Gait disturbances are described as any deviations from normal walking or gait. Numerous etiologies cause these disturbances. Due to their different clinical presentations, a high index of suspicion is required. The etiology can be determined through the clinical presentation, laboratory work, and diagnostic testing. Gait problems can be subdivided into episodic and chronic disturbances. Continous or chronic gait disturbances are those that the patient had adapted due to the chronicity of the neurological dysfunction. Episodic disturbances include those that occur suddenly, and the patient has not adapted to them and is a frequent cause for complications like unexpected falls. Examples of episodic disturbances include freezing gait, festinating gait, and disequilibrium. Most other gait disturbances belong to the chronic category.
Neurological causes are more common than non-neurological causes. Sensory ataxia caused by polyneuropathy, parkinsonism, subcortical vascular encephalopathy, and dementia is among the most common neurological causes. Hip and knee osteoarthritis causing pain and limit motion are common non-neurological causes of gait disorders. Gait disturbances have a tremendous impact on patients, especially on the quality of life, morbidity, and mortality.
Numerous diseases affect both the central and peripheral nervous systems, which ultimately affect gait. Due to the intricacies in the communications between these two systems, even subtle changes can lead to gait disturbances. Disease states, including Parkinson's, Huntington's, normal pressure hydrocephalus, can alter the neurocognitive functions to the point that walking can become a difficult task. The weakness of the hip and lower extremity muscles commonly cause gait disturbances. Cerebral palsy, muscular dystrophy, Charcot Marie Tooth disease, ataxia-telangiectasia, spinal muscular atrophy, peroneal neuropathy, and microvascular white-matter disease all cause significant gait disabilities.
Electrolyte disorders include hyponatremia, hypokalemia, and hypomagnesemia can cause gait disorders. Hyponatremia, being one of the most common, can lead to severe neurological symptoms that affect gait. Electrolyte balance is crucial to maintaining the proper musculoskeletal function, which contributes directly to normal gait.
Common vitamin deficiencies contributing to gait imbalances include folate, vitamin B12, vitamin E, and copper deficiency. The deficiency of these vitamins has been shown to cause neurological dysfunctions, which impede proper gait. Vitamin B12 deficiency, which causes subacute combined degeneration of the spinal cord, can lead to numbness and paresthesia, which ultimately affect gait.
Pain, vascular, traumatic, autoimmune, inflammatory (vasculitis), metabolic, neoplastic, paraneoplastic, and tabes dorsalis may be involved.
Anxiety, depression, and malingering have to be excluded.
Studies have demonstrated that gait disturbances occur as an individual age; these disturbances stemming from neurological and non-neurological causes. Studies have shown that while 85% of individuals 60-year-old have a normal gait, by the time they reach the age of 85, only 20% maintains normal gait. Gait disturbances are not commonly seen in the younger population unless they stem from a developmental or musculoskeletal etiology. No differences in incidence or prevalence between males and females have been found. Men had more neurological gait problems, while women had more non-neurologic gait problems.
The pathophysiology of gait disturbances is complex. Normal gait involves a gait cycle that has a stance phase and a swing phase. When one limb swings, the contralateral limb stance. The duration in each phase varies depending on the velocity of gait and can be altered in different gait disturbances. Normal gait is a combination of central nervous system control, as well as peripheral nervous system feedback.
Initially, the normal physiology must be delineated to understand how deviations from this norm contribute to gait disturbances. At rest, in the erect position, an individual relies on sensory feedback to maintain its center of gravity. Postural control is an essential component of gait. It depends on the integration of sensory inputs and spatiotemporal coordination. Postural control is influenced by the integration of visual, vestibular, and somatosensory information. With age, these inputs are reduced, worsening normal gait.
Gait occurs in a cycle from initiation of the first leg heel strike to termination with the next heel strike to propel the movement of an individual. Hip flexion changes the limb from a standing position to the swing position. The central nervous system interprets the position of an individual and helps balance the individual. When any part of the central nervous is diseased, this can lead to improper processing and lead to an unsteady gait, because the center of balance is thrown off. Cerebellar ataxia produces postural deficits in a quiet stance before voluntary limb movements are initiated. Integration of the spinal interneuronal network with the brainstem, cerebral cortex (motor and premotor), and cerebellum centers produce normal gait.
The typical presentation of gait disturbances may be apparent on the clinic exam. However, it may be subclinical. Therefore the entire clinical picture must be taken into account. An extensive history of the patient is required. Social history, as well as medical history, is critical in the evaluation. Understanding how long the symptoms have been present is essential, as well as determining whether the onset was sudden or insidious. Merely taking a history of the patient's symptoms can help narrow down the etiology of the gait disturbances. Understanding different aspects of a patient’s social history are important, specifically, their diet, ability to perform daily activities of living, and physical limitations.
Clinical examination should include:
The examination can separate gait disturbances in two categories; musculoskeletal or neuromuscular (lower motor neuron and upper motor neuron).
1. Antalgic Gait:
2. Vaulting gait: It can be real or apparent. Is common in children with limb length discrepancy
1. Trendelenburg gait: pelvis drops to the unaffected side
2. Posterior lurch gait: backward trunk lean with hyperextended hip during the stance phase of the affected limb
3. Knee buckling - genu recurvatum: posterior capsule locks affected knee joint, hyperextending knee by forwarding trunk leading
4. Steppage gait: unable to heel strike causing initial contact with toes (foot drop)
5. Calcaneal gait: knee flexion movement with excess tibial motion over ankle during mid to late stance
6. Waddling gait: toe walking (posterior lurch and bilateral Trendelenburg)
7. Scissor gait (Crouched gait): Cerebral palsy
8. Ataxic gait: broad-based, unsteady
9. Sensory ataxic gait (stomping gait): Romberg’s test positive. Vitamin B12 deficiency. The patients use visual control to compensate for the loss of proprioception
10. Hemiparetic gait (hemispastic): gait is slow, with a broad base, knee, and hip are extended, during the swing phase, the paretic leg performs a lateral movement (circumduction)
11. Festinating gait (Shuffling gait): short stepped, hurrying, with weak arm swing, or naturally very slow (parkinsonian), in some patients with freezing and slow turning
12. Apraxic frontal gait (Apractic or Bruns apraxia): gait ignition failure, or with walking difficulty (‘Marche à petit pas’). Bifrontal lesions
13. Hyperkinetic gait: (chorea, dystonia, Wilson disease)
14. Freezing gait: (Parkinson's disease) typically occur on turning or when approaching obstacles or narrow passages such as doors. Can fall easily
15. Neurogenic claudication: (spinal stenosis) bending forward to relief pressure - flexed position
16. Intermittent claudication: (peripherovascular disease), the patient stops walking
17. Myelopatic gait: (spastic) stiff gait
18. Propulsive gait: center of gravity anterior to the body
19. Magnetic gait: NPH slow and unsteady turns, slow, broad-based, short-stepped, "stuck to the floor," or "glued to the floor" words are often used
20. Paraspastic gait: the gait may appear stiff and insecure, narrow-based, stiff, toe-scuffing (spastic paraparesis)
21. Myoclonic gait: short-lasting, involuntary jerks that result in the movement of a joint
22. Thalamic astasia: fall backward or to the contralateral side while sitting or standing caused by thalamic lesions or stokes
23. Higher-level gait disorders: microvascular white-matter disease, small steps and disequilibrium due to alterations in the balance-locomotor circuits (cortex, brainstem, and cerebellum)
24. Psychogenic gait: rarely falls, bizarre walking, lack of persistence of a symptom or sign
Observation can provide a tremendous amount of feedback concerning the etiology of someone’s gait disturbance. Observing a patient’s tendencies during gait cycles, as well as identifying where they are compensating, is essential. Testing of joint motion, joint pain, extremity force, and coordination are all necessary. Knee, ankle, and foot coordination must be precise.
Laboratory tests are particularly relevant to rule out any metabolic disturbances or vitamin deficiency. A complete blood count and comprehensive metabolic panel can reveal most deficiencies. If the clinical suspicion is high enough, further laboratories can be drawn and evaluated. Testing with imaging is vital to diagnose structural causes of gait disturbances. Imaging modalities are chosen based on the patient’s symptoms.
Treatment of gait disturbances initially involves diagnosing the underlying cause. A proper diagnosis leads to more accurate treatment plans. These plans can require a multi-faceted approach incorporating, physiotherapy, medications, and deep brain stimulation. The treatment plans range in complexity based on the severity of one’s symptoms and where they stem.
Patients with vitamin deficiency can be educated and prescribed proper supplementation to increase their body’s levels. Following up with routine laboratory work is essential in these patients to ensure therapeutic levels of vitamins are reached. Similarly, lifestyle modifications can be employed to ensure that patients are repleting nutritional deficiencies through the foods they consume. Patients with neurologic causes of gait disturbances can be treated with medications to provide symptomatic relief as well as increasing neurotransmitter levels to improve gait.
Most of the improvements have been made with Parkinson's disease with effective medications, deep brain stimulation at the subthalamic nucleus, and allied healthcare gait improvement techniques (external cueing physiotherapy intervention which uses visual and auditory cues aimed at improving gait, treadmill walking, cognitive training, and home-based exercise programs). Intensive coordinative training on posture and gait is used in degenerative cerebellar disease.
Patients can benefit from multimodal rehabilitation, gait training, use of assistive devices, and fall prevention measures. Commonly used exercise interventions such as muscle strength, power, and resistance training, as well as coordination training, can improve routine and maximum gait speed in the elderly.
The suspicion of gait disturbances demands a broad differential encompassing numerous etiologies. The following potential causes should be ruled out and to come up with a final diagnosis.
Neurologic: Parkinson, dementia, delirium, stroke, cerebellar dysfunction, multiple sclerosis, amyotrophic lateral sclerosis
Metabolic: Diabetes mellitus, encephalopathy, obesity, vitamin B12 deficiency, uremia
Psychiatric: Substance abuse, depression, anxiety, malingering
The prognosis of gait disturbances depends on the etiology. Metabolic etiologies of gait disturbances have a relatively good prognosis. If the metabolic disorder is addressed, patients mostly recover without lasting symptoms. Some neurologic diseases often have no cure and must be treated symptomatically. Often neurologic disorders worsen over time, and medications become inadequate for managing symptoms.
The risks of having gait disturbances should be explained to the patient, so they are aware. These risks include:
Patient education and counseling, according to the patient's need, is a multidisciplinary team effort for better management and outcomes.
Gait and posture are extremely important for the quality of life of a patient. A normal gait leads a patient to functional independence. Patient education is a vital part of identifying gait disturbances; early detection can lead to better outcomes and prevent complications. Corrective rehabilitation, gait training, use of assistive devices, and fall prevention measures should be implemented.
Identifying patients with gait disturbances requires a high index of suspicion. A wide range of specialties and professions contribute to the proper diagnosis of gait disturbance. Initially, the caretakers who interact daily with patients should monitor for acute changes in the patient’s gait. Patients need to observe if they lose the ability to perform daily tasks, such as ambulating to the bathroom unassisted. Physicians should observe gait during a physical examination to identify any changes. Nursing staff who may be interacting with patients more directly should observe any gait changes in their patients. Medications should be reviewed by the specialists and nursing staff to ensure there are no interactions between drugs, which can cause a gait disturbance. Patients should engage in open dialogue with their caretakers, noting any specific changes in lifestyle or diet, which may help uncover the etiology for their gait disturbance.
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