Hypertonia is caused by upper motor neuron lesions which may result from injury, disease, or conditions that involve damage to the central nervous system. The lack of or decrease in upper motor neuron function leads to loss of inhibition with resultant hyperactivity of lower motor neurons. Different patterns of muscle weakness or hyperactivity can occur based on the location of the lesion, causing a multitude of neurological symptoms, including spasticity, rigidity, or dystonia.

Spastic hypertonia involves uncontrollable muscle spasms, stiffening or straightening out of muscles, shock-like contractions of all or part of a group of muscles, and abnormal muscle tone. It is seen in disorders such as cerebral palsy, stroke, and spinal cord injury. Rigidity is a severe state of hypertonia where muscle resistance occurs throughout the entire range of motion of the affected joint independent of velocity. It is frequently associated with lesions of the basal ganglia. Individuals with rigidity present with stiffness, decreased range of motion and loss of motor control. Dystonic hypertonia refers to muscle resistance to passive stretching (in which a therapist gently stretches the inactive contracted muscle to a comfortable length at very low speeds of movement) and a tendency of a limb to return to a fixed involuntary (and sometimes abnormal) posture following movement.

Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions. Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition. These consequences result in abnormally increased muscle tone of symptomatic muscles. Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug and/or physical therapy.

Symptoms associated with central nervous systems disorders are classified into positive and negative categories. Positive symptoms include those that increase muscle activity through hyper-excitability of the stretch reflex (i.e., rigidity and spasticity) where negative symptoms include those of insufficient muscle activity (i.e. weakness) and reduced motor function. Often the two classifications are thought to be separate entities of a disorder; however, some authors propose that they may be closely related.

Paratonia is the inability to relax muscles during muscle tone assessment. There are two types of paratonia: oppositional and facilitatory. Oppositional paratonia ("gegenhalten") occurs when subjects involuntary resist to passive movements, while facilitatory paratonia ("mitgehen") occurs when subjects involuntary assist passive movements.

Both types of paratonia have been associated with cognitive impairment or mental disorders, particularly in relation to frontal lobe dysfunction. Paratonia is frequently encountered in clinical practice.

Paratonia can be assessed with rating scales during clinical examination. Paratonia scale is a semi-quantitative score to rate the amount of oppositional and facilitatory paratonia separately. Kral modified procedure is a more objective semi-quantitative rating of upper limb facilitatory paratonia easily applicable while patients are seated. The Paratonia Assessment Instrument (PAI) was also used in a physiotherapic setting for the assessment of oppositional paratonia.

In 2017 facilitatory and oppositional paratonia have been assessed with surface electromyography, allowing a quantitative measure and better characterization of paratonia. Recording paratonia with electromyography on elbow flexor and extensors during repetitive continuous or discontinuous elbow movements may help distinguish paratonia from other forms of altered muscle tone. Both facilitatory and oppositional paratonia increase during continuous flexion and extension movements, moreover, oppositional paratonia increases with movement velocity. Spasticity also is velocity-dependent, but, differently from oppositional paratonia, if repeatedly elicited decreases instead of increasing. Conversely, parkinsonian rigidity is independent from movement velocity and probably also from movement repetition.

Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with an antipsychotic drug such as haloperidol (Haldol) or amoxapine (Asendin). The symptoms include tremors and writhing movements of the body and limbs, and abnormal movements in the face, mouth, and tongue including involuntary lip smacking, repetitive pouting of the lips, and tongue protrusions.

Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of Herpes simplex virus type 1.

Opisthotonus or opisthotonos, from Greek roots, ὄπισθεν, "opisthen" meaning "behind" and τόνος "tonos" meaning "tension", is a state of severe hyperextension and spasticity in which an individual's head, neck and spinal column enter into a complete "bridging" or "arching" position. This abnormal posturing is an extrapyramidal effect and is caused by spasm of the axial muscles along the spinal column.

It is seen in some cases of severe cerebral palsy and traumatic brain injury or as a result of the severe muscular spasms associated with tetanus. It can be a feature of severe acute hydrocephalus.

Opisthotonus can be produced experimentally in animals by transection of the midbrain (between the superior colliculus and the inferior colliculus), which results in severing all the corticoreticular fibers. Hyperextension occurs due to facilitation of the anterior reticulospinal tract caused by the inactivation of inhibitory corticoreticular fibers, which normally act upon the pons reticular formation. It has been shown to occur naturally only in birds and placental mammals.

Opisthotonus is more pronounced in infants. Opisthotonus in the neonate may be a symptom of meningitis, tetanus, severe kernicterus, or the rare Maple syrup urine disease. This marked extensor tone can cause infants to "rear backwards" and stiffen out as the mother or nurse attempts to hold or feed them. Opisthotonus can be induced by any attempt at movement such as smiling, feeding, vocalization, or by seizure activity. A similar tonic posturing may be seen in Sandifer syndrome. Individuals with opisthotonus are quite challenging to position, especially in wheelchairs and car seats.

Opisthotonus can sometimes be seen in lithium intoxication. It is a rare extrapyramidal side effect of phenothiazines, haloperidol, and metoclopramide.

Opisthotonus with the presence of the risus sardonicus is also a symptom of strychnine poisoning.

Opisthotonus is also described as a potential CNS symptom of heat stroke along with bizarre behavior, hallucinations, decerebrate rigidity, oculogyric crisis and cerebellar dysfunction.

Opisthotonus is seen with drowning victims – called the "Opisthotonic Death Pose". This pose is also common in complete dinosaur skeletal fossils and it has been suggested that this is due to the animal drowning or being immersed in water soon after death.

Two other types, primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are not movement disorders.

Spastic thrusting of hip area can occur in Sodemytopic Parkinson's.

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.

This gait pattern is reminiscent of a marionette. Hypertonia in the legs, hips and pelvis means these areas become flexed to various degrees, giving the appearance of crouching, while tight adductors produce extreme adduction, presented by knees and thighs hitting, or sometimes even crossing, in a scissors-like movement while the opposing muscles, the abductors, become comparatively weak from lack of use. Most common in patients with spastic cerebral palsy, the individual is often also forced to walk on tiptoe unless the plantarflexor muscles are released by an orthaepedic surgical procedure.

These features are most typical with the scissors gait and usually result in some form and to some degree regardless of the mildness or severity of the spastic CP condition:

- rigidity and excessive adduction of the leg in swing

- plantar flexion of the ankle

- flexion at the knee

- adduction and internal rotation at the hip

- progressive contractures of all spastic muscles

- complicated assisting movements of the upper limbs when walking.

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.

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

Although essential tremor is often mild, people with severe tremor have difficulty performing many of their routine activities of daily living. ET is generally progressive in most cases (sometimes rapidly, sometimes very slowly), and can be disabling in severe cases.

Patients with Parkinson's disease exhibit gait characteristics that are markedly different from normal gait. While the list of abnormal gait characteristics given below is the most discussed, it is certainly not exhaustive.

Though it is often most associated with Parkinson's disease, hypokinesia can be present in a wide variety of other conditions.

Parkinsonian gait (or festinating gait, from Latin "festinare" [to hurry]) is the type of gait exhibited by patients suffering from Parkinson's disease (PD). This disorder is caused by a deficiency of dopamine in the basal ganglia circuit leading to motor deficits. Gait is one of the most affected motor characteristics of this disorder although symptoms of Parkinson's disease are varied.

Parkinsonian gait is characterized by small shuffling steps and a general slowness of movement (hypokinesia), or even the total loss of movement (akinesia) in the extreme cases. Patients with PD demonstrate reduced stride length and walking speed during free ambulation while double support duration and cadence rate are increased. The patient has difficulty starting, but also has difficulty stopping after starting. This is due to muscle hypertonicity.

Movement disorders are clinical syndromes with either an excess of movement or a paucity of voluntary and involuntary movements, unrelated to weakness or spasticity. Movement disorders are synonymous with basal ganglia or extrapyramidal diseases. Movement disorders are conventionally divided into two major categories- "hyperkinetic" and "hypokinetic".

Hyperkinetic movement disorders refer to dyskinesia, or excessive, often repetitive, involuntary movements that intrude upon the normal flow of motor activity.

Hypokinetic movement disorders refer to akinesia (lack of movement), hypokinesia (reduced amplitude of movements), bradykinesia (slow movement) and rigidity. In primary movement disorders, the abnormal movement is the primary manifestation of the disorder. In secondary movement disorders, the abnormal movement is a manifestation of another systemic or neurological disorder.

Stress causes alterations of cerebral circulation, increasing blood flow in the supramarginal gyrus and angular gyrus of the parietal lobe, the frontal lobe, and the superior temporal gyrus of the left hemisphere. Also, an increase in cardiac activity and change in the tonus of the heart vessels occurs, which is an elementary indication of stress development. In patients with normal stress, an adaptive fight-or-flight response is usually triggered by sympathetic nervous system activation. Hypokinesia patients experience these typical stress symptoms on a regular basis because of damage to the basal ganglia system. Therefore, when a hypokinesia victim is under stress, he or she does not display a typical fight-or-flight response, placing the patient under greater danger from potentially harmful stimuli. Low-impact exercise, elimination of drug and alcohol use, and regular meditation can help to restore normal stress responses in hypokinesia patients.

Patients with stiff person syndrome (SPS) suffer progressive stiffness in their truncal muscles, which become rigid and stiff because the lumbar and abdominal muscles engage in constant contractions. Initially, stiffness occurs in the thoracolumbar paraspinal and

abdominal muscles. It later affects the proximal leg and abdominal wall muscles. The stiffness leads to a change in posture, and patients develop a rigid gait. Persistent lumbar hyperlordosis often occurs as it progresses. The muscle stiffness initially fluctuates, sometimes for days or weeks, but eventually begins to consistently impair mobility. As the disease progresses, patients sometimes become unable to walk or bend. Chronic pain is common and worsens over time but sometimes acute pain occurs as well. Stress, cold weather, and infections lead to an increase in symptoms, and sleep decreases them.

SPS patients suffer superimposed spasms and extreme sensitivity to touch and sound. These spasms primarily occur in the proximal limb and axial muscles. There are co-contractions of agonist and antagonist muscles. Spasms usually last for minutes and can recur over hours. Attacks of spasms are unpredictable and are often caused by fast movements, emotional distress, or sudden sounds or touches. In rare cases, facial muscles, hands, feet, and the chest can be affected and unusual eye movements and vertigo occur. There are brisk stretch reflexes and clonus occurs in patients. Late in the disease's progression, hypnagogic myoclonus can occur. Tachycardia and hypertension are sometimes also present.

Because of the spasms, patients may become increasingly fearful, require assistance, and lose the ability to work, leading to depression, anxiety, and phobias, including agoraphobia and dromophobia. Most patients are psychologically normal and respond reasonably to their situations.

Paraneoplastic SPS tends to affect the neck and arms more than other variations. It progresses very quickly, is more painful, and is more likely to include distal pain than classic SPS. Patients with paraneoplastic SPS generally lack other autoimmune issues but may have other paraneoplastic conditions.

Stiff-limb syndrome is a variant of SPS. This syndrome develops into full SPS about 25 percent of the time. Stiffness and spasms are usually limited to the legs and hyperlordoisis generally does not occur. The stiffness begins in one limb and remains most prominent there. Sphincter and brainstem issues often occur with stiff-limb syndrome. Progressive encephalomyelitis with rigidity, another variant of the condition, includes symptoms of SPS with brainstem issues and autonomic disturbances. It involves polio-encephalomyelitis in the spine and brainstem. There is cerebellar and brainstem involvement. In some cases, the limbic system is affected, as well. Most patients have upper motoneuron issues and autonomic disturbances. Jerking man syndrome or jerking SPS is another subtype of the condition. It begins like classical SPS and progresses for several years, up to 14 in some cases. It is then distinguished by the development of myoclonus as well as seizures and ataxia in some cases.

Acute dystonia nearly always develops a few weeks after a dopamine blocking agent/medication has begun or a substantial increase in antipsychotic dosage. An acute dystonic reaction consists of sustained, painful muscular spasms, producing twisting of the trunk/body and abnormal posture. The most frequent occurrences of these spasms have been reported in the neck, tongue, and jaw. Oculogyric crisis and opisthotonus are also very common. Acute effects of dopamine antagonists also include Parkinsons-like symptoms, manifested by bradykinesia, pin rolling tremor, and rigidity of the body. These movements may fluctuate over hours and temporarily dissipate in response to reassurance, and the individual episodes may last minutes to hours. Acute reactions are more common in older patients and females. The pathophysiology underlying these reactions is unknown, but the movements usually occur during the period when blood medication level is dropping. The acute syndromes which occur due to prolonged exposure to a dopamine antagonist are collectively termed extrapyramidal symptoms, EPS.

The disease typically starts in one limb, typically one leg. Progressive dystonia results in clubfoot and tiptoe walking. The symptoms can spread to all four limbs around age 18, after which progression slows and eventually symptoms reach a plateau. There can be regression in developmental milestones (both motor and mental skills) and failure to thrive in the absence of treatment.

In addition, SS is typically characterized by signs of parkinsonism that may be relatively subtle. Such signs may include slowness of movement (bradykinesia), tremors, stiffness and resistance to movement (rigidity), balance difficulties, and postural instability. Approximately 25 percent also have abnormally exaggerated reflex responses (hyperreflexia), particularly in the legs. These symptoms can result in a presentation that is similar in appearance to that of Parkinson's Disease.

Many patients experience improvement with sleep, are relatively free of symptoms in the morning, and develop increasingly severe symptoms as the day progresses (i.e., diurnal fluctuation). Accordingly, this disorder has sometimes been referred to as "progressive hereditary dystonia with diurnal fluctuations." Yet some SS patients do not experience such diurnal fluctuations, causing many researchers to prefer other disease terms.

- Other symptoms - footwear

- excessive wear at toes, but little wear on heels, thus replacement of shoes every college term/semester.

- Other symptoms - handwriting

- near normal handwriting at infants/kindergarten (ages 3–5 school) years.

- poor handwriting at pre-teens (ages 8–11 school) years.

- very poor (worse) handwriting during teen (qv GCSE/A level-public exams) years.

- bad handwriting (worsening) during post-teen (qv university exams) years.

- very bad handwriting (still worsening) during adult (qv post-graduate exams) years.

- worsening pattern of sloppy handwriting best observed by school teachers via termly reports.

- child sufferer displays unhappy childhood facial expressions (depression.?)

Scissor gait is a form of gait abnormality primarily associated with spastic cerebral palsy. That condition and others like it are associated with an upper motor neuron lesion.

The extrapyramidal system regulates posture and skeletal muscle tone. Extrapyramidal symptoms (also called extrapyramidal side effects) get their name because they are symptoms of disorders in this system.

The progression of SPS depends on whether it is a typical or abnormal form of the condition and the presence of comorbidities. Early recognition and neurological treatment can limit its progression. SPS is generally responsive to treatment, but the condition usually progresses and stabilizes periodically. Even with treatment, quality of life generally declines as stiffness precludes many activities. Some patients require mobility aids due to the risk of falls. About 65 percent of SPS patients are unable to function independently. About ten percent of SPS patients require intensive care at some point; sudden death occurs in about the same number of patients. These deaths are usually caused by metabolic acidosis or an autonomic crisis.

The predominant symptom of Pisa syndrome is dystonia. Dystonia is a neurological movement disorder characterized by sustained muscle contraction leading to abnormal posture, twisting, and repetitive movement. In Pisa Syndrome specifically there is commonly a tonic flexion of the trunk of the body to one side, leading to a slight lean (reminiscent of the Leaning Tower of Pisa, hence the name "Pisa syndrome"). This is usually associated with a backward axial rotation of the spine and indifferent to markedly abnormal posture. Patients diagnosed with Pisa Syndrome usually experience either acute dystonia or tardive dystonia, also known as tardive dyskinesia. Differential diagnosis between the two may be hard to accomplish without a complete patient history, since both types of dystonia may occur simultaneously in a patient. These symptoms generally disappear after discontinuation of the antipsychotic drug. The time of onset of symptoms may vary depending on drug being administered and the neurological characteristics of the patient in question.

Extrapyramidal symptoms are most commonly caused by typical antipsychotic drugs that antagonize dopamine D2 receptors. The most common typical antipsychotics associated with EPS are haloperidol and fluphenazine. Atypical antipsychotics have lower D2 receptor affinity or higher serotonin 5-HT2A receptor affinity which lead to lower rates of EPS. However, some research has shown that atypical antipsychotics are just as likely as conventional antipsychotics to cause EPS.

Other anti-dopaminergic drugs, like the antiemetic metoclopramide, can also result in extrapyramidal side effects. Short and long-term use of antidepressants such as selective serotonin reuptake inhibitors (SSRI), serotonin-norepinephrine reuptake inhibitors (SNRI), and norepinephrine-dopamine reuptake inhibitors (NDRI) have also resulted in EPS. Specifically, duloxetine, sertraline, escitalopram, fluoxetine, and bupropion have been linked to the induction of EPS. Other causes of extrapyramidal symptoms can include brain damage and meningitis.