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.

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.

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.

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

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-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".

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.

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.

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.

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.

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."

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.

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.

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.

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”).

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

Spastic gait is a form of gait abnormality.

Among the treatment options is chemodenervation.

Hypokinesia refers to decreased bodily movement. One of the two categories of movement disorders, hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Patients with hypokinetic disorders like Parkinson's disease experience muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.

The other category of movement disorder resulting from damage to the basal ganglia, hyperkinesia, features an exaggeration of unwanted motion, like twitching or writhing in Huntington's disease or Tourette syndrome.

Hyperkinesia, also known as hyperkinesis, refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. The word hyperkinesis comes from the Greek "hyper", meaning "increased," and "kinein", meaning "to move." Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease. Many hyperkinetic movements are the result of improper regulation of the basal ganglia-thalamocortical circuitry. Overactivity of a direct pathway combined with decreased activity of an indirect pathway results in activation of thalamic neurons and excitation of cortical neurons, resulting in increased motor output. Often, hyperkinesia is paired with hypotonia, a decrease in muscle tone. Many hyperkinetic disorders are psychological in nature and are typically prominent in childhood. Depending on the specific type of hyperkinetic movement, there are different treatment options available to minimize the symptoms, including different medical and surgical therapies.

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.

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.