Functional weakness is weakness of an arm or leg due to the nervous system not working properly. It is not caused by damage or disease of the nervous system. Patients with functional weakness experience symptoms of limb weakness which can be disabling and frightening such as problems walking or a ‘heaviness’ down one side, dropping things or a feeling that a limb just doesn’t feel normal or ‘part of them’. Functional weakness may also be described as functional neurological symptom disorder (FNsD), Functional Neurological Disorder (FND) or functional neurological symptoms. If the symptoms are caused by a psychological trigger, it may be diagnosed as 'dissociative motor disorder' or conversion disorder (CD).

To the patient and the doctor it often looks as if there has been a stroke or have symptoms of multiple sclerosis. However, unlike these conditions, with functional weakness there is no permanent damage to the nervous system which means that it can get better or even go away completely.

The diagnosis should usually be made by a consultant neurologist so that other neurological causes can be excluded. The diagnosis should be made on the basis of positive features in the history and the examination (such as Hoover's sign). It is dangerous to make the diagnosis simply because tests are normal. Neurologists usually diagnose wrongly about 5% of the time (which is the same for many other conditions.)

Many patients with functional weakness suffer from not being believed. Although psychological factors can be important for a some patients, for the majority of individuals the cause of their weakness has a physical trigger such as a virus, injury or other medical condition. The symptoms of functional weakness are real, and are as disabling and distressing as Multiple Sclerosis or Parkinson's.

The most effective treatment is physiotherapy, however it is also helpful for patients to understand the diagnosis, and some may find CBT helps them to cope with the emotions associated with being unwell. For those with conversion disorder, psychological therapy is key to their treatment as it is emotional or psychological factors which are causing their symptoms.

There are a great number of symptoms experienced by those with a functional neurological disorder. It is important to note that the symptoms experienced by those with an FND are very real , and should not be confused with malingering, factitious disorders, or Munchausen syndrome. At the same time, the origin of symptoms is complex since it can be associated with physical injury, severe psychological trauma (conversion disorder), and idiopathic neurological dysfunction. The core symptoms are those of motor or sensory function or episodes of altered awareness

- Limb weakness or paralysis

- Blackouts (also called dissociative or non-epileptic seizures/attacks) – these may look like epileptic seizures or faints

- Movement disorders including tremors, dystonia (spasms), myoclonus (jerky movements)

- Visual symptoms including loss of vision or double vision

- Speech symptoms including dysphonia (whispering speech), slurred or stuttering speech

- Sensory disturbance including hemisensory syndrome (altered sensation down one side of the body)

A functional neurological disorder (FND) is a condition in which patients experience neurological symptoms such as weakness, movement disorders, sensory symptoms and blackouts. The brain of a patient with functional neurological symptom disorder is structurally normal, but functions incorrectly. According to consensus from the literature and from physicians and psychologists practicing in the field, "functional symptoms, also called 'medically unexplained,' 'psychogenic,' or [in outdated terminology] 'hysterical,' are symptoms that are clinically recognisable as not being caused by a definable organic disease". The intended contrast is with an organic brain syndrome, although the terms imply a level of certainty about causation that is often clinically unconfirmed. Subsets of functional neurological disorders include functional neurological symptom disorder (FNsD), conversion disorder, and psychogenic movement disorder/non-epileptic seizures. Functional neurological disorders are common in neurological services, accounting for up to one third of outpatient neurology clinic attendances, and associated with as much physical disability and distress as other neurological disorders.

The diagnosis is made based on positive signs and symptoms in the history and examination during consultation of a neurologist (see below). Physiotherapy is particularly helpful for patients with motor symptoms (weakness, gait disorders, movement disorders) and tailored cognitive behavioural therapy has the best evidence in patients with dissociative (non-epileptic) attacks.

Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion.

Following upper motor neuron lesions, affected muscles potentially have many features of altered performance including:

- weakness (decreased ability for the muscle to generate force)

- decreased motor control including decreased speed, accuracy and dexterity

- altered muscle tone (hypotonia or hypertonia) – a decrease or increase in the baseline level of muscle activity

- decreased endurance

- exaggerated deep tendon reflexes including spasticity, and clonus (a series of involuntary rapid muscle contractions)

Such signs are collectively termed the "upper motor neuron syndrome". Affected muscles typically show multiple signs, with severity depending on the degree of damage and other factors that influence motor control. In neuroanatomical circles, it is often joked, for example, that hemisection of the cervical spinal cord leads to an "upper lower motor neuron syndrome and a lower upper motor neuron syndrome". The saying refers to lower motor neuron symptoms in the upper extremity (arm) and upper motor neurons symptoms in the lower extremity (leg).

The upper motor neuron syndrome signs are seen in conditions where motor areas in the brain and/or spinal cord are damaged or fail to develop normally. These include spinal cord injury, cerebral palsy, multiple sclerosis and acquired brain injury including stroke. The impact of impairment of muscles for an individual is problems with movement, and posture, which often affects their function.

Health professionals' understanding of impairments in muscles after an upper motor neuron lesion has progressed considerably in recent decades. However, a diagnosis of "spasticity" is still often used interchangeably with upper motor neuron syndrome, and it is not unusual to see patients labeled as spastic who demonstrate an array of UMN findings.

Spasticity is an exaggerated stretch reflex, which means that a muscle has a reflex contraction when stretched, and that this contraction is stronger when the stretch is applied more quickly. The commonly quoted definition by Lance (1980) describes "a motor disorder, characterised by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex as one component of the upper motor neurone (UMN) syndrome".

Spasticity is a common feature of muscle performance after upper motor neuron lesions, but is generally of much less clinical significance than other features such as decreased strength, decreased control and decreased endurance. The confusion in the use of the terminology complicates assessment and treatment planning by health professionals, as many confuse the other findings of upper motor neuron syndrome and describe them as spasticity. This confusion potentially leaves health professionals attempting to inhibit an exaggerated stretch reflex to improve muscle performance, potentially leaving more significant UMNS changes such as weakness unaddressed. Improved understanding of the multiple features of the upper motor neuron syndrome supports more rigorous assessment, and improved treatment planning.

Onset of PLS usually occurs spontaneously after age 50 and progresses gradually over a number of years, or even decades. The disorder usually begins in the legs, but it may start in the tongue or the hands. Symptoms may include difficulty with balance, weakness and stiffness in the legs, and clumsiness. Other common symptoms are spasticity (involuntary muscle contraction due to the stretching of muscle, which depends on the velocity of the stretch) in the hands, feet, or legs, foot dragging, and speech and swallowing problems due to involvement of the facial muscles. Breathing may also become compromised in the later stages of the disease, causing those patients who develop ventilatory failure to require noninvasive ventilatory support. Hyperreflexia is another key feature of PLS as seen in patients presenting with the Babinski's sign. Some people present with emotional lability and bladder urgency, and occasionally people with PLS experience mild cognitive changes detectable on neuropsychological testing, particularly on measures of executive function.

PLS is not considered hereditary when onset is in adulthood; however, juvenile primary lateral sclerosis (JPLS) has been linked to a mutation in the ALS2 gene which encodes the cell-signalling protein alsin.

The issue of whether PLS exists as a different entity from ALS is not clear, as some patients initially diagnosed as having PLS ultimately develop lower motor neuron signs.

There are no specific tests for the diagnosis of PLS. Therefore, the diagnosis occurs as the result of eliminating other possible causes of the symptoms and by an extended observation period.

Primary lateral sclerosis (PLS) usually presents with gradual-onset, progressive, lower-extremity stiffness and pain due to muscle spasticity. Onset is often asymmetrical. Although the muscles do not appear to atrophy as in ALS (at least initially), the disabling aspect of PLS is muscle spasticity and cramping, and intense pain when those muscles are stretched, resulting in joint immobility. A normal walking stride may become a tiny step shuffle with related instability and falling.

Giveway weakness (also "give-away weakness", "collapsing weakness", etc.) refers to a symptom where a patient's arm, leg, can initially provide resistance against an examiner's touch, but then suddenly "gives way" and provides no further muscular resistance.

Symptoms of JPLS begin in early childhood and progress over a period of 15 to 20 years. Early symptoms include clumsiness, muscle spasms, weakness and stiffness in the legs, and difficulty with balance. As symptoms progress, they become more serious and include weakness and stiffness in the arms and hands, slurred speech, drooling, difficulty swallowing, and an inability to walk.

Muscle weakness can also be classified as either "proximal" or "distal" based on the location of the muscles that it affects. Proximal muscle weakness affects muscles closest to the body's midline, while distal muscle weakness affects muscles further out on the limbs.

Proximal muscle weakness can be seen in Cushing's syndrome and hyperthyroidism.

The severity of muscle weakness can be classified into different "grades" based on the following criteria:

- Grade 0: No contraction or muscle movement.

- Grade 1: Trace of contraction, but no movement at the joint.

- Grade 2: Movement at the joint with gravity eliminated.

- Grade 3: Movement against gravity, but not against added resistance.

- Grade 4: Movement against external resistance with less strength than usual.

- Grade 5: Normal strength.

Classic symptoms of muscle imbalances are usually pain associated with the affected joint. Symptoms can vary depending on what stage their muscular imbalance is, functional or pathological, but commonly exhibit small tissue damage or lesions accompanied by a change in muscle movement patterns. Symptoms may occur after injury or surgery, where the recuperation of the joint affected is left untreated causing either tension or restriction to flexibility and strength of the prime movers.

Scoliosis, is a medical condition where a person's spine has several irregular curves that are located between the neck and the pelvis. Symptoms of scoliosis in mild cases usually exhibit abnormal posture, back pain, tingling or numbness in the legs and in worse cases can exhibit breathing problems, fatigue, permanent deformities and in rare cases heart problems.

Symptoms of CMT usually begin in early childhood or early adulthood, but can begin later. Some people do not experience symptoms until their early thirties or forties. Usually, the initial symptom is foot drop early in the course of the disease. This can also cause hammer toe, where the toes are always curled. Wasting of muscle tissue of the lower parts of the legs may give rise to a "stork leg" or "inverted champagne bottle" appearance. Weakness in the hands and forearms occurs in many people as the disease progresses.

Loss of touch sensation in the feet, ankles and legs, as well as in the hands, wrists and arms occur with various types of the disease. Early and late onset forms occur with 'on and off' painful spasmodic muscular contractions that can be disabling when the disease activates. High-arched feet (pes cavus) or flat-arched feet (pes planus) are classically associated with the disorder. Sensory and proprioceptive nerves in the hands and feet are often damaged, while unmyelinated pain nerves are left intact. Overuse of an affected hand or limb can activate symptoms including numbness, spasm, and painful cramping.

Symptoms and progression of the disease can vary. Involuntary grinding of teeth as well as squinting are prevalent and often go unnoticed by the person affected. Breathing can be affected in some; so can hearing, vision, as well as the neck and shoulder muscles. Scoliosis is common, causing hunching and loss of height. Hip sockets can be malformed. Gastrointestinal problems can be part of CMT, as can difficulty chewing, swallowing, and speaking (due to atrophy of vocal cords). A tremor can develop as muscles waste. Pregnancy has been known to exacerbate CMT, as well as severe emotional stress. Patients with CMT must avoid periods of prolonged immobility such as when recovering from a secondary injury as prolonged periods of limited mobility can drastically accelerate symptoms of CMT.

Pain due to postural changes, skeletal deformations, muscle fatigue and cramping is fairly common in people with CMT. It can be mitigated or treated by physical therapies, surgeries, and corrective or assistive devices. Analgesic medications may also be needed if other therapies do not provide relief from pain. Neuropathic pain is often a symptom of CMT, though, like other symptoms of CMT, its presence and severity varies from case to case. For some people, pain can be significant to severe and interfere with daily life activities. However, pain is not experienced by all people with CMT. When neuropathic pain is present as a symptom of CMT, it is comparable to that seen in other peripheral neuropathies, as well as postherpetic neuralgia and complex regional pain syndrome, among other diseases.

The primary symptom of camptocormia is abnormal forward bending of the torso. This bending becomes worse while walking but does not appear when the affected individual is lying down in a horizontal position. This alleviation of the condition indicates that it is a manifestation of another disease or ailment and is not due to a spine that is actually bent. This is somewhat ironic, since the medically accepted name for the condition is bent spine syndrome.

In an afflicted individual, the abnormal bending consists of an anterior flexion greater than 45 degrees. Because of this bending and the physical limitations caused by the conditions associated with the disease, it is usually impossible for an afflicted person to achieve a fully erect position. In addition, patients suffering from camptocormia often experience low back pain as a result of the condition. BSS often appears in individuals afflicted with Parkinson’s disease, muscular dystrophies, endocrine disorders, inflammatory conditions (myositis), or mitochondrial myopathies. As previously mentioned, the disease is more common in older individuals.

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Interventions for neurological disorders include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. The World Health Organization estimated in 2006 that neurological disorders and their sequelae (direct consequences) affect as many as one billion people worldwide, and identified health inequalities and social stigma/discrimination as major factors contributing to the associated disability and suffering.

Assessment of motor control may involve several health professionals depending on the affected individual's situation, and the severity of their condition. This may include physical therapists, physicians (including neurologists and psychiatrists ) and rehabilitation physicians, orthotists, occupational therapists, and speech-language pathologists. Assessment is needed of the affected individual's goals, their function, and any symptoms that may be related to the movement disorder, such as pain. A thorough assessment then uses a clinical reasoning approach to determine why difficulties are occurring. Elements of assessment will include analysis of posture, active movement, muscle strength, movement control and coordination, and endurance, as well as muscle tone and spasticity. Impaired muscles typically demonstrate a loss of selective movement, including a loss of eccentric control (decreased ability to actively lengthen); this decreased active lengthening of a muscle is a key factor that limits motor control. While multiple muscles in a limb are usually affected in the Upper Motor Neuron Syndrome, there is usually an imbalance of muscle activity (muscle tone), such that there is a stronger pull on one side of a joint, such as into elbow flexion. Decreasing the degree of this imbalance is a common focus of muscle strengthening programs. Impaired motor control also typically features a loss of stabilisation of an affected limb or the head from the trunk, so a thorough assessment requires this to be analysed as well, and exercise to improve proximal stability may be indicated.

Secondary effects are likely to impact on assessment of impaired muscles. If muscle tone is assessed with passive muscle lengthening, increased muscle stiffness may affect the feeling of resistance to passive stretch, in addition to neurological resistance to stretch. Other secondary changes such as loss of muscle fibres following acquired muscle weakness are likely to compound the weakness arising from the upper motor neuron lesion. In severely affected muscles, there may be marked secondary changes, such as muscle contracture, particularly if management has been delayed or absent.

When initially identified, camptocormia was classified as a psychogenic disease. Although the condition is sometimes a psychogenic manifestation, camptocormia typically originates from either muscular or neurological diseases. However, due to the wide variety of pathologies resulting in camptocormia, there is no singular cause that is most influential for the condition.

Neurological disorders can be categorized according to the primary location affected, the primary type of dysfunction involved, or the primary type of cause. The broadest division is between central nervous system disorders and peripheral nervous system disorders. The Merck Manual lists brain, spinal cord and nerve disorders in the following overlapping categories:

- Brain:

- Brain damage according to cerebral lobe "(see also 'lower' brain areas such as basal ganglia, cerebellum, brainstem)":

- Frontal lobe damage

- Parietal lobe damage

- Temporal lobe damage

- Occipital lobe damage

- Brain dysfunction according to type:

- Aphasia (language)

- Dysgraphia (writing)

- Dysarthria (speech)

- Apraxia (patterns or sequences of movements)

- Agnosia (identifying things or people)

- Amnesia (memory)

- Spinal cord disorders (see spinal pathology, injury, inflammation)

- Peripheral neuropathy and other Peripheral nervous system disorders

- Cranial nerve disorder such as Trigeminal neuralgia

- Autonomic nervous system disorders such as dysautonomia, Multiple System Atrophy

- Seizure disorders such as epilepsy

- Movement disorders of the central and peripheral nervous system such as Parkinson's disease, Essential tremor, Amyotrophic lateral sclerosis, Tourette's Syndrome, Multiple Sclerosis and various types of Peripheral Neuropathy

- Sleep disorders such as Narcolepsy

- Migraines and other types of Headache such as Cluster Headache and Tension Headache

- Lower back and neck pain (see Back pain)

- Central neuropathy (see Neuropathic pain)

- Neuropsychiatric illnesses (diseases and/or disorders with psychiatric features associated with known nervous system injury, underdevelopment, biochemical, anatomical, or electrical malfunction, and/or disease pathology e.g. Attention deficit hyperactivity disorder, Autism, Tourette's syndrome and some cases of obsessive compulsive disorder as well as the neurobehavioral associated symptoms of degeneratives of the nervous system such as Parkinson's disease, essential tremor, Huntington's disease, Alzheimer's disease, multiple sclerosis and organic psychosis.)

Many of the diseases and disorders listed above have neurosurgical treatments available (e.g. Tourette's Syndrome, Parkinson's disease, Essential tremor and Obsessive compulsive disorder).

- Delirium and dementia such as Alzheimer's disease

- Dizziness and vertigo

- Stupor and coma

- Head injury

- Stroke (CVA, cerebrovascular attack)

- Tumors of the nervous system (e.g. cancer)

- Multiple sclerosis and other demyelinating diseases

- Infections of the brain or spinal cord (including meningitis)

- Prion diseases (a type of infectious agent)

- Complex regional pain syndrome (a chronic pain condition)

Neurological disorders in non-human animals are treated by veterinarians.

Irritable Bowel Syndrome (IBS),

Fibromyalgia (FMS),

Chronic Fatigue Syndrome (CFS),

Chronic Pelvic Pain (CPP),

Interstitial Cystitis (IC),

Temporomandibular Joint Pain (TMJ), Functional Neurological Symptom Disorder (FNsD),

Non-Cardiac Chest Pain (NCCP),

Post-Traumatic Stress Disorder (PTSD),

Dysuria (Pain On Urination),

and Multiple Chemical Sensitivity

Patients with spinal accessory nerve palsy often exhibit signs of lower motor neuron disease such as diminished muscle mass, fasciculations, and partial paralysis of the sternocleidomastoid and trapezius muscles. Interruption of the nerve supply to the sternocleidomastoid muscle results in an asymmetric neckline, while weakness of the trapezius muscle can produce a drooping shoulder, winged scapula, and a weakness of forward elevation of the shoulder.

Whether a given medical condition is termed a "functional disorder" depends in part on the state of knowledge. Some diseases, including epilepsy, schizophrenia, and migraine headaches were once considered functional disorders, but are no longer generally classified that way.

Juvenile primary lateral sclerosis (JPLS) ", also known as primary lateral sclerois (PLSJ)," is a rare genetic disorder, with a small number of reported cases, characterized by progressive weakness and stiffness of muscles in the arms, legs, and face. The disorder damages motor neurons, which are specialized nerve cells in the brain and spinal cord that control muscle movement.

Many patients report that temperature may affect the severity of symptoms, especially cold as being an aggravating factor. However, there is some scientific debate on this subject, and some even report that cold may alleviate symptoms.

Hypotonic patients may display a variety of objective manifestations that indicate decreased muscle tone. Motor skills delay is often observed, along with hypermobile or hyperflexible joints, drooling and speech difficulties, poor reflexes, decreased strength, decreased activity tolerance, rounded shoulder posture, with leaning onto supports, and poor attention. The extent and occurrence of specific objective manifestations depends upon the age of the patient, the severity of the hypotonia, the specific muscles affected, and sometimes the underlying cause. For instance, some people with hypotonia may experience constipation, while others have no bowel problems.

The prolonged muscle contractions, which occur most commonly in the leg muscles in recessive mutations, and more commonly in the hands, face, and eyelids in dominant mutations, are often enhanced by inactivity, and in some forms are relieved by repetitive movement known as "the warm-up effect". This effect often diminishes quickly with rest. Some individuals with myotonia congenita are prone to falling as a result of hasty movements or an inability to stabilize themselves after a loss of balance. During a fall, a person with myotonia congenita may experience partial or complete rigid paralysis that will quickly resolve once the event is over. However, a fall into cold water may render the person unable to move for the duration of submergence. As with myotonic goats, children are more prone to falling than adults, due to their impulsivity.

The two major types of myotonia congenita are distinguished by the severity of their symptoms and their patterns of inheritance. Becker disease usually appears later in childhood than Thomsen disease, and causes more severe myotonia, muscle stiffness and transient weakness. Although myotonia in itself is not normally associated with pain, cramps or myalgia may develop. People with Becker disease often experience temporary attacks of muscle weakness, particularly in the arms and hands, brought on by movement after periods of rest. They may also develop mild, permanent muscle weakness over time. This muscle weakness is not observed in people with Thomsen disease. However, in recent times, as more of the individual mutations that cause myotonia congenita are identified, these limited disease classifications are becoming less widely used.

Early symptoms in a child may include:

- Difficulty swallowing

- Gagging

- Stiff movements that improve when they are repeated

- Frequent falling

- Difficulties opening eyelids after strenuous contraction or crying (von Graefe's sign)

Possible complications may include:

- Aspiration pneumonia (caused by swallowing difficulties)

- Frequent choking or gagging in infants (also caused by swallowing difficulties)

- Abdominal muscle weakness

- Chronic joint problems

- Injury due to falls