The most effective treatment of astasia seems to be a removal of stress inducing stimuli and allowing the patient to rest and regain strength. Despite the lack of a direct prescribable cure for the effect of astasia on the motor system of the legs, in almost all documented cases physical rehabilitation and relief from mental stressors have led to a full recovery. Although astasia is not expressly associated with any neurological disorders, there is a strong correlation between general mental hysteria and the symptoms of astasia. Therefore, isolation of the patient from the situation causing them hysteria is the most efficient way to rid them of disabling motor symptoms. Another method for treatment that patients who experience astasia is to have therapy for the triceps surae muscle. This therapy can help strengthen these muscles to help maintain an upright posture. It has also been suggested that ankle-foot orthoses be prescribed for these patients. This would help patients with astasia maintain balance by preventing ankle dorsiflexion.

Currently, physical therapy and rehabilitation are widely accepted as the best treatments for the symptoms of astasia. There is, however, evidence to suggest that regulation of a patient's social situation and behavioral influences can influence the effectiveness of rehabilitation. A 1975 study shows that when a patient is given direct encouragement and social distractions their physical recovery proceeds much faster than when only basic instructions are provided to them.

Mobility issues associated with falls and freezing of gait have a devastating impact in the lives of PD patients. Fear of falling in itself can have an incapacitating effect in PD patients and can result in social seclusion leaving patients largely isolated leading to depression. Immobility can also lead to osteoporosis which in-turn facilitates future fracture development. This then becomes a vicious circle with falls leading to immobility and immobility facilitating future falls. Hip fractures from falls are the most common form of fracture among PD patients. Fractures increase treatment costs associated with health care expenditures in PD. Also, when gait is affected it often heralds the onset of Lewy body dementia.

Persons suffering from peripheral neuropathy experience numbness and tingling in their hands and feet. This can cause ambulation impairment, such as trouble climbing stairs or maintaining balance. Gait abnormality is also common in persons with nervous system problems such as cauda equina syndrome, multiple sclerosis, Parkinson's disease, Alzheimer's disease, myasthenia gravis, normal pressure hydrocephalus, and Charcot–Marie–Tooth disease. Research has shown that neurological gait abnormalities are associated with an increased risk of falls in older adults.

Orthopedic corrective treatments may also manifest into gait abnormality, such as lower extremity amputation, post-fracture, and arthroplasty (joint replacement). Difficulty in ambulation that results from chemotherapy is generally temporary in nature, though recovery times of six months to a year are common. Likewise, difficulty in walking due to arthritis or joint pains (antalgic gait) sometimes resolves spontaneously once the pain is gone. Hemiplegic persons have circumduction gait and those with cerebral palsy often have scissoring gait.

Gait abnormality is a deviation from normal walking (gait). Watching a patient walk is the most important part of the neurological examination. Normal gait requires that many systems, including strength, sensation and coordination, function in an integrated fashion. Many common problems in the nervous system and musculoskeletal system will show up in the way a person walks.

Gluteal gait is an abnormal gait caused by neurological problems. If the superior gluteal nerve or obturator nerves are injured, they fail to control the gluteus minimus and medius muscles properly, thus producing an inability to tilt the pelvis upward while swinging the leg forward to walk. To compensate for this loss, the leg swings out laterally so that the foot can move forward, producing a shuffling or waddling gait.

Injury to the superior gluteal nerve results in a characteristic motor loss, resulting in a disabling gluteus medius limp, to compensate for weakened abduction of the thigh by the gluteus medius and minimus, and/or a gluteal gait, a compensatory list of the body to the weakened gluteal side.

As a result of this compensation, the center of gravity is placed over the supporting lower limb. Medial rotation of the thigh is also severely impaired. When a person is asked to stand on one leg, the gluteus medius and minimus normally contract as soon as the contralateral foot leaves the floor, preventing tipping of the pelvis to the unsupported side. When a person with paralysis of the superior gluteal nerve is asked to stand on one leg, the pelvis descends on the unsupported side, indicating that the gluteus medius on the contralateral side is weak or non-functional. This observation is referred to clinically as a positive Trendelenburg's sign.

When the pelvis descends on the unsupported side, the lower limb becomes, in effect, too long and does not clear the ground when the foot is brought forward in the swing phase of walking. To compensate, the individual leans away from the unsupported side, raising the pelvis to allow adequate room for the foot to clear the ground as it swings forward.

Attention strategies:

By consciously paying more attention to walking and rehearsing each step before actually making it, PD patients have shown to improve their gait. Sometimes, a companion walking alongside reminds the patient to concentrate on gait or they create a visual cue to step over by putting a foot in front of the person with PD over which the person must step. This causes the patient to focus their attention on the stepping action, thus making this a voluntary action and hence bypassing the faulty basal ganglia pathway (which is responsible for involuntary actions like walking). Avoidance of dual tasks that require motor attention or cognitive attention has also been shown to normalize gait in the PD patients.

Exercise:

Physical therapy and exercise have been shown to have positive effects on gait parameters in PD patients.

Physiotherapists may help improve gait by creating training programs to lengthen a patient's stride length, broaden the base of support, improve the heel-toe gait pattern, straighten out a patient's posture, and increase arm swing patterns.

Research has shown gait training combining an overhead harness with walking on a treadmill has shown to improve both walking speed and stride length. The harness assists the patient in maintaining an upright posture by eliminating the need to use a mobility aid, a practice which normally promotes a forward flexed posture. It is believed the activation of the central pattern generator leads to the improvement in gait pattern.

Improving trunk flexibility, along with strengthening of the core muscles and lower extremities has been associated with increased balance and an improvement in gait pattern. Aerobic exercises such as tandem bicycling and water aerobics are also crucial in improving strength and overall balance. Due to PD’s progressive nature it is important to sustain an exercise routine to maintain its benefits.

Strategies such as using a vertical walking pole can also help to improve upright postural alignment. The therapist may also use tiles or footprints on the ground to improve foot placement and widen the patient's base of support. Creative visualization of walking with a more normalized gait pattern, and mentally rehearsing the desired movement has also shown to be effective.

The patient should also be challenged by walking on a variety of surfaces such as tile, carpet, grass, or foamed surfaces will also benefit the individual’s progress towards normalizing their gait pattern.

Tandem gait is a gait (method of walking or running) where the toes of the back foot touch the heel of the front foot at each step. Neurologists sometimes ask patients to walk in a straight line using tandem gait as a test to help diagnose ataxia, especially truncal ataxia, because sufferers of these disorders will have an unsteady gait. However, the results are not definitive, because many disorders or problems can cause unsteady gait (such as vision difficulties and problems with the motor neurons or associative cortex). Therefore, inability to walk correctly in tandem gait does not prove the presence of ataxia.

Profoundly affected tandem gait with no other perceptible deficits is a defining feature of posterior vermal split syndrome.

Suspects may also be asked to perform a tandem gait walk during the "walk and turn" part of a field sobriety test.

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.

"For many years, it was thought that postural and balance disorders in cerebellar ataxia were not treatable. However, the results of several recent studies suggest that rehabilitation can relieve postural disorders in patients with cerebellar ataxia...There is now moderate level evidence that rehabilitation is efficient to improve postural capacities of patients with cerebellar ataxia – particularly in patients with degenerative ataxia or multiple sclerosis. Intensive rehabilitation programs with balance and coordination exercises are necessary. Although techniques such as virtual reality, biofeedback, treadmill exercises with supported bodyweight and torso weighting appear to be of value, their specific efficacy has to be further investigated. Drugs have only been studied in degenerative ataxia, and the level of evidence is low."

One approach is that it can be ameliorated to varying degrees by means of Frenkel exercises.

One main objective of the treatment is to re-establish the physiological inhibition exerted by the cerebellar cortex over cerebellar nuclei. Research using Transcranial direct-current stimulation (TCDCS) and Transcranial magnetic stimulation (TMS) shows promising results.

Additionally, mild to moderate cerebellar ataxia may be treatable with buspirone.

It is thought that the buspirone increases the serotonin levels in the cerebellum and so decreases ataxia.

There are many speculations as to what is the main cause of astasis. A combination of weakness of the triceps surae muscle, peripheral neuropathy, and irregular postural movements are the leading theories thus far. Diabetes, spinal root or spinal cord lesions, and traumas or injuries to the motor cortex of the brain can also cause similar symptoms that are seen in patients with astasis. However, none of these have been proven definite. Many scientists also believe that this is a conversion disorder, in which patients exhibit symptoms without any neurological cause.

Medications remain the basis of therapy in many cases. Symptomatic drug therapy is available for several forms of tremor:

- Parkinsonian tremor drug treatment involves L-DOPA and/or dopamine-like drugs such as pergolide, bromocriptine and ropinirole; They can be dangerous, however, as they may cause symptoms such as tardive dyskinesia, akathisia, clonus, and in rare instances tardive (late developing) psychosis. Other drugs used to lessen parkinsonian tremor include amantadine and anticholinergic drugs like benztropine

- Essential tremor may be treated with beta blockers (such as propranolol and nadolol) or primidone, an anticonvulsant

- Cerebellar tremor symptoms may decrease with the application of alcohol (ethanol) or benzodiazepine medications, both of which carry some risk of dependence and/or addiction

- Rubral tremor patients may receive some relief using L-DOPA or anticholinergic drugs. Surgery may be helpful

- Dystonic tremor may respond to diazepam, anticholinergic drugs, and intramuscular injections of botulinum toxin. Botulinum toxin is also prescribed to treat voice and head tremors and several movement disorders

- Primary orthostatic tremor sometimes is treated with a combination of diazepam and primidone. Gabapentin provides relief in some cases

- Enhanced physiological tremor is usually reversible once the cause is corrected. If symptomatic treatment is needed, beta blockers can be used

Bruns apraxia, or frontal ataxia is a gait apraxia found in patients with bilateral frontal lobe disorders. It is characterised by an inability to initiate the process of walking, despite the power and coordination of the legs being normal when tested in the seated or lying position. The gait is broad-based with short steps with a tendency to fall backwards. It was originally described in patients with frontal lobe tumours, but is now more commonly seen in patients with cerebrovascular disease.

It is named after Ludwig Bruns.

Treatment consists of physical rehabilitation programs designed to improve overall function, increase strength and improve balance. The ultimate goal is to increase the patient's degree of independence, thus improving the patient's quality of life. Exercise typically begins with simple movements, gradually transitioning into more complex actions. Various aspects of treatment are assessed based on the individual patient's condition, utilizing many assessment tools:

- Functional Reach Test

- External Perturbation Test – Push, Release

- External Perturbation Test – Pull

- Clinical Sensory Integration Test

- Single Leg Stance Test

- Five Times Sit to Stand Test

Various scales are also utilized

- Brief Ataxia Rating Scale

- Friedreich's Ataxia Impact Scale

- Scale For Assessment and Rating of Ataxia

Eliminating tremor “triggers” such as caffeine and other stimulants from the diet is often recommended.

Essential tremor may benefit from slight doses of ethanol, but the potential negative consequences of regular ethanol intake need to be taken into account. Beta blockers have been used as an alternative to alcohol in sports such as competitive dart playing and carry less potential for addiction.

Physical therapy and occupational therapy may help to reduce tremor and improve coordination and muscle control for some patients. A physical therapist and/or occupational therapist will evaluate the patient for tremor positioning, muscle control, muscle strength, and functional skills. Teaching the patient to brace the affected limb during the tremor or to hold an affected arm close to the body is sometimes useful in gaining motion control. Coordination and balancing exercises may help some patients. Some occupational therapists recommend the use of weights, splints, other adaptive equipment, and special plates and utensils for eating.

Individuals with cerebellar ataxia have full cognitive awareness: it is usually only the physical deterioration that prohibits them from participating in activities of daily living and any other relevant or desired interests. One of the most significant barriers in the lives of these individuals is dysarthria. Due to their cognitive stability, it is important that people who spend time with individuals with this disease are able to communicate as fully as possible with them. This is necessary in order to improve their day-to-day interactions.

Behavioral intervention is successful when it involves engaging knowledge of the interests and general backgrounds of individuals with cerebellar ataxia. Communication maximizing strategies are also useful, such as exaggeration of articulatory gestures, giving full attention to their responses, repeating where necessary, and slowing down speaking rate. Another intervention technique for speech is to focus on optimizing respiratory and vocal resources as well as training compensatory strategies.

These listed intervention techniques can improve quality of life in individuals with this disease and can be helpful for professionals/clinicians in the field as well as loved ones of those affected.

Astasia-abasia refers to the inability to either stand or walk in a normal manner. Astasia refers to the inability to stand upright unassisted. Abasia refers to lack of motor coordination in walking. The term "abasia" literally means that the base of gait (the lateral distance between the two feet) is inconstant or unmeasurable. When seen in conversion disorder, the gait is bizarre and is not suggestive of a specific organic lesion: often the patient sways wildly and nearly falls, recovering at the last moment.

An acquired total inability to stand and walk can be seen in true neurological diseases, including stroke, Parkinson's disease, damage to the cerebellum, Guillain–Barré syndrome, normal pressure hydrocephalus and many others. In normal pressure hydrocephalus, for example, when the condition remains untreated, the patient's gait becomes shortened, with frequent shuffling and falls; eventually standing, sitting, and even rolling over in bed become impossible. This advanced state is referred to as "hydrocephalic astasia-abasia".

Myopathic gait (or waddling gait) is a form of gait abnormality.

The "waddling" is due to the weakness of the proximal muscles of the pelvic girdle.

The patient uses circumduction to compensate for gluteal weakness.

Conditions associated with a myopathic gait include pregnancy, congenital hip dysplasia, muscular dystrophies and spinal muscular atrophy

Blocq's disease was first considered by Paul Blocq (1860–1896), who described this phenomenon as the loss of memory of specialized movements causing the inability to maintain an upright posture, despite normal function of the legs in the bed. The patient is able to stand up, but as soon as the feet are on the ground, the patient cannot hold himself upright nor walk; however when lying down, the subject conserved the integrity of muscular force and the precision of movements of the lower limbs. The motivation of this study came when a fellow student Georges Marinesco (1864) and Paul published a case of parkinsonian tremor (1893) due to a tumor located in the substantia nigra.

In the third paper published by Paul Blocq, he was trying to determine the neurophysiology behind this disease by relating the cerebral cortex (the decision making) and the spinal cord (the decision executer). His hypothesis was that there would exist an inhibitory influence which exerted and influenced the cortical or spinal centers for standing and walking.

Spastic gait is a form of gait abnormality.

Among the treatment options is chemodenervation.

The Trendelenburg gait pattern (or gluteus medius lurch) is an abnormal gait (as with walking) caused by weakness of the abductor muscles of the lower limb, gluteus medius and gluteus minimus. People with a lesion of superior gluteal nerve have weakness of abducting the thigh at the hip.

This type of gait may also be seen in L5 radiculopathy and after poliomyelitis, but is then usually seen in combination with foot drop.

During the stance phase, the weakened abductor muscles allow the pelvis to tilt down on the opposite side. To compensate, the trunk lurches to the weakened side to attempt to maintain a level pelvis throughout the gait cycle. The pelvis sags on the opposite side of the lesioned superior gluteal nerve.

This gait is precipitated by strain to the gluteus maximus and gluteus minimus. Sufferers frequently complain that an overly strenuous session at the gym, particularly with glute-isolating equipment, result in this awkward gait, or worse.

This gait may be caused by cleidocranial dysostosis.

Biofeedback and physical therapy have been used in treatment.

When the hip abductor muscles (gluteus medius and minimus) are weak, the stabilizing effect of these muscles during gait is lost.

When standing on the right leg, if the left hip drops, it's a positive right Trendelenburg sign (the contralateral side drops because the ipsilateral hip abductors do not stabilize the pelvis to prevent the droop).

"When the patient walks, if he swings his body to the right to compensate for left hip drop, he will present with a compensated Trendelenburg gait; the patient exhibits an excessive lateral lean in which the thorax is thrust laterally to keep the center of gravity over the stance leg."

There is no known cure for PSP and management is primarily supportive. PSP cases are often split into two subgroups, PSP-Richardson, the classic type, and PSP-Parkinsonism, where a short-term response to levodopa can be obtained. Dyskinesia is an occasional but rare complication of treatment. Amantadine is also sometimes helpful. After a few years the Parkinsonian variant tends to take on Richardson features. Other variants have been described. Botox can be used to treat neck dystonia and blephrospasm, but this can aggravate dysphagia.

Two studies have suggested that rivastigmine may help with cognitive aspects, but the authors of both studies have suggested a larger sampling be used. There is some evidence that the hypnotic zolpidem may improve motor function and eye movements, but only from small-scale studies.

Stomping gait (or sensory ataxia gait) is a form of gait abnormality.

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.

There is currently no effective treatment or cure for PSP, although some of the symptoms can respond to nonspecific measures. The average age at symptoms onset is 63 and survival from onset averages 7 years with a wide variance. Pneumonia is a frequent cause of death.

Astasia and/or abasia are associated with the corresponding fears of walking and/or standing, variously called stasophobia, basophobia, stasiphobia, basiphobia, stasobasophobia, stasibasiphobia, etc., sometimes turning into pathological forms, i.e. phobias.