerk reflex is absent in peripheral neuropathy.
A physical examination will involve testing the deep ankle reflex as well as examining the feet for any ulceration. For large fiber neuropathy, an exam will usually show an abnormally decreased sensation to vibration, which is tested with a 128-Hz tuning fork, and decreased sensation of light touch when touched by a nylon monofilament.Diagnostic tests include electromyography (EMG) and nerve conduction studies (NCSs), which assess large myelinated nerve fibers. Testing for small-fiber peripheral neuropathies often relates to the autonomic nervous system function of small thinly- and unmyelinated fibers. These tests include a sweat test and a tilt table test. Diagnosis of small fiber involvement in peripheral neuropathy may also involve a skin biopsy in which a 3 mm-thick section of skin is removed from the calf by a punch biopsy, and is used to measure the skin intraepidermal nerve fiber density (IENFD), the density of nerves in the outer layer of the skin. Reduced density of the small nerves in the epidermis supports a diagnosis of small-fiber peripheral neuropathy.
In EMG testing, demyelinating neuropathy characteristically shows a reduction in conduction velocity and prolongation of distal and F-wave latencies, whereas axonal neuropathy shows a reduction in amplitude.Laboratory tests include blood tests for vitamin B-12 levels, a complete blood count, measurement of thyroid stimulating hormone levels, a comprehensive metabolic panel screening for diabetes and pre-diabetes, and a serum immunofixation test, which tests for antibodies in the blood.

Treatment
The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.

Medications
A range of medications that act on the central nervous system have been used to symptomatically treat neuropathic pain. Commonly used medications include tricyclic antidepressants (such as nortriptyline, amitriptyline. imapramine, and desipramine,) serotonin-norepinephrine reuptake inhibitor (SNRI) medications (duloxetine, venlafaxine, and milnacipran) and antiepileptic medications (gabapentin, pregabalin, oxcarbazepine zonisamide levetiracetam, lamotrigine, topiramate, clonazepam, phenytoin, lacosamide, sodium valproate and carbamazepine). Opioid and opiate medications (such as buprenorphine, morphine, methadone, fentanyl, hydromorphone, tramadol and oxycodone) are also often used to treat neuropathic pain.
As is revealed in many of the Cochrane systematic reviews listed below, studies of these medications for the treatment of neuropathic pain are often methodologically flawed and the evidence is potentially subject to major bias. In general, the evidence does not support the usage of antiepileptic and antidepressant medications for the treatment of neuropathic pain. Better designed clinical trials and further review from non-biased third parties are necessary to gauge just how useful for patients these medications truly are. Reviews of these systematic reviews are also necessary to assess for their failings.
It is also often the case that the aforementioned medications are prescribed for neuropathic pain conditions for which they had not been explicitly tested on or for which controlled research is severely lacking; or even for which evidence suggests that these medications are not effective. The NHS for example explicitly state that amitriptyline and gabapentin can be used for treating the pain of sciatica. This is despite both the lack of high quality evidence that demonstrates efficacy of these medications for that symptom, and also the prominence of generally moderate to high quality evidence that reveals that antiepileptics in specific, including gabapentin, demonstrate no efficacy in treating it.

Antidepressants
In general, according to Cochranes systematic reviews, antidepressants have shown to either be ineffective for the treatment of neuropathic pain or the evidence available is inconclusive. Evidence also tends to be tainted by bias or issues with the methodology.Cochrane systematically reviewed the evidence for the antidepressants nortriptyline, desipramine, venlafaxine and milnacipran and in all these cases found scant evidence to support their use for the treatment of neuropathic pain. All reviews were done between 2014 and 2015.A 2015 Cochrane systematic review of amitriptyline found that there was no evidence supporting the use of amitriptyline that did not possess inherent bias. The authors believe amitriptyline may have an effect in some patients but that the effect is overestimated. A 2014 Cochrane systematic review of imipramine notes that the evidence suggesting benefit were "methodologically flawed and potentially subject to major bias."A 2017 Cochrane systematic review assessed the benefit of antidepressant medications for several types of chronic non-cancer pains (including neuropathic pain) in children and adolescents and the authors found the evidence inconclusive.

Antiepileptics
A 2017 Cochrane systematic review found that daily dosages between (1800 - 3600) mg of gabapentin could provide good pain relief for pain associated with diabetic neuropathy only. This relief occurred for roughly (30 - 40)% of treated patients, while placebo had a (10 - 20)% response. Three of the seven authors of the review had conflicts of interest declared. In a 2019 Cochrane review of pregabalin the authors conclude that there is some evidence of efficacy in the treatment of pain deriving from post-herpetic neuralgia, diabetic neuropathy and post-traumatic neuropathic pain only. They also warned that many patients treated will have no benefit. Two of the five authors declared receiving payments from pharmaceutical companies.A 2017 Cochrane systematic review found that oxcarbazepine had little evidence to support its use for treating diabetic neuropathy, radicular pain and other neuropathies. The authors also call for better studies. In a 2015 Cochrane systematic review the authors found a lack of evidence showing any effectiveness of zonisamide for the treatment of pain deriving from any peripheral neuropathy. A 2014 Cochrane review found that studies of levetiracetam showed no indication for its effectiveness at treating pain from any neuropathy. The authors also found that the evidence was possibly biased and that some patients experienced adverse events.A 2013 Cochrane systematic review concluded that there was high quality evidence to suggest that lamotrigine is not effective for treating neuropathic pain, even at high dosages (200 - 400) mg. A 2013 Cochrane systematic review of topimirate found that the included data had a strong likelihood of major bias; despite this, it found no effectiveness for the drug in treating the pain associated with diabetic neuropathy. It had not been tested for any other type of neuropathy. Cochrane reviews from 2012 of clonazepam and phenytoin uncovered no evidence of sufficient quality to support their use in chronic neuropathic pain."A 2012 Cochrane systematic review of lacosamide found it very likely that the drug is ineffective for treating neuropathic pain. The authors caution against positive interpretations of the evidence. For sodium valproate the authors of a 2011 Cochrane review found that "three studies no more than hint that sodium valproate may reduce pain in diabetic neuropathy". They discuss how there is a probable overestimate of effect due to the inherent problems with the data and conclude that the evidence does not support its usage. In a 2014 systematic review of carbamazepine the authors believe the drug to be of benefit for some people. No trials were considered greater than level III evidence; none were longer than 4 weeks in length or were deemed as having good reporting quality.A 2017 Cochrane systematic review aiming to assess the benefit of antiepileptic medications for several types of chronic non-cancer pains (including neuropathic pain) in children and adolescents found the evidence inconclusive. Two of the ten authors of this study declared receiving payments from pharmaceutical companies.

Opioids
A Cochrane review of buprenorphine, fentanyl, hydromorphone and morphine, all dated between 2015 and 2017, and all for the treatment of neuropathic pain, found that there was insufficient evidence to comment on their efficacy. Conflicts of interest were declared by the authors in this review. A 2017 Cochrane review of methadone found very low quality evidence, three studies of limited quality, of its efficacy and safety. They could not formulate any conclusions about its relative efficacy and safety compared to a placebo.For tramadol, Cochrane found that there was only modest information about the benefits of its usage for neuropathic pain. Studies were small, had potential risks of bias and apparent benefits increased with risk of bias. Overall the evidence was of low or very low quality and the authors state that it "does not provide a reliable indication of the likely effect". For oxycodone the authors found very low quality evidence showing its usefulness in treating diabetic neuropathy and postherpetic neuralgia only. One of the four authors declared receiving payments from pharmaceutical companies.More generally, a 2013 review examining the overall efficacy of opioid therapy for the treatment of neuropathic pain found studies were often subject to bias and that their efficacy and safety was not deducible with the evidence available. A 2017 Cochrane review examining opioid therapy as a treatment for many non-cancer pain syndromes (including neuropathic pain) concluded, "There was no evidence from randomised controlled trials to support or refute the use of opioids to treat chronic non-cancer pain in children and adolescents."

Others
A 2016 Cochrane review of paracetamol for the treatment of neuropathic pain concluded that its benefit alone or in combination with codeine or dihydrocodeine is unknown.Few studies have examined whether nonsteroidal anti-inflammatory drugs are effective in treating peripheral neuropathy.There is some evidence that symptomatic relief from the pain of peripheral neuropathy may be obtained by application of topical capsaicin. Capsaicin is the factor that causes heat in chili peppers. However, the evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option.Evidence supports the use of cannabinoids for some forms of neuropathic pain. A 2018 Cochrane review of cannabis-based medicines for the treatment of chronic neuropathic pain included 16 studies. All of these studies included THC as a pharmacological component of the test group. The authors rated the quality of evidence as very low to moderate. The primary outcome was quoted as, "Cannabis-based medicines may increase the number of people achieving 50% or greater pain relief compared with placebo" but "the evidence for improvement in Patient Global Impression of Change (PGIC) with cannabis to be of very low quality". The authors also conclude, "The potential benefits of cannabis-based medicine... might be outweighed by their potential harms."A 2014 Cochrane review of topical lidocaine for the treatment of various peripheral neuropathies found its usage supported by a few low quality studies. The authors state that there are no high quality randomised control trials demonstrating its efficacy or safety profile.A 2015 (updated in 2022) Cochrane review of topical clonidine for the treatment of diabetic neuropathy included two studies of 8 and 12 weeks in length; both of which compared topical clonidine to placebo and both of which were funded by the same drug manufacturer. The review found that topical clonidine may provide some benefit versus placebo. However, the authors state that the included trials are potentially subject to significant bias and that the evidence is of low to moderate quality.A 2007 Cochrane review of aldose reductase inhibitors for the treatment of the pain deriving from diabetic polyneuropathy found it no better than placebo.

Medical devices
Transcutaneous electrical nerve stimulation (TENS) therapy is often used to treat various types of neuropathy. A 2010 review of three trials, for the treatment of diabetic neuropathy explicitly, involving a total of 78 patients found some improvement in pain scores after 4 and 6, but not 12 weeks of treatment and an overall improvement in neuropathic symptoms at 12 weeks </s>