The main symptom of benign fasciculation syndrome is focal or widespread involuntary muscle activity (twitching), which can occur at random or specific times (or places). Presenting symptoms of benign fasciculation syndrome may include:

- Fasciculations (primary symptom)

- Blepharospasms (eye spasms)

- Generalized fatigue

- Muscle pain

- Anxiety (which can also be a cause)

- Exercise intolerance

- Globus sensation

- Paraesthesias

- Muscle cramping or spasms

Other symptoms include:

- Hyperreflexia

- Muscle stiffness

- Tremors

- Itching

- Myoclonic jerks

BFS symptoms are typically present when the muscle is at rest and are not accompanied by severe muscle weakness. In some BFS cases, fasciculations can jump from one part of the body to another. For example, it could start in a leg muscle, then in a few seconds jump to the forehead, then the abdomen, etc. Because fasciculations can occur on the head, this strongly suggests the brain as the generator due to its exclusive non-dependence on the spinal cord. (Together, the brain and spinal cord comprise the central nervous system.)

Anxiety is often caused as a result of BFS, and a lot of sufferers have hypochondria as BFS mimics symptoms of much more serious diseases such as amyotrophic lateral sclerosis (ALS).

Symptoms are very similar to those found in benign fasciculation syndrome and include:

- Fasciculations (Primary Symptom)

- Muscle cramping (Primary Symptom)

- Muscle pain

- Muscle Stiffness

- Generalized fatigue

- Anxiety

- Exercise intolerance

- Globus sensations

- Paraesthesias.

- Hyperreflexia

Cramp fasciculation syndrome (CFS) is a rare peripheral nerve hyperexcitability disorder. It is more severe than the related (and common) disorder known as benign fasciculation syndrome; it causes fasciculations, cramps, pain, fatigue, and muscle stiffness similar to those seen in neuromyotonia (another related condition). Patients with CFS, like those with neuromyotonia, may also experience paresthesias.

Most cases of cramp fasciculation syndrome are idiopathic.

Cramp fasciculation syndrome is diagnosed by clinical examination and electromyography (EMG). Fasciculation is the only abnormality (if any) seen with EMG.

Cramp fasciculation syndrome is a chronic condition. Treatment options include anti-seizure medications such as carbamazepine, immunosuppressive drugs and plasmapheresis.

Benign fasciculation syndrome (BFS) is a neurological disorder characterized by fasciculation (twitching) of various voluntary muscles in the body. The twitching can occur in any voluntary muscle group but is most common in the eyelids, arms, legs, and feet. Even the tongue may be affected. The twitching may be occasional or may go on nearly continuously. Usually intentional movement of the involved muscle causes the fasciculations to cease immediately, but they may return once the muscle is at rest again.

NMT is a diverse disorder. As a result of muscular hyperactivity, patients may present with muscle cramps, stiffness, myotonia-like symptoms (slow relaxation), associated walking difficulties, hyperhidrosis (excessive sweating), myokymia (quivering of a muscle), fasciculations (muscle twitching), fatigue, exercise intolerance, myoclonic jerks and other related symptoms. The symptoms (especially the stiffness and fasciculations) are most prominent in the calves, legs, trunk, and sometimes the face and neck, but can also affect other body parts. NMT symptoms may fluctuate in severity and frequency. Symptoms range from mere inconvenience to debilitating. At least a third of people also experience sensory symptoms.

There are three main types of NMT:

- Chronic

- Monophasic (symptoms that resolve within several years of onset; postinfection, postallergic)

- Relapsing Remitting

The most effective way to detect fasciculations may be surface electromyography (EMG). Surface EMG is more sensitive than needle electromyography and clinical observation in the detection of fasciculation in people with amyotrophic lateral sclerosis.

A fasciculation , or muscle twitch, is a small, local, involuntary muscle contraction and relaxation which may be visible under the skin. Deeper areas can be detected by electromyography (EMG) testing, though they can happen in any skeletal muscle in the body. Fasciculations arise as a result of "spontaneous depolarization" of a lower motor neuron leading to the synchronous contraction of all the skeletal muscle fibers within a single motor unit. An example of normal spontaneous depolarization is the constant contractions of cardiac muscle, causing the heart to beat. Usually, intentional movement of the involved muscle causes fasciculations to cease immediately, but they may return once the muscle is at rest again.

Fasciculations have a variety of causes, the majority of which are benign, but can also be due to disease of the motor neurons. They are encountered by virtually all healthy people, though for most, it is quite infrequent. In some cases, the presence of fasciculations can be annoying and interfere with quality of life. If a neurological examination is otherwise normal and EMG testing does not indicate any additional pathology, a diagnosis of benign fasciculation syndrome is usually made.

Symptoms vary according to the kind of dystonia involved. In most cases, dystonia tends to lead to abnormal posturing, in particular on movement. Many sufferers have continuous pain, cramping, and relentless muscle spasms due to involuntary muscle movements. Other motor symptoms are possible including lip smacking.

Early symptoms may include loss of precision muscle coordination (sometimes first manifested in declining penmanship, frequent small injuries to the hands, and dropped items), cramping pain with sustained use, and trembling. Significant muscle pain and cramping may result from very minor exertions like holding a book and turning pages. It may become difficult to find a comfortable position for arms and legs with even the minor exertions associated with holding arms crossed causing significant pain similar to restless leg syndrome. Affected persons may notice trembling in the diaphragm while breathing, or the need to place hands in pockets, under legs while sitting or under pillows while sleeping to keep them still and to reduce pain. Trembling in the jaw may be felt and heard while lying down, and the constant movement to avoid pain may result in the grinding and wearing down of teeth, or symptoms similar to temporomandibular joint disorder. The voice may crack frequently or become harsh, triggering frequent throat clearing. Swallowing can become difficult and accompanied by painful cramping.

Electrical sensors (EMG) inserted into affected muscle groups, while painful, can provide a definitive diagnosis by showing pulsating nerve signals being transmitted to the muscles even when they are at rest. The brain appears to signal portions of fibers within the affected muscle groups at a firing speed of about 10 Hz causing them to pulsate, tremble and contort. When called upon to perform an intentional activity, the muscles fatigue very quickly and some portions of the muscle groups do not respond (causing weakness) while other portions over-respond or become rigid (causing micro-tears under load). The symptoms worsen significantly with use, especially in the case of focal dystonia, and a "mirror effect" is often observed in other body parts: Use of the right hand may cause pain and cramping in that hand as well as in the other hand and legs that were not being used. Stress, anxiety, lack of sleep, sustained use and cold temperatures can worsen symptoms.

Direct symptoms may be accompanied by secondary effects of the continuous muscle and brain activity, including disturbed sleep patterns, exhaustion, mood swings, mental stress, difficulty concentrating, blurred vision, digestive problems, and short temper. People with dystonia may also become depressed and find great difficulty adapting their activities and livelihood to a progressing disability. Side-effects from treatment and medications can also present challenges in normal activities.

In some cases, symptoms may progress and then plateau for years, or stop progressing entirely. The progression may be delayed by treatment or adaptive lifestyle changes, while forced continued use may make symptoms progress more rapidly. In others, the symptoms may progress to total disability, making some of the more risky forms of treatment worth considering. In some cases with patients who already have dystonia, a subsequent tramatic injury or the effects of general anethesia during an unrelated surgery can cause the symptoms to progress rapidly.

An accurate diagnosis may be difficult because of the way the disorder manifests itself. Sufferers may be diagnosed as having similar and perhaps related disorders including Parkinson's disease, essential tremor, carpal tunnel syndrome, TMD, Tourette's syndrome, conversion disorder or other neuromuscular movement disorders. It has been found that the prevalence of dystonia is high in individuals with Huntington's disease, where the most common clinical presentations are internal shoulder rotation, sustained fist clenching, knee flexion, and foot inversion. Risk factors for increased dystonia in patients with Huntington's disease include long disease duration and use of antidopaminergic medication.

Although the cause of writer's cramp is not well known, it was historically believed to be the result of excessive fine motor activity, possibly complicated by a tense or otherwise inappropriate writing technique. More recently, Karin Rosenkranz et al. have suggested that this is not necessarily the case. Musician's cramp (a similar focal dystonia which affects some 1% of instrumentalists) has historically been grouped together with writer's cramp because of this and their common task-specificity. Rosenkranz et al. have more recently identified significant differences between the two populations, however. No matter exactly how it arises, researchers generally agree that these types of focal dystonia are the result of a basal ganglia and/or sensorimotor cortex malfunction in the brain.

Early symptoms may include loss of precision muscle coordination (sometimes first manifested in declining penmanship, frequent small injuries to the hands, dropped items and a noticeable increase in dropped or chipped dishes), cramping pain with sustained use and trembling. Significant muscle pain and cramping may result from very minor exertions like holding a book and turning pages. It may become difficult to find a comfortable position for arms and legs with even the minor exertions associated with holding arms crossed causing significant pain similar to restless leg syndrome. Affected persons may notice trembling in the diaphragm while breathing, or the need to place hands in pockets, under legs while sitting or under pillows while sleeping to keep them still and to reduce pain. Trembling in the jaw may be felt and heard while lying down, and the constant movement to avoid pain may result in the grinding and wearing down of teeth, or symptoms similar to TMD. The voice may crack frequently or become harsh, triggering frequent throat clearing. Swallowing can become difficult and accompanied by painful cramping. Patients may also present with varying degree of disability and symptoms, such as experiencing more difficulty writing down-stroke as compared to writing upstroke.

Electrical sensors (EMG) inserted into affected muscle groups, while painful, can provide a definitive diagnosis by showing pulsating nerve signals being transmitted to the muscles even when they are at rest. The brain appears to signal portions of fibers within the affected muscle groups at a firing speed of about 10 Hz causing them to pulsate, tremble and contort. When called upon to perform an intentional activity, the muscles fatigue very quickly and some portions of the muscle groups do not respond (causing weakness) while other portions over-respond or become rigid (causing micro-tears under load). The symptoms worsen significantly with use, especially in the case of focal dystonia, and a "mirror effect" is often observed in other body parts: use of the right hand may cause pain and cramping in that hand as well as in the other hand and legs that were not being used. Stress, anxiety, lack of sleep, sustained use and cold temperatures can worsen symptoms.

Direct symptoms may be accompanied by secondary effects of the continuous muscle and brain activity, including disturbed sleep patterns, exhaustion, mood swings, mental stress, difficulty concentrating, blurred vision, digestive problems and short temper. People with dystonia may also become depressed and find great difficulty adapting their activities and livelihood to a progressing disability. Side effects from treatment and medications can also present challenges in normal activities.

In some cases, symptoms may progress and then plateau for years, or stop progressing entirely. The progression may be delayed by treatment or adaptive lifestyle changes, while forced continued use may make symptoms progress more rapidly. In others, the symptoms may progress to total disability, making some of the more risky forms of treatment worth considering in the future.

There are several types of torsion dystonia that affect different areas of the body. However, it is unknown if the gene that causes Early Onset Torsion Dystonia is responsible for the other dystonias as well.

- Cervical dystonia (spasmodic torticollis): A type of dystonia that affects the head, neck and spine. It can create problems by the characteristic turning of the head and neck from side to side.

- Blepharospasm: This type of dystonia causes involuntary contraction of the eyelids. The main concern for this dystonia is that it can cause the eyelids to close involuntarily and for indefinite periods of time.

- Oromandibular dystonia: A dystonia of the jaw, lips, and/or the tongue. It can make eating and swallowing very complicated due to the jaw being held open or shut for periods of time.

- Spasmodic dysphonia: A dystonia of the vocal cords. The complications surrounding this form of dystonia are speech related and can cause symptoms such as speech that wavers, speech that sounds like a whisper, or speech that is hesitant.

- Writer's cramp (occupational dystonia): A dystonia that affects the muscles of the hand and forearm. It is triggered by attempting to write or execute other fine-motor hand functions.

- Orofacial-Buccal dystonia (Meige's or Brueghal's Syndrome): A combination of blepharospasm and oromandibular dystonia.

- Early-onset torsion dystonia: The most severe type of dystonia, it begins in an arm or leg and progresses to the rest of the body until the person — in most cases, a child — is confined to a wheel chair.

Segmental dystonias affect two adjoining parts of the body:

- Hemidystonia affects an arm and foot on one side of the body.

- Multifocal dystonia affects many different parts of the body.

- Generalized dystonia affects most of the body, frequently involving the legs and back.

Writer's cramp, also called mogigraphia and scrivener's palsy, is a disorder caused by cramps or spasms of certain muscles of the hand and/or forearm, and presents itself while performing fine motor tasks, such as writing or playing an instrument. Writer's cramp is a task-specific focal dystonia of the hand. 'Focal' refers to the symptoms being limited to one location (the hand in this case), and 'task-specific' means that symptoms first occur only when the individual engages in a particular activity. Writer's cramp first affects an individual by interfering with their ability to write, especially for prolonged periods of time.

Torsion dystonia, also known as dystonia musculorum deformans, is a disease characterized by painful muscle contractions resulting in uncontrollable distortions. This specific type of dystonia is frequently found in children, with symptoms starting around the ages of 11 or 12. It commonly begins with contractions in one general area such as an arm or a leg that continue to progress throughout the rest of the body. It takes roughly 5 years for the symptoms to completely progress to a debilitating state.

Proctalgia fugax (a variant of levator ani syndrome) is a severe, episodic pain in the regions of the rectum and anus. It can be caused by cramp of the levator ani muscle, particularly in the pubococcygeal part.

It most often occurs in the middle of the night and lasts from seconds to minutes, an indicator for the differential diagnosis of levator ani syndrome, which presents as pain and aching lasting twenty minutes or longer. In a study published in 2007 involving 1809 patients, the attacks occurred in the daytime (33 per cent) as well as at night (33 per cent) and the average number of attacks was 13. Onset can be in childhood; however, in multiple studies the average age of onset was 45. Many studies showed that women are affected more commonly than men. This can be at least partly explained by men's reluctance to seek medical advice concerning such a delicate case as rectal pain.

During an episode, the patient feels spasm-like, sometimes excruciating, pain in the anus, often misinterpreted as a need to defecate. The pain must arise de novo, that is in absence of clear cause. As such, pain associated with penetrative anal intercourse, trauma or rectal foreign body insertion preclude a diagnosis of proctalgia fugax. Simultaneous stimulation of the local autonomic system can cause erection in males. In some people, twinges sometimes occur shortly after orgasm. Because of the high incidence of internal anal sphincter thickening with the disorder, it is thought to be a disorder of the internal anal sphincter or that it is a neuralgia of pudendal nerves. It is recurrent and there is also no known cure. However, some studies show effective use of botulinum toxin, pudendal nerve block, and calcium channel blockers. It is not known to be linked to any disease process and data on the number of people afflicted vary, but prevalence may be as high as 8–18%. It is thought that only 17–20% of sufferers consult a physician, so obtaining accurate data on occurrence presents a challenge.

The pain episode subsides by itself as the spasm disappears on its own, but may reoccur.

Myoclonus dystonia includes the rapid contractions of myoclonus alongside the abnormal postures classified under dystonia, as well as neurological and psychiatric issues. This disease typically begins during childhood with symptoms of myoclonus and slight dystonia, most commonly cervical dystonia or writer’s cramp. Dystonia symptoms tend to not get exaggerated over the course of the disease and is rarely the only associated symptom, while the myoclonus symptoms can become more severe. Psychiatric issues are clinically diagnosed with the aforementioned symptoms and include depression, anxiety, personality disorders and addiction. Obsessive-compulsive disorder is associated with myoclonus dystonia as both have been found to have a commonality on chromosome 7 in various studies.

Neurological symptoms are relatively common in those with myoclonus dystonia. Any neurological abnormalities won’t normally be present in those affected at a young age. Neurological testing has been performed to determine the origins of these symptoms and multiple parts of the brain have been pinpointed including the brainstem, neocortex, pallidum, and thalamus. These cause various effects in those diagnosed with myoclonus dystonia including changes in posture and tremors, and very rarely dementia and ataxia.

Dystonia is a response to simultaneous contraction of agonist and antagonist muscles seen as twisting and contorting that affect posture and stance. Other symptoms can include tremors and muscle spasms due to various interactions of muscle, contractions and movement. Dystonia can be either primary or secondary with the latter being more common. Primary dystonia or “pure” dystonia is only physiological in origin. Secondary dystonia has multiple origins that are physiological, pathological or neurological.

Prognosis for PBP patients is poor. Progressive bulbar palsy symptoms can include progressive difficulty with chewing, talking, and swallowing. Patients can also exhibit reduced gag reflexes, weak palatal movements, fasciculations, and weak movement of the facial muscles and tongue. In advanced cases of PBP, the patient may be unable to protrude their tongue or manipulate food in their mouth.

Patients with early cases of PBP have difficulty with pronunciations, particularly lateral consonants (linguals) and velars, and may show problems with drooling saliva. If the corticobulbar tract is affected a pseudobulbar affect with emotional changes may occur. Because PBP patients have such difficulty swallowing, food and saliva can be inhaled into the lungs. This can cause gagging and choking, and it increases the risk of pneumonia. Death, which is often from pneumonia, usually occurs 1 to 3 years after the start of the disorder.

In mild cases, ET can manifest as the inability to stop the tongue or hands from shaking, the ability to sing only in vibrato, and difficulty doing small precise tasks such as threading a needle. Even simple tasks like cutting in a straight line or using a ruler can range from difficult to impossible, depending on the severity of the condition. In disabling cases, ET can interfere with a person's activities of daily living, including feeding, dressing, and taking care of personal hygiene. Essential tremor generally presents as a rhythmic tremor (4–12 Hz) that occurs only when the affected muscle is exerting effort. Any sort of physical or mental stress will tend to make the tremor worse.

The tremor may also occur in the head (neck), jaw and voice as well as other body regions, with the general pattern being that the tremor begins in the arms and then spreads to these other regions in some people. Women are more likely to develop the head tremor than are men. Other types of tremor may also occur, including postural tremor of the outstretched arms, intention tremor of the arms and rest tremor in the arms. Some people may have unsteadiness and problems with gait and balance.

ET-related tremors do not occur during sleep, but people with ET sometimes complain of an especially coarse tremor upon awakening that becomes noticeably less coarse within the first few minutes of wakefulness. Tremor and disease activity/intensity can worsen in response to fatigue, strong emotions, low blood sugar, cold and heat, caffeine, lithium salts, some antidepressants, and other factors. It is typical for the tremor to worsen in "performance" situations, such as when writing a check for payment at a store or giving a presentation.

Parkinson's disease and Parkinsonism can also occur simultaneously with ET. In those cases the degree of tremor, rigidity, and functional disability does not differ from those people with idiopathic Parkinson's disease. Hand tremor predominates (as it does in Parkinson’s disease), and occurs in nearly all cases, followed by head tremor, voice tremor, neck, face, leg, tongue and trunk tremor. Most other tremors occur in association with hand tremor. Walking difficulties in essential tremor are common. About half of patients have associated dystonia, including cervical dystonia, writer's cramp, spasmodic dysphonia, and cranial dystonia, and 20% of the patients had associated parkinsonism. Olfactory dysfunction (loss of sense of smell) is common in Parkinson’s disease, and has also been reported to occur in patients with essential tremor. A number of patients with essential tremor also exhibit many of the same neuropsychiatric disturbances seen in idiopathic Parkinson's disease.

Essential tremor with tremor onset after the age of 65 is associated with Mild cognitive impairement and dementia.

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.

Progressive bulbar palsy (PBP) is a medical condition. It belongs to a group of disorders known as motor neuron diseases. PBP is a disease that attacks the nerves supplying the bulbar muscles. These disorders are characterized by the degeneration of motor neurons in the cerebral cortex, spinal cord, brain stem, and pyramidal tracts. This specifically involves the glossopharyngeal nerve (IX), vagus nerve (X), and hypoglossal nerve (XII).

This disorder should not be confused with pseudobulbar palsy or progressive spinal muscular atrophy. The term Infantile progressive bulbar palsy is used to describe progressive bulbar palsy in children. Some neurologists consider this disorder to be a subset of amyotrophic lateral sclerosis (ALS), but others disagree with that classification.

This type of tremor is often referred to as "kinetic tremor".

Essential tremor has been known as "benign essential tremor", but the adjective "benign" has been removed in recognition of the sometimes disabling nature of the disorder.

Myoclonus is defined as a sequence of repeated, often nonrhythmic, brief, shock-like jerks due to sudden involuntary contraction or relaxation of one or more muscles. These movements may be asynchronous, in which several muscles contract variably in time, synchronous, in which muscles contract simultaneously, or spreading, in which several muscles contract sequentially. It is characterized by a sudden, unidirectional movement due to muscle contraction, followed by a relaxation period in which the muscle is no longer contracted. However, when this relaxation phase is decreased, as when muscle contractions become faster, a myoclonic tremor results. Myoclonus can often be associated with seizures, delirium, dementia, and other signs of neurological disease and gray matter damage.

Hemifacial spasm (HFS) is characterized by involuntary contraction of facial muscles, typically occurring only on one side of the face. Like blepharospasm, the frequency of contractions in hemifacial spasm may range from intermittent to frequent and constant. The unilateral blepharospasm of HFS may interfere with routine tasks such as driving. In addition to medication, patients may respond well to treatment with Botox. HFS may be due to vascular compression of the nerves going to the muscles of the face. For these patients, surgical decompression may be a viable option for the improvement of symptoms.