Diagnosis consists of a variety of tests, including but not limited to:

- Measurement of orthostatic blood pressure

- Coordination

- rapid, alternating movements

- stroking of heel from along the opposite shin from knee to ankle

- finger-to-nose testing.

- Primary sensory modalities are examined with the following methods, searching for focal sensory loss, graded distal sensory loss, or levels of decreased sensation, hyperesthesia or dysesthesia.

- light touch

- pin-prick

- temperature

- position

- vibration

- Focused gait examination, which examines stationary position and walking abnormalities. Walking generally exposes any faults within the complex neurological communication between systems as weight is shifted from one foot to the other.

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.

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.

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.

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.

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

- Functional Reach Test

- External Perturbation Test – Push, Release

- External Perturbation Test – Pull

- Clinical Sensory Integration Test

- Single Leg Stance Test

- Five Times Sit to Stand Test

Various scales are also utilized

- Brief Ataxia Rating Scale

- Friedreich's Ataxia Impact Scale

- Scale For Assessment and Rating of Ataxia

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.

Initial diagnosis often is made during routine physical examination. Such diagnosis can be confirmed by a medical professional such as a neurologist, orthopedic surgeon or neurosurgeon. A person with foot drop will have difficulty walking on his or her heels because he will be unable to lift the front of the foot (balls and toes) off the ground. Therefore, a simple test of asking the patient to dorsiflex may determine diagnosis of the problem. This is measured on a 0-5 scale that observes mobility. The lowest point, 0, will determine complete paralysis and the highest point, 5, will determine complete mobility.

There are other tests that may help determine the underlying etiology for this diagnosis. Such tests may include MRI, MRN, or EMG to assess the surrounding areas of damaged nerves and the damaged nerves themselves, respectively. The nerve that communicates to the muscles that lift the foot is the peroneal nerve. This nerve innervates the anterior muscles of the leg that are used during dorsi flexion of the ankle. The muscles that are used in plantar flexion are innervated by the tibial nerve and often develop tightness in the presence of foot drop. The muscles that keep the ankle from supination (as from an ankle sprain) are also innervated by the peroneal nerve, and it is not uncommon to find weakness in this area as well. Paraesthesia in the lower leg, particularly on the top of the foot and ankle, also can accompany foot drop, although it is not in all instances.

A common yoga kneeling exercise, the Varjrasana has, under the name "yoga foot drop," been linked to foot drop.

Hereditary spastic paraplegias can be classified based on the symptoms; mode of inheritance; the patient’s age at onset; the affected genes; and biochemical pathways involved.

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

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.

A working diagnosis is made from a neurological examination and evaluation. Parts of a complete examination include a physical examination, MRI, patient history, and electrophysiological and accelerometric studies. A diagnosis of solely intention tremor can only be made if the tremor is of low frequency (below 5 Hz) and without the presence of any resting tremors. Electrophysiological studies can be useful in determining frequency of the tremor, and accelerometric studies quantify tremor amplitude. MRI is used to locate damage to and degradation of the cerebellum that may be causing the intention tremor. Focal lesions such as neoplasms, tumors, hemorrhages, demyelination, or other damage may be causing dysfunction of the cerebellum and correspondingly the intention tremor.

Physical tests are an easy way to determine the severity of the intention tremor and impairment of physical activity. Common tests that are used to assess intention tremor are the finger-to-nose and heel-to-shin tests. In a finger-to-nose test, a physician has the individual touch their nose with their finger while monitoring for irregularity in timing and control of the movement. An individual with intention tremors will have coarse side-to-side movements that increase in severity as the finger approaches the nose. Similarly, the heel-to-shin test evaluates intention tremors of the lower extremities. In such a test, the individual, in a supine position, places one heel on top of the opposite knee and is then instructed to slide the heel down the shin to the ankle while being monitored for coarse and irregular side-to-side movement as the heel approaches the ankle.

Important historical elements to the diagnosis of intention tremor are:

1. age at onset

2. mode of onset (sudden or gradual)

3. anatomical affected sites

4. rate of progression

5. exacerbating and remitting factors

6. alcohol abuse

7. family history of tremor

8. current medications

Secondary symptoms commonly observed are dysarthria (a speech disorder characterized by poor articulation and slurred speech), nystagmus (rapid involuntary eye movement, especially rolling of the eyes), gait problems (abnormality in walking), and postural tremor or titubation (to-and-fro movements of the neck and trunk). A postural tremor may also accompany intention tremors.

Although HSP is a progressive condition, the prognosis for individuals with HSP varies greatly. It primarily affects the legs although there can be some upperbody involvement in some individuals. Some cases are seriously disabling while others are less disabling and are compatible with a productive and full life. The majority of individuals with HSP have a normal life expectancy.

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."

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

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.

There are two types of normal pressure hydrocephalus: idiopathic and secondary. The secondary type of NPH can be due to a subarachnoid hemorrhage, head trauma, tumor, infection in the central nervous system, or a complication of cranial surgery.

As stated earlier, musculoskeletal disorders can cost up to $15–$20 billion in direct costs or $45–$55 billion in indirect expenses. This is about $135 million a day Tests that confirm or correct TTS require expensive treatment options like x-rays, CT-scans, MRI and surgery. 3 former options for TTS detect and locate, while the latter is a form of treatment to decompress tibial nerve pressure Since surgery is the most common form of TTS treatment, high financial burden is placed upon those diagnosed with the rare syndrome.

Diagnosis of NPH is usually first led by brain imaging, either CT or MRI, to rule out any mass lesions in the brain. This is then followed by lumbar puncture and evaluation of clinical response to removal of CSF. This can be followed by continuous external lumbar CSF drainage during 3 or 4 days.

- CT scan may show enlarged ventricles without convolutional atrophy.

- MRI may show some degree of transependymal migration of CSF surrounding the ventricles on T2/FLAIR sequence. Imaging however cannot differentiate between pathologies with similar clinical picture like Alzheimer's dementia, vascular dementia or Parkinson's disease.

- Following imaging, lumbar puncture is usually the first step in diagnosis and the CSF opening pressure is measured carefully. In most cases, CSF pressure is usually above 155 mmHO. Clinical improvement after removal of CSF (30 mL or more) has a high predictive value for subsequent success with shunting. This is called the "lumbar tap test" or Miller Fisher test. On the contrary, a "negative" test has a very low predictive accuracy, as many patients may improve after a shunt in spite of lack of improvement after CSF removal.

- Infusion test is a test that may have higher sensitivity and specificity than a lumbar puncture, but is not performed in most centers. The outflow conductance (Cout) of the cerebrospinal fluid (CSF) system is a parameter considered by some centers to be predictive in selection for hydrocephalus surgery. Cout can be determined through an infusion test. This is not a test that is normally performed prior to shunting, but may become more accepted.

- In some centers, External lumbar drainage has been shown to have the highest sensitivity and specificity with regards to predicting a successful outcome following surgery.

Diagnosis of clubfoot deformity is by physical examination. Typically, a newborn is examined shortly after delivery with a head to toe assessment. Examination of the lower extremity and foot reveals the deformity, which may affect one or both feet. Examination of the foot shows four components of deformity.

- First, there is a higher arch on the inside of the foot. This component of the deformity can occur without the other aspects of clubfoot deformity. In isolation, this aspect of the deformity is called cavus deformity.

- Second, the forefoot is curved inward or medially (toward the big toe). This component of the deformity can occur without the other aspects of clubfoot deformity. In isolation, this aspect of the deformity is called metatarsus adductus.

- Third, the heel is turned inward. This is a natural motion of the heel and subtalar joint, typically referred to as inversion. In clubfoot deformity, the turning in (inversion) of the heel is fixed (not passively correctable) and considered a varus deformity.

- Fourth, and finally, the ankle is pointed downward. This is a natural motion of the ankle referred to as plantar flexion. In clubfoot deformity, this position is fixed (not correctable) and is referred to as equinus deformity.

A foot that shows all four components are diagnosed as having clubfoot deformity. These four components of a clubfoot deformity can be remembered with the acronym CAVE (cavus, forefoot adductus, varus, and equinus).

The severity of the deformity can also be assessed on physical exam, but is subjective to quantify. One way to assess severity is based on the stiffness of the deformity or how much it can be corrected with manual manipulation of the foot to bring it into a corrected position. Other factors used to assess severity include the presence of skin creases in the arch and at the heel and poor muscle consistency.

In some cases, it may be possible to detect the disease prior to birth during a prenatal ultrasound. Prenatal diagnosis by ultrasound can allow parents the opportunity to get information about this condition and make plans for treatment after their baby is born.

Other testing and imaging is typically not needed. Further testing may be needed if there are concerns for other associated conditions.

An upper motor neuron lesion (also known as pyramidal insufficiency) occurs in the neural pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves. Conversely, a lower motor neuron lesion affects nerve fibers traveling from the anterior horn of the spinal cord or the cranial motor nuclei to the relevant muscle(s).

Upper motor neuron lesions occur in the brain or the spinal cord as the result of stroke, multiple sclerosis, traumatic brain injury and cerebral palsy.

In many cases, conservative treatment consisting of physical therapy and new shoes with soft, spacious toe boxes is enough to resolve the condition, while in more severe or longstanding cases Hammertoe Surgery may be necessary to correct the deformity. The patient's doctor may also prescribe some toe exercises that can be done at home to stretch and strengthen the muscles. For example, the individual can gently stretch the toes manually, or use the toes to pick things up off the floor. While watching television or reading, one can put a towel flat under the feet and use the toes to crumple it. The doctor can also prescribe a brace that pushes down on the toes to force them to stretch out their muscles.

The French method for treatment of clubfoot is a conservative method of treatment of a newborn which requires daily physical therapy for the first two months. The goal of this treatment is to avoid future need of surgery, but the success rate varies and after release surgery may still be necessary. The treatment includes daily manipulations of the feet along with stretching of the feet, followed by taping in order to maintain the range of motion gains achieved at the end of each session. The French method differs from the Ponseti method in that the taping techniques allow some motion in the feet. Another focus is to strengthen the peroneal muscles which is thought to contribute towards long-term correction. After the two month mark physical therapy sessions can be weaned down to three times per week instead of daily until the child reaches six months old. Parents are required to continue on with home exercises and night splinting even after the program has achieved proper foot correction in order to maintain the correction. The Ponseti method is generally preferred.

Diagnosis is based upon physical examination findings. Patients' pain history and a positive Tinel's sign are the first steps in evaluating the possibility of tarsal tunnel syndrome. X-ray can rule out fracture. MRI can assess for space occupying lesions or other causes of nerve compression. Ultrasound can assess for synovitis or ganglia. Nerve conduction studies alone are not, but they may be used to confirm the suspected clinical diagnosis. Common causes include trauma, varicose veins, neuropathy and space-occupying anomalies within the tarsal tunnel. Tarsal tunnel syndrome is also known to affect both athletes and individuals that stand a lot.

A Neurologist or a Physiatrist usually administers nerve conduction tests or supervises a trained technologist. During this test, electrodes are placed at various spots along the nerves in the legs and feet. Both sensory and motor nerves are tested at different locations. Electrical impulses are sent through the nerve and the speed and intensity at which they travel is measured. If there is compression in the tunnel, this can be confirmed and pinpointed with this test. Some doctors do not feel that this test is necessarily a reliable way to rule out TTS. Some research indicates that nerve conduction tests will be normal in at least 50% of the cases.

Given the unclear role of electrodiagnostics in the diagnosis of tarsal tunnel syndrome, efforts have been made in the medical literature to determine which nerve conduction studies are most sensitive and specific for tibial mononeuropathy at the level of the tarsal tunnel. An evidence-based practice topic put forth by the professional organization, the American Association of Neuromuscular & Electrodiagnostic Medicine has determined that Level C, Class III evidence exists for the use of tibial motor nerve conduction studies, medial and lateral plantar mixed nerve conduction studies, and medial and lateral plantar sensory nerve conduction studies. The role of needle electromyography remains less defined.

Tarsal Tunnel Syndrome (TTS) is most closely related to Carpal Tunnel Syndrome (CTS). However, the commonality to its counterpart is much less or even rare in prevalence Studies have found that patients with rheumatoid arthritis (RA) show signs of distal limb neuropathy. The posterior tibial nerve serves victim to peripheral neuropathy and often show signs of TTS amongst RA patients. Therefore, TTS is a common discovery found in the autoimmune disorder of rheumatoid arthritis