For idiopathic toe walking in young children, doctors may prefer to watch and wait: the child may "outgrow" the condition. If there is a reduction in the child's range of motion, there are several options.

- Wearing a brace or splint either during the day, night or both which limits the ability of the child to walk on their toes and stretches the Achilles tendon. One type of brace used is an AFO (ankle-foot orthosis).

- Serial casting where the foot is cast with the tendon stretched, and the cast is changed weekly with progressive stretching. However, these casts may not be changed weekly and instead every 2-3 weeks.

- Botox therapy is used to paralyze the calf muscles to reduce the opposition of the muscles to stretching the Achilles tendon, usually together with serial casting or splinting.

- If conservative measures fail to correct the toe walking after about 12–24 months, surgical lengthening of the tendon is an option. The surgery is typically done under full anesthesia but if there are no issues, the child is released the same day. After the surgery, a below-the-knee walking cast is worn for six weeks and then an AFO is worn to protect the tendon for several months.

For toe walking which results from more serious neuro-muscular conditions, additional specialists may need to be consulted.

A doctor will typically evaluate whether there is bilateral (both legs) toe walking, what the child's range of motion is (how far they can flex their feet) and perform a basic neurological exam. Treatment will depend on the cause of the condition.

The underlying disorder must be treated. For example, if a spinal disc herniation in the low back is impinging on the nerve that goes to the leg and causing symptoms of foot drop, then the herniated disc should be treated. If the foot drop is the result of a peripheral nerve injury, a window for recovery of 18 months to 2 years is often advised. If it is apparent that no recovery of nerve function takes place, surgical intervention to repair or graft the nerve can be considered, although results from this type of intervention are mixed.

Non-surgical treatments for spinal stenosis include a suitable exercise program developed by a physical therapist, activity modification (avoiding activities that cause advanced symptoms of spinal stenosis), epidural injections, and anti-inflammatory medications like ibuprofen or aspirin. If necessary, a decompression surgery that is minimally destructive of normal structures may be used to treat spinal stenosis.

Non-surgical treatments for this condition are very similar to the non-surgical methods described above for spinal stenosis. Spinal fusion surgery may be required to treat this condition, with many patients improving their function and experiencing less pain.

Nearly half of all vertebral fractures occur without any significant back pain. If pain medication, progressive activity, or a brace or support does not help with the fracture, two minimally invasive procedures - vertebroplasty or kyphoplasty - may be options.

Ankles can be stabilized by lightweight orthoses, available in molded plastics as well as softer materials that use elastic properties to prevent foot drop. Additionally, shoes can be fitted with traditional spring-loaded braces to prevent foot drop while walking. Regular exercise is usually prescribed.

Functional electrical stimulation (FES) is a technique that uses electrical currents to activate nerves innervating extremities affected by paralysis resulting from spinal cord injury (SCI), head injury, stroke and other neurological disorders. FES is primarily used to restore function in people with disabilities. It is sometimes referred to as Neuromuscular electrical stimulation (NMES)

The latest treatments include stimulation of the peroneal nerve, which lifts the foot when you step. Many stroke and multiple sclerosis patients with foot drop have had success with it. Often, individuals with foot drop prefer to use a compensatory technique like steppage gait or hip hiking as opposed to a brace or splint.

Treatment for some can be as easy as an underside "L" shaped foot-up ankle support (ankle-foot orthoses). Another method uses a cuff placed around the patient's ankle, and a topside spring and hook installed under the shoelaces. The hook connects to the ankle cuff and lifts the shoe up when the patient walks.

Most of these conditions are self-correcting during childhood. In the worst cases, surgery may be needed. Most of the time, this involves lengthening the Achilles tendon. Less severe treatment options for pigeon toe include keeping a child from crossing his or her legs, use of corrective shoes, and casting of the foot and lower legs, which is normally done before the child reaches 12 months of age or older.

If the pigeon toe is mild and close to the center, treatment may not be necessary.

Ballet has been used as a treatment for mild cases. Dance exercises can help to bend the legs outward.

Patients with symptomatic isthmic anterolisthesis are initially offered conservative treatment consisting of activity modification, pharmacological intervention, and a physical therapy consultation.

- Physical therapy can evaluate and address postural and compensatory movement abnormalities.

- Anti-inflammatory medications (NSAIDS) in combination with paracetamol (Tylenol) can be tried initially. If a severe radicular component is present, a short course of oral steroids such as Prednisone or Methylprednisolone can be considered. Epidural steroid injections, either interlaminal or transforaminal, performed under fluoroscopic guidance can help with severe radicular (leg) pain. Lumbosacral orthoses may be of benefit for some patients but should be used on a temporary basis to prevent spinal muscle atrophy and loss of proprioception.

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."

The goal of non-surgical treatment of tarsal coalition is to relieve the symptoms by reducing the movement of the affected joint. This might include non-steroidal anti-inflammatory drugs (NSAIDs), steroidal anti-inflammatory injection, stabilizing orthotics or immobilization via a leg cast. At times, short term immobilization followed by long term orthotic use may be sufficient to keep the area free of pain.

Surgery is very commonly required. The type and complexity of the surgery will depend on the location of the coalition. Essentially, there are two types of surgery. Wherever possible, the bar will be removed to restore normal motion between the two bones. If this is not possible, it may be necessary to fuse the affected joints together by using screws to connect them solidly. Cutting away the coalition is more likely to succeed the younger the patient. With age comes extra wear in the affected and adjacent joints that makes treatment more difficult.

Degenerative anterolisthesis with spinal stenosis is one of the most common indications for spine surgery (typically a laminectomy) among older adults. Both minimally invasive and open surgical techniques are used to treat anterolisthesis.

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.

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.

Appropriate treatment for lameness depends on the condition diagnosed, but at a minimum it usually includes rest or decreased activity and anti-inflammatory medications. Other treatment options, such as corrective shoeing, joint injections, and regenerative therapies, are pursued based on the cause of lameness and the financial limits of the owner. Consultation with a veterinarian is generally recommended, even for mild cases, as some types of lameness may worsen if not properly diagnosed and treated.

Physical therapy is the predominant treatment of symptoms. Orthopedic shoes and foot surgery can be used to manage foot problems.

Trendelenburg's sign is found in people with weak or paralyzed abductor muscles of the hip, namely gluteus medius and gluteus minimus. It is named after the German surgeon Friedrich Trendelenburg.

The gluteus medius is very important during the stance phase of the gait cycle to maintain both hips at the same level. Moreover, one leg stance accounts for about 60% of the gait cycle. Furthermore, during the stance phase of the gait cycle, there is approximately three times the body weight transmitted to the hip joint. The hip abductors' action accounts for two thirds of that body weight. The Trendelenburg sign is said to be positive if, when standing on one leg, the pelvis drops on the side opposite to the stance leg to reduce the load by decreasing the lever arm. By reducing the lever arm, this decreases the work load on the hip abductors. The muscle weakness is present on the side of the stance leg. A Trendelenburg sign can occur when there is presence of a muscular dysfunction (weakness of the gluteus medius or minimus) or when someone is experiencing pain. The body is not able to maintain the center of gravity on the side of the stance leg. Normally, the body shifts the weight to the stance leg, allowing the shift of the center of gravity and consequently stabilizing or balancing the body. However, in this scenario, when the patient/person lifts the opposing leg, the shift is not created and the patient/person cannot maintain balance leading to instability.

Intravenously administered penicillin is the treatment of choice. Associated pain can be treated with opiates, valproate, or carbamazepine. Those with tabes dorsalis may also require physical therapy to deal with muscle wasting and weakness. Preventive treatment for those who come into sexual contact with an individual with syphilis is important.

A number of treatments have some evidence for benefits include an exercise program. Paracetamol (acetaminophen) has not been found effective but is safe. NSAIDs are sometimes effective but should not be used after 30 weeks of pregnancy. There is tentative evidence for acupuncture.

Some pelvic joint trauma will not respond to conservative type treatments and orthopedic surgery might become the only option to stabilize the joints.

No specific treatment is known that would prevent, slow, or reverse HSP. Available therapies mainly consist of symptomatic medical management and promoting physical and emotional well-being. Therapeutics offered to HSP patients include:

- Baclofen – a voluntary muscle relaxant to relax muscles and reduce tone. This can be administered orally or intrathecally. (Studies in HSP )

- Tizanidine – to treat nocturnal or intermittent spasms (studies available )

- Diazepam and clonazepam – to decrease intensity of spasms

- Oxybutynin chloride – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Tolterodine tartate – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Botulinum toxin – to reduce muscle overactivity (existing studies for HSP patients)

- Antidepressants (such as selective serotonin re-uptake inhibitors, tricyclic antidepressants and monoamine oxidase inhibitors) – for patients experiencing clinical depression

- Physical therapy – to restore and maintain the ability to move; to reduce muscle tone; to maintain or improve range of motion and mobility; to increase strength and coordination; to prevent complications, such as frozen joints, contractures, or bedsores.

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.

Foot drop is a gait abnormality in which the dropping of the forefoot happens due to weakness, irritation or damage to the common fibular nerve including the sciatic nerve, or paralysis of the muscles in the anterior portion of the lower leg. It is usually a symptom of a greater problem, not a disease in itself. Foot drop is characterized by inability or impaired ability to raise the toes or raise the foot from the ankle (dorsiflexion). Foot drop may be temporary or permanent, depending on the extent of muscle weakness or paralysis and it can occur in one or both feet. In walking, the raised leg is slightly bent at the knee to prevent the foot from dragging along the ground.

Foot drop can be caused by nerve damage alone or by muscle or spinal cord trauma, abnormal anatomy, toxins, or disease. Toxins include organophosphate compounds which have been used as pesticides and as chemical agents in warfare. The poison can lead to further damage to the body such as a neurodegenerative disorder called organophosphorus induced delayed polyneuropathy. This disorder causes loss of function of the motor and sensory neural pathways. In this case, foot drop could be the result of paralysis due to neurological dysfunction. Diseases that can cause foot drop include trauma to the posterolateral neck of fibula, stroke, amyotrophic lateral sclerosis, muscular dystrophy, poliomyelitis, Charcot Marie Tooth disease, multiple sclerosis, cerebral palsy, hereditary spastic paraplegia, Guillain–Barré syndrome, and Friedreich's ataxia. It may also occur as a result of hip replacement surgery or knee ligament reconstruction surgery.

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.

There is no pharmacological treatment for Roussy–Lévy syndrome.

Treatment options focus on palliative care and corrective therapy. Patients tend to benefit greatly from physical therapy (especially water therapy as it does not place excessive pressure on the muscles), while moderate activity is often recommended to maintain movement, flexibility, muscle strength and endurance.

Patients with foot deformities may benefit from corrective surgery, which, however, is usually a last resort. Most such surgeries include straightening and pinning the toes, lowering the arch, and sometimes, fusing the ankle joint to provide stability. Recovering from these surgeries is oftentimes long and difficult. Proper foot care including custom-made shoes and leg braces may minimize discomfort and increase function.

While no medicines are reported to treat the disorder, patients are advised to avoid certain medications as they may aggravate the symptoms.

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.

As a matter of everyday maintenance, muscle stretching, range of motion exercises, yoga, contact improvisation, modern dance, resistance training, and other physical activity regimens are often utilized by those with spastic CP to help prevent contractures and reduce the severity of symptoms.

Major clinical treatments for spastic diplegia are:

- Baclofen (and its derivatives), a gamma amino butyric acid (GABA) substitute in oral (pill-based) or intrathecal form. Baclofen is essentially chemically identical to the GABA that the damaged, over-firing nerves cannot absorb, except that it has an extra chemical 'marker' on it that makes the damaged nerves 'think' it is a different compound, and thus those nerves will absorb it. Baclofen is noted for being the sole medication available for GABA-deficiency-based spasticity which acts on the actual cause of the spasticity rather than simply reducing symptomatology as muscle relaxants and painkillers do. The intrathecal solution is a liquid injected into the spinal fluid for trial, and if successful in reducing spasticity, thereafter administered via an intrathecal pump, which has variously been proven potentially very dangerous on one or another level with long-term use (see article), including sudden and potentially lethal baclofen overdose, whereas the oral route, which comes in 10- or 20-milligram tablets and the dosage of which can be gently titrated either upward or downward, as well as safely ceased entirely, has not.

- Antispasmodic muscle relaxant chemicals such as tizanidine and botulinum toxin (Botox), injected directly into the spastic muscles; Botox wears off every three months.

- Phenol and similar chemical 'nerve deadeners', injected selectively into the over-firing nerves in the legs on the muscle end to reduce spasticity in their corresponding muscles by preventing the spasticity signals from reaching the legs; Phenol wears off every six months.

- Orthopedic surgery to release the spastic muscles from their hypertonic state, a usually temporary result because the spasticity source is the nerves, not the muscles; spasticity can fully reassert itself as little as one year post-surgery.

- Selective dorsal rhizotomy, a neurosurgery directly targeting and eliminating ("cutting" or "lesioning") the over-firing nerve rootlets and leaving the properly firing ones intact, thereby permanently eliminating the spasticity but compelling the person to spend months re-strengthening muscles that will have been severely weakened by the loss of the spasticity, due to the fact of those muscles not really having had actual strength to begin with.

Spastic gait is a form of gait abnormality.

Among the treatment options is chemodenervation.

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 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.