Toe walking refers to a condition where a person walks on their toes without putting much weight on the heel or any other part of the foot. Toe walking in toddlers is common. These children usually adopt a normal walking pattern as they grow older. If a child continues to walk on their toes past the age of three, they should be evaluated by a doctor.

Toe walking can be caused by different factors. One type of toe walking is also called "habitual" or "idiopathic" toe walking, where the cause is unknown. Other causes include a congenital short Achilles tendon, muscle spasticity (especially as associated with cerebral palsy) and paralytic muscle disease such as Duchenne muscular dystrophy. A congenital shortening of the Achilles tendon can be hereditary, can take place over time as the result of abnormal foot structure which shortens the tendon, or can shorten over time if its full length is not being used. Toe walking is sometimes caused by a bone block located at the ankle which prevents the antagonist movement, dorsiflexion. This cause is often associated with trauma or arthritis. It may also be one way of accommodating a separate condition, foot drop. Persistent toe walking in children has been identified as a potential early sign of autism.

Toe walking has been found to be more prevalent in males than females when tested with very large numbers of children. This study looked for family history of toe walking and the connection to children demonstrating ITW. 64.2% of the subjects with ITW were males showing a relationship between ITW and males. Of 348 subjects with positive family history of toe walking, about 60% had family history on the paternal side showing it may be genetically related to paternal genes. In 30-42% of idiopathic toe walkers, a family link has been observed.

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.

Studies have been performed to determine the source of the association between toe walking and cerebral palsy patients. One study suggests that the toe walking—sometimes called an equinus gait—associated with cerebral palsy presents with an abnormally short medial and lateral gastrocnemius and soleus—the primary muscles involved in plantarflexion. A separate study found that the gait could be a compensatory movement due to weakened plantarflexion muscles. The study performed clinical studies to determine that a greater plantarflexion force is required for normal heel-to-toe walking than for toe walking. Able bodied children were tasked to perform gaits at different levels of toe walking and the study discovered that their toe walking could not reduce the force to the levels that cerebral palsy patients indicated in their walk. This suggests that cerebral palsy in which an equinus gait is present may be due to abnormally weakened plantarflexion that can only manage toe walking.

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.

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.

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 person's feet seem attached to the floor as if by a magnet. In magnetic gait, each step is initiated in a "wresting" motion carrying feet upward and forward. Magnetic gait can be visualized in terms of a powerful magnet being forcefully pulled from a

steel plate.

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.

The causes of foot drop, as for all causes of neurological lesions, should be approached using a localization-focused approach before etiologies are considered. Most of the time, foot drop is the result of neurological disorder; only rarely is the muscle diseased or nonfunctional. The source for the neurological impairment can be central (spinal cord or brain) or peripheral (nerves located connecting from the spinal cord to an end-site muscle or sensory receptor). Foot drop is rarely the result of a pathology involving the muscles or bones that make up the lower leg. The anterior tibialis is the muscle that picks up the foot. Although the anterior tibialis plays a major role in dorsiflexion, it is assisted by the fibularis tertius, extensor digitorum longus and the extensor halluces longus. If the drop foot is caused by neurological disorder all of these muscles could be affected because they are all innervated by the deep fibular (peroneal) nerve, which branches from the sciatic nerve. The sciatic nerve exits the lumbar plexus with its root arising from the fifth lumbar nerve space. Occasionally, spasticity in the muscles opposite the anterior tibialis, the gastrocnemius and soleus, exists in the presence of foot drop, making the pathology much more complex than foot drop. Isolated foot drop is usually a flaccid condition. There are gradations of weakness that can be seen with foot drop, as follows: 0=complete paralysis, 1=flicker of contraction, 2=contraction with gravity eliminated alone, 3=contraction against gravity alone, 4=contraction against gravity and some resistance, and 5=contraction against powerful resistance (normal power). Foot drop is different from foot slap, which is the audible slapping of the foot to the floor with each step that occurs when the foot first hits the floor on each step, although they often are concurrent.

Treated systematically, possible lesion sites causing foot drop include (going from peripheral to central):

1. Neuromuscular disease;

2. Peroneal nerve (common, i.e., frequent) —chemical, mechanical, disease;

3. Sciatic nerve—direct trauma, iatrogenic;

4. Lumbosacral plexus;

5. L5 nerve root (common, especially in association with pain in back radiating down leg);

6. Cauda equina syndrome, which is cause by impingement of the nerve roots within the spinal canal distal to the end of the spinal cord;

7. Spinal cord (rarely causes isolated foot drop) —poliomyelitis, tumor;

8. Brain (uncommon, but often overlooked) —stroke, TIA, tumor;

9. Genetic (as in Charcot-Marie-Tooth Disease and hereditary neuropathy with liability to pressure palsies);

10. Nonorganic causes.

If the L5 nerve root is involved, the most common cause is a herniated disc. Other causes of foot drop are diabetes (due to generalized peripheral neuropathy), trauma, motor neuron disease (MND), adverse reaction to a drug or alcohol, and multiple sclerosis.

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.

Yoga foot drop is a kind of drop foot, a gait abnormality. It is caused by a prolonged sitting on heels, a common yoga position of vajrasana. The name was suggested by Joseph Chusid, MD, in 1971, who reported a case of foot drop in a student who complained about increasing difficulty to walk, run, or climb stairs. The cause was thought to be injury to the common peroneal nerve, which is compressed and thereby deprived of blood flow while kneeling.

Yoga foot drop is a potential adverse effect of yoga, allegedly unmentioned by yoga teachers and books.

Pigeon toe (also known as metatarsus varus, metatarsus adductus, in-toe gait, intoeing or false clubfoot) is a condition which causes the toes to point inward when walking. It is most common in infants and children under two years of age and, when not the result of simple muscle weakness, normally arises from underlying conditions, such as a twisted shin bone or an excessive anteversion (femoral head is more than 15° from the angle of torsion) resulting in the twisting of the thigh bone when the front part of a person's foot is turned in.

Severe cases are considered a form of clubfoot.

The tibia or lower leg slightly or severely twists inward when walking or standing.

Steppage gait (High stepping, Neuropathic gait) is a form of gait abnormality characterised by foot drop due to loss of dorsiflexion. The foot hangs with the toes pointing down, causing the toes to scrape the ground while walking, requiring someone to lift the leg higher than normal when walking.

It can be caused by damage to the deep peroneal nerve.

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.

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.

An antalgic gait is a gait that develops as a way to avoid pain while walking ("" = "" + "", "against pain"). It is a form of gait abnormality where the stance phase of gait is abnormally shortened relative to the swing phase. It can be a good indication of pain with weight-bearing.

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.

A limp at one hospital emergency department was the presenting complaint in 4% of children. It occurs twice as commonly in boys as in girls.

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

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".

Subcortical arteriosclerotic encephalopathy (SAE), also called lower-body parkinsonism, and cerebellar ataxia are two other gait disorders whose symptoms seem to closely resemble that of Parkinson's. However, through regression analysis studies have revealed that in Parkinson's, increasing the velocity of walking changes the stride length linearly (which resembles that of controls). However, in SAE and cerebellar ataxia stride length had a disproportionate contribution to increasing velocity, indicating that SAE and cerebellar ataxia have common underlying mechanisms different from those of Parkinson's.

Accidental or deliberate physical trauma may result in either a fracture, muscle bruising, or a contusion. It is the leading cause of a limp. Deliberate abuse is important to consider.

A detailed history is the first step of a lameness exam.

1. Age: Foals are more likely to have infectious causes of lameness (septic arthritis). Horses just starting training may be lame due to a developmental orthopedic disease, such as osteochondrosis. Older animals are more likely to experience osteoarthritis.

2. Breed: Breed-specific diseases, such as HYPP, can be ruled out. Additionally, some breeds or types are more prone to certain types of lameness.

3. Discipline: Certain lamenesses are associated with certain uses. For example, racehorses are more likely to have fatigue-related injuries such as stress fractures and injury to the flexor tendons, while western show horses are more likely to suffer from navicular syndrome and English sport horses are more likely to have osteoarthritis or injury to the suspensory ligament.

4. Past history of lameness: An old injury may be re-injured. In the case of progressive disease, such as osteoarthritis, a horse will often experience recurrent lameness that must be managed. Shifting lameness may suggest a bilateral injury or infectious cause of lameness.

5. Duration and progression the lameness: Acute injury is more common with soft tissue injury. Chronic, progressive disease is more common in cases such as osteoarthritis and navicular disease.

6. Recent changes in management: such as turn-out, exercise level, diet, or shoeing.

7. Effect of exercise on degree of lameness.

8. Any treatment implemented, including rest.