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.

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.

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.

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.

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".

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.

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.

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.

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."

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.

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.

Unlike ataxias of cerebellar origin, Bruns apraxia exhibits many frontal lobe ataxia characteristics, with some or all present.

- Difficulty in initiating movement

- Poor truncal mobility

- Falls due to minor balance disturbances

- Greatly hindered postural responses

- Characteristic magnetic gait, the inability to raise one's foot off of the floor.

- Wide base, poor balance control when in stance

- Short stride

- En bloc turns

Often patients with frontal lobe ataxia may experience minute cognitive changes that accompany the gait disturbances, such as frontal dementia and presentation of frontal release signs (Plantar reflex). Urinary incontinence may also be present.

Bruns apraxia can be distinguished from Parkinsonian ataxia and cerebellar ataxia in a number of ways. Patients typically afflicted with Parkinsonian ataxia typically have irregular arm swing, a symptom not typically present in frontal ataxia. Walking stride in cerebellar ataxia varies dramatically, accompanied by erratic foot placement and sudden, uncontrolled lurching, not generally characteristic of Bruns apraxia.

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.

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.

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.

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

In the industrialized world, the incidence of overall cerebral palsy, which includes but is not limited to spastic diplegia, is about 2 per 1000 live births. Thus far, there is no known study recording the incidence of CP in the overall nonindustrialized world. Therefore, it is safe to assume that not all spastic CP individuals are known to science and medicine, especially in areas of the world where healthcare systems are less advanced. Many such individuals may simply live out their lives in their local communities without any medical or orthopedic oversight at all, or with extremely minimal such treatment, so that they are never able to be incorporated into any empirical data that orthopedic surgeons or neurosurgeons might seek to collect. It is shocking to note that—as with people with physical disability overall—some may even find themselves in situations of institutionalization, and thus barely see the outside world at all.

From what "is" known, the incidence of spastic diplegia is higher in males than in females; the Surveillance of Cerebral Palsy in Europe (SCPE), for example, reports a M:F ratio of 1.33:1. Variances in reported rates of incidence across different geographical areas in industrialized countries are thought to be caused primarily by discrepancies in the criteria used for inclusion and exclusion.

When such discrepancies are taken into account in comparing two or more registers of patients with cerebral palsy and also the extent to which children with mild cerebral palsy are included, the incidence rates still converge toward the average rate of 2:1000.

In the United States, approximately 10,000 infants and babies are born with CP each year, and 1200–1500 are diagnosed at preschool age when symptoms become more obvious. It is interesting to note that those with extremely mild spastic CP may not even be aware of their condition until much later in life: Internet chat forums have recorded men and women as old as 30 who were diagnosed only recently with their spastic CP.

Overall, advances in care of pregnant mothers and their babies has not resulted in a noticeable decrease in CP; in fact, because medical advances in areas related to the care of premature babies has resulted in a greater survival rate in recent years, it is actually "more" likely for infants with cerebral palsy to be born into the world now than it would have been in the past. Only the introduction of quality medical care to locations with less-than-adequate medical care has shown any decreases in the incidences of CP; the rest either have shown no change or have actually shown an increase. The incidence of CP increases with premature or very low-weight babies regardless of the quality of care.

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.

Dystonia is a neurological motor disorder that affects muscles and causes involuntary muscle spasms, and it occurs when the part of the brain called the basal ganglia malfunctions. The basal ganglia is located in the cerebrum and is responsible for controlling the coordination, speed, and fluidity of movement as well as suppressing involuntary or unwanted movements. Dystonias can be classified by the affected part(s) of the body.

1. General Dystonia - affects most or all of the body.

2. Focal Dystonia - localized to a specific part of the body.

3. Multifocal Dystonia - localized to two or more unrelated parts of the body.

4. Segmental Dystonia - localized to two or more adjacent parts of the body.

5. Hemidystonia - Involves the arm and leg on the same side of the body.

Body parts usually affected by focal dystonias include the neck, lower face, eyelids, or hands.

Typical treatments for dystonia include medication, surgery, and botox injections. Botox can reduce involuntary movements by blocking signals between muscles and nerves. When all other treatments are unsuccessful, surgery is usually used as a last resort (“Movement Disorders”).

Ataxia is a motor disorder that affects the spinal cord, brain and brainstem. Symptoms of ataxia include tremors, lack of coordination, loss of balance, instability, inaccuracy, clumsiness, gait problems, speech problems, and involuntary eye movements. Medication is the main treatment of ataxia. Some of these medicines include selegiline, amantadine, entacapone, dopamine agonists, and anticholinergics (“Movement Disorders”).

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.

Foot drop is characterized by steppage gait. While walking, people suffering the condition drag their toes along the ground or bend their knees to lift their foot higher than usual to avoid the dragging. This serves to raise the foot high enough to prevent the toe from dragging and prevents the slapping. To accommodate the toe drop, the patient may use a characteristic tiptoe walk on the opposite leg, raising the thigh excessively, as if walking upstairs, while letting the toe drop. Other gaits such as a wide outward leg swing (to avoid lifting the thigh excessively or to turn corners in the opposite direction of the affected limb) may also indicate foot drop.

Patients with painful disorders of sensation (dysesthesia) of the soles of the feet may have a similar gait but do not have foot drop. Because of the extreme pain evoked by even the slightest pressure on the feet, the patient walks as if walking barefoot on hot sand.

Spastic gait is a form of gait abnormality.

Among the treatment options is chemodenervation.