Gait

Written by: Dr Jeremy Steinberg – created: 19 October 2020; last modified: 22 April 2025

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Gait Cycle Terminology; graphical representation of stride and step lengths

Humans possess two primary gaits: walking and running. This article focuses on the walking gait, a complex, coordinated action requiring the seamless integration of sensory and motor functions throughout the neuromuscular and skeletal systems.

A gait disturbance is defined as any deviation from a smooth, symmetrical, and efficient walking pattern. Such disturbances can affect the synchrony, fluency, and symmetry of movement. Identifying a gait disturbance is often a crucial step in diagnosing underlying pathologies, which can occur at any level of the neuraxis (central and peripheral nervous system) or within the musculoskeletal system itself.

Gait disorders can be broadly classified based on the anatomical level of the primary deficit:

• Lower-Level: Involving peripheral structures (muscles, bones, joints, peripheral nerves, vestibular system, visual input).
• Middle-Level: Involving spinal cord pathways, brainstem, cerebellum, or basal ganglia.
• Higher-Level: Involving cortical and subcortical pathways, often related to planning, initiation, or adaptation of gait.

It is important to note, particularly in elderly individuals, that gait disturbances frequently result from multiple contributing factors. The most commonly observed abnormal gait patterns include hemiplegic, parkinsonian, marche à petits pas, ataxic, and unsteady gaits. A thorough gait assessment is a fundamental part of the clinical examination.

Gait Cycle

Primary Terminology

The walk and run gait cycle.

Gait is a cyclical process, typically defined from the point one foot contacts the ground (initial contact, often heel-strike) to the point the same foot contacts the ground again.

• Stance phase. The stance phase of a limb is when some part of the foot is touching the ground. It makes up 60% of the gait cycle and incorporates heel strike, foot flat, mid-stance, and push-off (heels-off and toes-off).
• Swing phase. The swing phase is when it is off the ground. This phase has an acceleration, mid-swing, and deceleration components.

Gait can also be divided into support phases:

• Single support phases: Only one foot is in contact with the ground (occurs during each limb's mid-stance and terminal stance).
• Double support phases: Because the stance phase is longer than the swing phase there are periods when both feet are in contact with the ground. The duration of double support decreases as walking speed increases.

Spatial and Temporal Definitions:

• Stride Length: Distance between two consecutive initial contacts of the same foot (e.g., right heel strike to next right heel strike).
• Step Length: Distance between the initial contact of one foot and the initial contact of the opposite foot (e.g., right heel strike to left heel strike). Typically 0.6-0.7m.
• Cadence (Step Frequency): Number of steps taken per unit time (e.g., steps per minute or steps per second). A typical value is around 100-120 steps/min (approx. 2 steps/sec).
• Stride Frequency: Number of strides taken per unit time.
• Walking Speed: Product of step length and cadence (or stride length and stride frequency). Healthy adults typically walk at 1.2-1.4 m/s on level ground.
• Step Width: Lateral distance between the midline of the heels during double support. Normally around 5-10 cm (or ~10% of leg length). Increased step width often indicates instability.
• Foot Progression Angle: Angle between the long axis of the foot and the line of forward progression. A positive value is termed toe-out and a negative value is termed toe-in. A slight toe-out angle (approx. 10 degrees) is typical.

Stance Phase

Initial contact (heel strike): This occurs when the foot contacts the ground. The hip extensors contract to stabilize the hip. The quadriceps and tibialis anterior contract eccentrically to control plantar flexion (foot slap).

Loading response (initial double limb support): This marks the beginning of the initial double limb stance. It occurs after initial contact until elevation of the contralateral limb. The bodyweight is transferred on to the supporting limb. The ankle dorsiflexors (tibialis anterior) contract eccentrically to control plantar flexion moment. The quadriceps contract to stabilise knee and counteract the flexion moment (about the knee).

Mid-stance (single limb support): This is the initial period of single leg support. It is from elevation of opposite limb until both ankles are aligned in coronal plane. The hip extensors and quadriceps undergo concentric contraction.

Terminal stance (single limb support): This begins when the supporting heel rises from the ground and continues until the opposite heel touches the ground. The toe flexors contract and are the most active during this phase

Pre-swing (second double limb support): This is the start of the second double limb stance in the gait cycle. It is from initial contact of opposite limb to just prior to elevation of ipsilateral limb. The hip flexors contract to propel advancing limb

Swing Phase

Initial swing (toe off): This is the start of single limb support for the contralateral limb. It is from elevation of limb to point of maximal knee flexion. The hip flexors concentrically contract to advance the swinging leg

Mid-swing (foot clearance). This follows knee flexion to point where tibia is vertical. The ankle dorsiflexors contract to ensure foot clearance

Terminal swing (tibia vertical): This is from point where tibia is vertical to just prior to initial contact. The hamstring muscles decelerate forward motion of thigh.

Key Kinematics and Centre of Gravity Movement

Efficient walking involves coordinated movements that minimize energy expenditure:

Pelvis Kinematics:

• Pelvic rotation: The pelvis rotates 4 degrees medially (anteriorly) on swing side. It lengthens the limb as it prepares to accept weight contributing to step length.
• Pelvic tilt: The pelvis drops about 4 degrees on the swing side during the stance phase of the opposite limb (Trendelenburg physiology, controlled by hip abductors), lowering the centre of gravity slightly at mid-stance.
• Lateral displacement of pelvis: The pelvis and trunk shift laterally about 2-5 cm over the stance limb to keep the centre of gravity balanced over the base of support.

Knee mechanisms: early knee flexion (15 degrees) at heel strike. This lowers the centre of gravity, decreasing energy expenditure. It also absorbs shock of heel strike. At midstance, the knee extends as the ankle plantarflexes and foot supinates. This restores leg to original length.

Hip mechanisms: Starts flexed at foot contact, extends through the stance phase (peaking just before toe-off), and flexes during swing.

Foot/Ankle mechanisms: Neutral at foot contact. Controlled plantar flexion after initial contact, followed by dorsiflexion through mid-stance, and powerful plantar flexion at push-off smooth the vertical path of the body.

Centre of gravity (COG) movement: In standing position the centre of gravity (COG) is 5cm anterior to S2 vertebral body. There is vertical displacement during gait cycle in a rhythmic pattern. The highest point is during midstance phase, and the lowest point occurs at the time of double limb support. There is also horizontal displacement of the COG, where it displaces horizontally during adult male step

As walking speed increases, the range of motion at the hip, knee, and ankle generally increases, while the relative duration of the stance phase (and particularly double support) decreases.

Ground Reaction Forces

Components of the ground reaction force (GRF), moment, and center of pressure (COP) across the walking gait cycle measured with one force platform per foot. Functional phases of the gait cycle are separated by vertical dashed lines.

Walking can be further studied by measuring the ground reaction forces (GRFs) exerted by the floor onto the feet using force plates. These forces, measured in vertical, forward/backward (anteroposterior), and side-to-side (mediolateral) directions, are reactions to muscle-generated forces.

GRFs are important because, according to Newton's second law (Fexternal​=m(aCOM​+g)), they directly relate to the acceleration of the body's center of mass (COM).

Key characteristics of GRFs during walking include:

1. Vertical GRF: Typically shows a "double-hump" pattern. It rises above body weight shortly after initial contact (impact absorption), dips below body weight during mid-stance, and rises again during push-off (propulsion). Averaged over the cycle, it equals body weight. The amplitude of the peaks increases with walking speed. Clinical Relevance: Reduced peak forces may indicate muscle weakness or pain avoidance (e.g., antalgic gait, severe OA), while altered timing can reflect instability or specific pathologies.
2. Anteroposterior (AP) GRF: Initially directed backward (braking force) as the foot contacts the ground ahead of the COM, then shifts to a forward direction (propulsive force) during push-off. Averages to zero during steady-speed walking. Clinical Relevance: Reduced propulsive force is common in conditions affecting plantar flexor strength or hip extension (e.g., elderly gait, some neurological conditions).
3. Mediolateral (M/L) GRF: Generally smaller magnitude, reflecting forces needed for lateral stability and balance control. Changes can indicate balance issues or compensatory strategies.

Double Support: When both feet are on the ground, the AP (fore-aft) forces largely oppose each other, while vertical forces add up.

Energy Exchange: Analysis of GRFs allows calculation of the COM's kinetic energy (Ekf​) and gravitational potential energy (Epv​). During walking, these fluctuate largely out of phase (like a pendulum), allowing for efficient energy exchange and reducing the metabolic cost. Pathological gaits often disrupt this mechanism, increasing energy expenditure.

Obesity: Individuals with obesity exhibit increased peak GRFs (due to higher mass), often adopt a wider step width, and may show altered joint moments, potentially increasing joint stress.

Gait Disorder Classifications

Higher, Middle, and Lower Level Gait Disorder Anatomical Correlations.

Levels	Anatomical Level	Balance and Gait Pattern
Higher	Psychological / psychiatric	Variable: slow, buckling knees
Higher	Cortical and subcortical	Different patterns: cautious, parkinsonian, ataxic, spastic, magnetic, gait ignition failure, disequilibrium
Middle	Basal ganglia	Parkinsonian / dystonic / choreic
Middle	Thalamus	Astasia / ataxia
Middle	Cerebellum	Cerebellar ataxia
Middle	Brain stem	Ataxia / spasticity
Middle	Spinal cord	Spastic gait / tabetic gait
Lower	Peripheral nerve Proprioception, vestibular visual	Sensory ataxia / vestibular disequilibrium / visual disequilibrium
Lower	Neuromuscular junction	Waddling
Lower	Muscle	Waddling, steppage, Trendelenburg
Lower	Skeleton	Antalgic / compensatory for deformities

See below for a demonstration of neurological gait conditions (Hemiplegic, Parkinsonian, Cerebellar, Stomping, Scissoring, Trendelenburg, Foot-drop, Choreiform)

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Gait Disorders

Lower Level Gait Disorders

Lower level gait disorders are caused by pathology of the muscles, skeleton, peripheral nerves, peripheral vestibular system, and anterior visual pathway.

Antalgic Gait: The occurs when there is a protective adaptation to minimise pain during weightbearing. The patient removes weight from the painful side as quickly as possible. The stance phase of the affected side, and the swing phase of the unaffected side are lessened. Stride length and velocity are decreased.

Trendelenburg Gait: The distance from the midline to the femoral head is almost twice that between the abductors and femoral head. The abductors generate very large forces across the hip weight bearing area, about 3 times that of upper body weight. Trendelenburg gait manifests as ipsilateral lurching of the torso with a contralateral hip drop during the stance phase of the affected side. It is caused by unilateral hip abductor weakness. There is an exaggerated up and down motion of the pelvic.

Waddling Gait: A waddling gait pattern is seen with weakness of the bilateral hip abductors as well as in bilateral hip joint osteoarthritis or other bilateral hip joint diseases such as bilateral congenital hip dislocation. The gait is wide based, and has short steps. There is increased alternating lateral body sway, and excessive drop of the hips. By swaying laterally the patient places their weight down the centre of gravity through each hip to reduce pain. There may be increased arm abduction and an exaggerated lumbar lordosis.

Abductor Lurch: The abductor lurch is seen with further abductor mechanism weakness, where the trunk muscles come into play. The entire body and shoulder tilts to the diseased side in the stance phase of the ipsilateral limb. The abductor lurch can also occur in the setting of a painful hip. By tilting the body to the affected side the centre of gravity is shifted towards the centre of the femoral head, thereby reducing the reaction force and resultant pain. In this situation there is no drop of the hemipelvis as seen with a Trendelenburg gait.

Short Limb Gait: To compensate for length, the pelvis on the affected short side tilts down (hip hiking). This allows the longer limb to more easily clear the ground. The foot may supinate or there may be toe walking. The longer limb may compensate by flexing at the hip or knee.

Steppage Gait: This is seen with weakness of foot dorsiflexion, which may be due to peroneal nerve injury, radiculopathy, and demyelinating neuropathy. It may be unilateral or bilateral. The patient exaggerates knee and hip flexion to avoid tripping. The step is high and short, and at the end of each swing phase the foot may slap the floor.

Gluteus Maximus or Extensor Lurch: Normally the gluteus maximus prevents the torso toppling forward in the stance phase, because the centre of gravity is anterior to the hip. With gluteus maximus weakness, the torso lurches backwards at heel strike on the affected side. This is a compensatory mechanism to interrupt forward motion of the trunk due to a weakness of hip extension. The pelvis is thrusted forward, and the torso backwards, in order to shift the centre of gravity more posteriorly.

Gait Affected by Joint Contractures/Stiffness:

• Hip/Knee Flexion Contracture: Results in a stooped posture, increased lumbar lordosis, and short strides. Evaluate this laterally
• Stiff Knee Gait (Extended): May be adopted to avoid patellofemoral pain or to compensate for quadriceps weakness (locking the knee in extension during stance). Circumduction may be needed during swing.
• Stiff Knee Gait (Flexed): Even mild flexion contracture (e.g., 5 degrees) shortens the functional limb length, disrupting normal heel strike (leading to flat-foot contact) and causing jerky vertical motion. Common after knee surgery or in severe OA.
• Ankle Equinus Contracture: Causes premature heel rise during stance and may lead to compensatory knee hyperextension. A high-stepping gait may be seen during swing.
• Stiff First MTP Joint (Hallux Rigidus): Patients avoid rolling over the big toe during late stance/push-off. They may walk on the lateral border of the foot (check shoe wear) and push off more from the heel or lateral forefoot, leading to a shortened, less efficient stride.

Genu Varus and Valgus Thrust: Evaluate varus and valgus thrusting by squatting or sitting to inspect the patient from the level of their knees. Varus thrust is the most common. In the stance phase the knee collapses into varus with the lateral border laterally thrusting. This can be seen in advanced osteoarthritis, varus from malunited tibial plateau fracture, and tibia varum. A ligamentous laxity will usually add a recurvatum thrust visualised laterally. Valgus thrust is less common, and patients may circumduct their limb to avoid knocking their knees. See also Knee Examination

Pes Planus: In flexible flatfoot, the arch collapses during weight-bearing. In severe or rigid cases, normal heel rise and push-off may be compromised, with the foot lifting off the ground more as a single unit. Often associated with foot eversion/abduction (toe-out). See also Ankle Examination and Adult Acquired Flat Foot Deformity.

Sensory Ataxia: The sensory ataxic gait is wide based with a variable step length and marked stride-to-stride variability. There is usually unsteadiness. Romberg sign is often positive. This gait pattern is not specific to any anatomical location, and may be seen in pathology of proprioception (sensory ataxia), cerebellum (cerebellar ataxia), pons, and thalamus. Common causes are peripheral neuropathy and posterior column loss.

Visual Disequilibrium: Acute visual distortion such as using new prescription glasses may cause a sense of loss of balance. There may be cautiousness in gait, with tentative steps and an increased base of support.

Vestibular Disequilibrium: Acutely there may be vertigo, nystagmus, and a tendency to fall onto the affected side. Chronically, the symptoms may be less marked, but the gait is often still wide based and cautious. There is difficulty with Romberg test and tandem walking, but assistance is not required to walk.

Sensory Disequilibrium: There is conflict among inputs from the visual, proprioceptive, and vestibular pathways. Loss of two of these pathways, or loss of one without CNS adaptation, may lead to this becoming chronic. The gait is slow and cautious, and there is increased bipedal support.

Middle Level Gait Disorders

In middle level gait disorders are caused by lesions in the ascending or descending sensorimotor tract, cerebellar dysfunction, bradykinesia, and hyperkinetic movement disorders.

Spastic Gait and Scissoring: Corticospinal tract lesions cause spastic gaits that can be hemi or paraparetic depending on whether the lesion is unilateral or bialteral. There is often an associated weakness. Common causes of spastic paraparesis are cerebral palsy, multiple sclerosis, and cord compression.

Spastic hemiparetic gaits show lower limb hyperextension with difficulty in hip and knee flexion and excessive plantarflexion and inversion of the foot. The arm may have a flexor posture or may dangle. The support base is narrowed, and there is a semicircular movement at the hip during the swing phase which is needed to clear the ground due to the hyperextension of the leg. With more mild spasticity and good proximal muscle strength the patient may clear the floor during the swing phase with increased hip flexion.

Spastic paraparetic gaits is more common in spinal cord injury and there is some shared features with hemiparetic gaits. Arm swing and the posture of the upper limb may be relatively normal depending on the lesion level.

Spastic diplegic gait is a bilatearl hemiparetic gait with particular features. The knees and hips are significantly flexed. The hips are adducted during the gait cycle causing a scissoring pattern from leg crossing. Compared to bilateral hemiparesis, in spastic diplegia the upper limbs and bulbar muscles are much less affected than the lower limbs.

Crouch Gait: Individuals with cerebral palsy may walk with a crouched gait. This is characterised by excessive flexion of the knee during stance phase, commonly accompanied by increased hip flexion. This increases forces in the knee during stance, reduces toe-ground clearance during swing, and increases overall energy expenditure.

Stiff-Knee Gait (Neurological): Individuals who have cerebral palsy or have had a stroke may walk with a stiff-knee gait, thought to be due to inappropriate activation of rectus femoris. This is where knee flexion is reduced or delayed during swing. Like crouch gait, this pattern also affects toe-ground clearance leading to tripping and increased energy expenditure.

Cerebellar Ataxia: The patient veers towards side of lesion. The common causes are drugs (e.g. phenytoin), alcohol, multiple sclerosis, and cerebrovascular disease.

Parkinsonian Gait: A parkinsonian gait indicates basal ganglion dysfunction. There are small paces and reduce arm swing. The reduced arm swing is usually unilateral, and is one of the earliest signs of parkinsonism. There may be be difficulty in starting and stopping. Festination may be worse on one side. The tremor may increase with walking. The common causes are Parkinson's disease and major tranquillisers. See also Parkinson's Disease and Chronic Pain

Marche à Petit Pas: This indicates bilateral diffuse cortical dysfunction. The common cause is diffuse cerebrovascular disease ‘lacunar state.’

Apraxic Gait: This indicates that cortical integration of the movement is abnormal and there is usually frontal lobe pathology. Common causes are normal pressure hydrocephalus and cerebrovascular disease.

Hemiplegic Gait: There is seen in unilateral upper motor neurone lesion. Common causes are stroke and multiple sclerosis.

Choreic Gait: Choreic gait is a type of abnormal walking pattern observed in individuals with chorea, a neurological disorder characterized by involuntary, rapid, and irregular movements. In patients with choreic gait, the involuntary movements interfere with the coordination required for smooth walking, resulting in jerky and unpredictable steps, as well as imbalance and difficulty in maintaining a steady pace.

Dystonic Gait: Dystonic gait is associated with dystonia, a neurological movement disorder marked by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements or postures. In individuals with dystonic gait, the muscle contractions can affect walking by causing twisting, turning, or dragging movements of the legs or feet, leading to an unsteady, bizarre, and awkward walking pattern. The severity of dystonic gait can vary and may be exacerbated by specific triggers, such as stress or voluntary movements.

Higher Level Gait Disorders

These gait disorders are caused by impairment of the cortico-basal ganglia-thalamocortical pathways.

Cautious Gait: Slow speed, shortened stride length, widened base, reduced arm swing, and often turning "en bloc." Common in elderly individuals, often related to fear of falling or mild balance deficits.

Frontal Gait Disorder / Gait Apraxia: Difficulty initiating gait ("magnetic gait" - feet seem stuck to the floor), shuffling steps, impaired balance, and difficulty integrating movements, despite normal motor strength and sensation. Associated with frontal lobe dysfunction (e.g., normal pressure hydrocephalus (NPH), diffuse vascular disease, frontal tumours).

Subcortical Disequilibrium: Profound instability and postural impairment, often unable to stand or walk without assistance, despite minimal or no focal neurological signs. May be seen in advanced white matter disease or NPH.

Psychogenic/Functional Gait: Gait pattern is inconsistent, often bizarre, may worsen with observation, and doesn't fit a recognized neurological or musculoskeletal pattern. May involve excessive slowness, exaggerated effort, buckling knees, or unusual postures inconsistent with findings on examination (e.g., normal strength/coordination when tested lying down).

Examination

Observation

• Overall Pattern: Is it symmetrical or asymmetrical? Smooth or jerky? Stable or unstable?
• Initiation: Any hesitation or freezing?
• Pace & Stride: Normal, small (shuffling), or variable steps? Normal or reduced speed?
• Base of Support: Normal width, narrow, or wide-based?
• Posture: Upright, stooped, listing to one side?
• Arm Swing: Present, reduced, absent, symmetrical?
• Foot Clearance: Normal, slapping, dragging, high-stepping (steppage), circumduction?
• Heel Strike: Present or replaced by flat-foot or toe contact?
• Push-off: Appears normal or reduced?
• Trunk/Pelvic Movement: Normal rotation/tilt, excessive sway (waddling), lurching?
• Turning: Smooth pivot or multiple small steps ("en bloc")?

Specific Gait Observation Heuristics

There should be a general, neurological, and musculoskeletal examination in order to localise the lesion. The gait should be assessed by observing the gait parameters, posture, range of motion, and tandem walking.

• Symmetrical gait
  • Size of the paces are they small or normal
    • If small paces, look at the posture and arm-swing
      • If they are stooped with reduced arm-swing this is a parkinsonian gait
      • Upright with marked arm-swing: marche à petits pas
    • If normal paces, look at the lateral distance between the feet
      • Widely separated is broad-based
      • Legs uncoordinated is cerebellar
      • Crossing over with toes dragging is scissoring
  • Normal paces
    • Look at the knees
      • Knees lifting high is high-stepping
    • Look at the pelvis and shoulders
      • Marked rotation of pelvis and shoulders is waddling
    • Look at the whole movement
      • Disjointed movements as if the patient has forgotten how to walk, and is frequently rooted to the spot is apraxic
      • Bizarre, elaborate, and inconsistent is functional.
• asymmetrical gait
  • Is there pain?
    • Painful or antalgic gait
    • Bony deformity is an orthopaedic gait
    • Leg swinging out to the side is a hemiplegic gait
    • One leg lifting higher than the other is foot drop

Romberg's Test

The Romberg test is done after gait assessment and is a test of joint position sense. Ask the patient to stand with his feet together. Allow them to stand like this for a few seconds. Reassure them that you will catch them if they fall. If they falls with their eyes open do not proceed. Romberg’s test is not positive in cerebellar disease.

• Negative Romberg's test: stands with eyes open, stands with eyes closed
• Positive Romberg's test: stands with eyes open, falls with eyes closed
  • This indicates loss of joint position sense.
  • It can occur with:
    • A posterior column lesion in the spinal cord with cord compression (cervical spondylosis, tumour). Rare causes include tabes dorsalis, vitamin B12 deficiency, and degenerative spinal cord disease.
    • Peripheral neuropathy
• Severe unsteadiness: unable to stand with eyes open and feet together
  • Common causes are cerebellar syndromes, central and peripheral vestibular syndromes.
• Cerebellar syndrome: Stands with eyes open, rocks backwards and forwards with eyes closed.

Other Tests

Other tests to consider are

• Tandem Gait: Ask patient to walk heel-to-toe as if on a tightrope. Sensitive for ataxia (cerebellar) and balance impairment. Mild difficulty can be normal in the elderly.
• Heel Walking: Tests ankle dorsiflexor strength (L4/L5, peroneal nerve). Inability suggests foot drop.
• Toe Walking: Tests ankle plantar flexor strength (S1/S2, gastrocnemius/soleus).
• Focused Neurological Exam: Assess strength, tone, reflexes (pyramidal signs), sensation (especially vibration/proprioception), coordination (finger-nose, heel-shin for dysmetria), tremor.
• Focused Musculoskeletal Exam: Assess joint range of motion (especially hips, knees, ankles), check for contractures, leg length discrepancy, joint instability, tenderness, muscle strength (MMT), especially hip abductors, extensors, knee extensors, ankle plantar/dorsiflexors.
• Vestibular Exam: If indicated (e.g., Dix-Hallpike for BPPV, head impulse test).
• Cognitive Screen: Especially if higher-level disorder suspected.

Investigations

Following a thorough clinical examination, investigations are directed by the suspected underlying cause of the gait disturbance. The goal is to confirm the diagnosis, identify the specific pathology, and guide management. Common investigations include:

Blood Tests: These can help identify systemic causes contributing to gait problems. Examples include:

• Complete Blood Count (CBC): To check for anaemia.
• Vitamin B12 and Folate levels: Deficiency can cause sensory ataxia and spasticity (subacute combined degeneration of the cord).
• Thyroid Function Tests (TFTs): Hypothyroidism can cause ataxia or myopathy.
• Blood Glucose/HbA1c: To screen for diabetes, a common cause of peripheral neuropathy.
• Inflammatory markers (ESR, CRP): May be elevated in inflammatory conditions affecting joints or the nervous system.
• Creatine Kinase (CK): Elevated in muscle diseases (myopathies).

Neuroimaging: Essential for identifying structural lesions in the central nervous system.

• MRI Brain: The investigation of choice for suspected stroke, multiple sclerosis, tumours, cerebellar degeneration, Parkinsonism (may show specific patterns or rule out mimics), and normal pressure hydrocephalus (NPH).
• MRI Spine: Used to evaluate for spinal cord compression (disc herniation, stenosis, tumour), myelitis (inflammation), or syringomyelia.

• Musculoskeletal Imaging: To assess bones, joints, and soft tissues.
  • X-rays: Useful for evaluating arthritis, fractures, bony deformities, or limb length discrepancy. Weight-bearing views are often preferred.
  • CT/MRI of Joints/Limbs: Provide more detailed views of joint structures, cartilage, ligaments, and muscles if specific joint pathology or soft tissue injury is suspected.

Neurophysiological Studies: Assess the function of the peripheral and central nervous system pathways.

• Nerve Conduction Studies (NCS) and Electromyography (EMG): Crucial for diagnosing peripheral neuropathy, radiculopathy (nerve root compression), neuromuscular junction disorders (e.g., myasthenia gravis), and myopathy (muscle disease). Helps differentiate nerve vs. muscle problems causing weakness (e.g., steppage gait, waddling gait).
• Evoked Potentials (e.g., Somatosensory Evoked Potentials - SSEPs): Can assess the integrity of sensory pathways in the spinal cord and brain, particularly useful if posterior column dysfunction (sensory ataxia) is suspected.

Lumbar Puncture (LP): Involves analysing cerebrospinal fluid (CSF). Indicated if infection (meningitis, encephalitis), inflammation (multiple sclerosis), or specific conditions like NPH (therapeutic trial of CSF removal) are suspected.

Vestibular Laboratory Testing: Performed in specialised centres if a peripheral (inner ear) or central vestibular cause for disequilibrium is suspected based on history and examination (e.g., vertigo, nystagmus).

Formal Gait Analysis: Specialised laboratories use motion capture systems, force plates, and surface EMG to provide detailed quantitative data on gait kinematics and kinetics. This is typically reserved for complex cases, pre-operative planning, or research purposes.

Resources

Neurological gait assessment - Mermelstein 2023.pdf - 1.1 MB (f)

Normal Gait - Armand 2015.pdf - 785 KB (f)

Literature Review

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