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Gait -Normal and Abnormal gait :Physiology and Management

  2. References  Dejong  Jankovic  Neurological disorders of gait, balance and posture: a sign-based approach (NATURE REVIEWS | NEUROLOGY)  Neurological gait disorders in elderly people: clinical approach and classification (Lancet Neurol)  Gait Disorders ( Fasano, MD, PhD; Bastiaan R. Bloem, MD, PhD)  Gait disorders in adults and the elderly A clinical guide (Walter Pirker · Regina Katzenschlager)  Higher-Level Gait Disorders: An Open Frontier John G. Nutt, MD*
  3. Contents  Definition  Requirements Of Normal Gait  Physiology Of Gait  Classification Of Gait Disorders  Clinical Assessment Of Gait Disorders  Rules In Gait Disorders  Treatment Of Gait Disorders
  4. Definition  Station is the way a patient stands and gait the way she walks  Stance is the posture of standing  Balance is the ability to maintain stance without falling or excessive lurching (Benvenuti, 2001)
  5. Introduction  The prevalence of gait and balance disorders markedly increases with age, from around 10 % between the ages of 60 and 69 years to more than 60 % in those over 80 years  Greatly affect the quality of life and restrict the personal independence of those affected  Balance and gait problems may be precursors of falls, which are the most common cause of severe injuries in the elderly . Ebersbach G, Sojer M, Muller J, Heijmenberg M, Poewe W. Sociocultural differences in gait. Mov Disord. 2000;15(6):1145–7
  6. 3 Components and 3 Systems 3 Components  Locomotion  Balance  Ability to adapt to environments 3 Systems (Normal gait requires a delicate balance between various interacting systems)  Efferent motor (including nerves, muscles, bones, joints, and tendons)  Afferent sensory (visual, vestibular, and proprioceptive senses)  Surveillance by higher centre
  7. Requirement of normal gait
  8. Frequency of etiologies of neurologically referred undiagnosed gait disorders  Sensory deficits 18.3%  Myelopathy 16.7%  Multiple infarcts 15.0%  Unknown 14.2%  Parkinsonism 11.7%  Cerebellar degeneration 6.7%  Hydrocephalus 6.7%  Psychogenic 3.3%  Other 7.5% In: Masdeu J, Sudarsky L, Wolfson L, eds. Gait Disorders of Aging: Falls and Therapeutic Strategies. Philadelphia: Lippincott-Raven; 1997, pp. 147– 158,
  9. Neurophysiology of Gait
  10. Cognitive information processing
  11.  The movements are generated by a locomotor generator in the spinal cord, but they are under control by supraspinal mechanisms  The spinal cord generator can produce only simple, primitive stepping (Burke, 2001)  Supraspinal mechanisms are required for a person to go in desired directions, with desired velocities and to deal well with perturbations
  12.  The pattern generators control the activity in lower motor neurons that execute the mechanics of walking  Higher centers in the subthalamus and midbrain, particularly the pedunculopontine nucleus, modulate the activity in the spinal cord pattern generators through the reticulospinal tracts
  13.  Aim of this study –to understand the role of the supplementary motor area (SMA) and posterior cerebellum in the gait initiation process  Procedure -Gait initiation parameters were recorded in 22 controls both before and after continuous theta burst transcranial stimulation (cTBS) of the SMA and cerebellum, and were compared to sham stimulation  The two phases of gait initiation process were analyzed: anticipatory postural adjustments (APAs) and execution, with recordings of soleus and tibialis anterior muscles
  14.  Functional inhibition of the SMA led to a shortened APA phase duration with advanced and increased muscle activity; during execution, it also advanced muscle co-activation and decreased the duration of stance soleus activity  Cerebellar functional inhibition did not influence the APA phase duration and amplitude but increased muscle co-activation, it decreased execution duration and showed a trend to increase velocity, with increased swing soleus muscle duration and activity
  15. Conclusion  The results support distinct roles for the SMA and the lateral posterior cerebellum in human gait initiation, with the SMA coding for the timing, and probably amplitude, of the preparatory phase of the gait initiation, and the posterior cerebellum contributing to the inter- and intra-limb muscle coordination, and probably coupling between the APAs and the execution phases
  16. Gait Cycle  The gait cycle refers to the events that transpire between the time that one heel strikes the ground and the time the same heel strikes the ground again
  17. The functional task during the stance phase is to bear weight; the functional task during swing phase is to advance the limb
  18. Basic terminology  Step width-The distance between the two feet at the perpendicular axis to the walking direction for a given step  Step height -The maximum distance between the forefoot and ground during the swing time  Step length: The distance advanced by one foot compared to the position of the other  Stride length: The sum of two consecutive step lengths or the distance advanced by one foot compared to its prior position
  19. Basic terminology
  20. Basic terminology  Stance time: The time that the foot is on the floor, measured as the time between heel strike and toe or heel off, whichever is last  Swing time: The time that the foot is in the air, measured as the time between toe off and heel strike  Cadence: The number of steps per minute  Step time: The time from heel strike of one foot to the subsequent heel strike of the contralateral foot.
  21. Normal adult walking  Walks at a velocity of about 80 m/min,taking about 113 steps per minute,Stride length of 1.41 m  About 60% of the gait cycle is spent in stance, 40% in swing, and 10% in double limb support
  22. Body’s center of mass  This located just anterior to the S2 vertebral body  An efficient gait minimizes the displacement of the center of mass by rotating and tilting the pelvis and flexing and extending the various joints involved.
  23. Classification Of Gait Disorders
  24. J.G. Nutt, MD; C.D. Marsden, DSc; and P.D. Thompson, MD
  25. Clinical Assessment of Gait Disorders
  26. History in gait  Temporal Nature Continuous Episodic, which can be subdivided into: Random (eg, paroxysmal dyskinesias) Pseudoperiodic (after a given amount of steps, eg, freezing of gait, claudication)  Type of Onset and Progression Sudden (eg, stroke) Insidious (eg, neurodegenerative disorders) Step-wise (eg, vascular parkinsonism)  Walking Worse in the Dark? Yes (consider sensory ataxia or vestibulopathy) No
  27. History in gait  Use of Walking Aids? Yes (consider latency to using aids: months versus years) No (if not, why not? Embarrassment or inability? Consider higher-level gait disorder)  Medical History Prior/current diseases Psychoactive medications Intoxication (alcohol)  Protective Factors Exercise/fitness level Amount of daily walking Adaptation of behavior/activities
  28. Anke H Snijders, Bart P van de Warrenburg, Nir Giladi, Bastiaan R Bloem
  29. Fall History  Frequency of prior falls and near-falls Single (in absence of extrinsic cause, search for risk factors) Recurrent  Specific fall pattern?  Apparent cause of the fall(s): None (spontaneous, consider intrinsic causes) Extrinsic (environmental, eg, slippery floor)
  30. Fall History  Intrinsic (patient-related) Symptoms preceding the fall: Loss of consciousness (consider syncope, epilepsy, or psychiatric conditions) ‘‘Funny turns’’ (vertigo, presyncope) Palpitations, chest pain, breathlessness Sudden weakness of the legs (drop-attack, cataplexy) Behavior: Performing several activities simultaneously Hazardous behavior Inappropriate footwear
  31.  Symptoms after the fall: Confusion (consider epilepsy) Inability to stand up Physical injury Fear of falling
  32. Signs based examination
  33. NATURE 2018
  34. Signs based examination  Sitting  Rising from chair  Quite standing  walking
  35. Sitting  Leaning sideways  Drifting backwards  Forwards dropping of the head  Backwards dropping of the head
  36. Disproportionate Antecollis In Msa (the lancet 1989)  The clinical picture of a severely aphonic parkinsonian patient with chin-on-chest, and with a poor response to levodopa, should therefore lead to consideration of a possible diagnosis of MSA.
  37. 2.Rising from chair  Inappropriate motor strategies  Slow ,requiring multiple attempts, or needing to push off with arms  Reckless rising  Shaking of leg upon standing  Leg wide apart while arising
  38. 3.Quiet standing (eyes open)  1.Normal to narrowed base of support  2.Widened base of support  3.Progressive instability  4.Excessive spontaneous sway  5.Leaning or drifting sideways  6.Excessive trunk flexion that persist when lying down  7.Excessive trunk flexion that disappears when lying down 
  39. Step length, height and cadence  Reduced step height –PD ;foot drop  Small step –Pain(orthopaedic disorders),PD, atypical parkinsonism, NPH  Irregular step size-Cerebellar ataxia, vestibular ataxia, chorea, higher level of gait disorders  Reduced stance phase on affected side(limping) –pain (trauma ,arthritis ,functional gait disorders )
  40. Gait speed  Slow (Nonspecific) –PD, higher–level gait disorders, functional, pain  Fast, safe- Vestibular syndrome, orthostatic tremor  Fast ,unsafe- AD, frontal disinhibition
  41. UMN GAIT  Circumduction Gait  Scissoring Gait  Cerebral Diplegic Gait  Cervical Myelopathic Gait
  42. Hemiparetic gait  Caused by a unilateral lesion interrupting the corticospinal pathways  The patient stands with a hemiparetic posture, arm flexed, adducted, and internally rotated, and leg extended  With each step, the pelvis tilts upward on the involved side to aid in lifting the foot off the floor (hip hike)and during swing phase, the entire extremity sweeps around in a semicircle from the hip (circumduction)  Loss of normal arm swing and slight circumduction of the leg -mild hemiparesis
  43. Hemiparetic gait
  44. Spastic gait / Scissoring gait  Bilateral hemiparetic gait affecting the legs  There is characteristic tightness of the hip adductors  Walks on an abnormally narrow base, with a stiff shuffling gait, dragging both legs and scraping the toe  The shuffling, scraping sound— together with worn areas at the toes of the shoes—are characteristic  Patients to walk on tiptoe  Congenital spastic diplegia (Little’s disease, cerebral palsy), chronic myelopathies
  45. Scissoring gait
  46. The Spastic-Ataxic Gait  Involvement of both the corticospinal and the proprioceptive pathways  The ataxic component may be either cerebellar or sensory  In vitamin B12 deficiency, it is predominantly sensory; in MS, both components may be present
  47. Cerebellar Ataxia  The only sign of mild ataxia may be the inability to walk tandem  A clumsy, staggering, unsteady, irregular, lurching, titubating, and wide-based gait, and the patient may sway to either side, back, or forward  Leg movements are erratic, and step length varies unpredictably  Walking a few steps backward and forward with eyes closed may bring out “compass deviation” or a “star-shaped gait”  Either unilateral cerebellar or vestibular disease may cause turning toward the side of the lesion on the Unterberger-Fukuda stepping test
  48. LMN GAIT  High Steppage Gait  Waddling Gait  Dragging Gait  Quadriceps Gait
  49. Waddling Gait  Myopathic gaits occur when there is weakness of the hip girdle muscles  If the hip flexors are weak-pronounced lordosis  The hip abductor muscles are vital in stabilizing the pelvis, while walking  Trendelenburg’s sign is an abnormal drop of the pelvis on the side of the swing leg because of hip abductor weakness  When the weakness is bilateral, there is an exaggerated pelvic swing that results in a waddling gait.
  51. Gaits Associated with Focal Weakness  With paralysis of the gastrocnemius and soleus muscles, the patient is unable to stand on the toes  In weakness of the quadriceps muscle (e.g., femoral neuropathy), there is weakness of knee extension, and the patient can only accept weight on the affected extremity by bracing the knee  Lumbosacral radiculopathy may cause either foot drop or a unilateral Trendelenburg’s gait, or both
  52. High Steppage Gait  The patient takes a high step, throws out her foot, and slams it down on the floor in order to increase the proprioceptive feedback  The heel may land before the toe, creating an audible “double tap.”  Unilateral steppage gait - peroneal nerve palsy and L5 radiculopathy  Bilateral steppage gait -ALS, CMT and other severe peripheral neuropathies, certain forms of muscular dystrophy
  53. Cock walk gait  High stepping gait  Strutting on toes  Flexed elbows and erect spine  Seen in manganese toxicity (welders),methcathinone poisioning ,PANK associated neurodegenration ,SCA3
  54. Cock walk gait
  55. Dromedary gait  Rolling ,high Stepping gait with protrusion of buttocks due to excessive lordosis  Seen in patients with generalised dystonia especially DYT1 primary dystonia
  56. Hobby Horse Gait  Toe walking ,stiff legs and skipping gait  Seen in DYT4 due to TUBB4a mutation  Begins as whispering dysphonia and dystonia generalises
  57. Hobby Horse Gait
  58. Choreic Gait  Dancing gait  Represents the superimposition of chorea on the locomotor movements  Stepping is also uncoordinated and appears dysmetric like an ataxic gait
  59. Choreic Gait
  60. Freezing  Motor blocks  Characterized by lack of movement with the feet looking like they are glued to the floor (Snijders et al., 2008)  Patients often look like they are trying to move, but they cannot  Can occur when trying to initiate gait, in which circumstance it has also been called “start hesitation”
  61. Pathophysiology Of Freezing  Defective bilateral coordination of stepping (Plotnik et al., 2008)  There is an association of freezing with loss of frontal lobe executive function (Amboni et al., 2008)  Sequence effect where sequential movements become progressively smaller (Iansek et al., 2006; Chee et al., 2009)
  62.  In addition to the absence of movement, another form of Freezing is characterized by rapid, side-to-side shifting of weight, but no lifting of the feet and no forward progression (“slipping clutch syndrome”)  IPD,PSP, Vascular parkinsonism and normal pressure hydrocephalus  It seems less common in MSA and drug-induced parkinsonism (Giladi, 2001).
  63. Additional test Helps to differentiate  Turning of head during gait –Worsening of gait seen in vestibular ataxia  Walking backwards compared to walking forwards –Discrepant features seen in Dystonia and functional gait disorders (inconsistency )  Tandem walking –impaired in atypical PD  Better running than regular walking—Dystonia ,PD, functional gait disorders
  64. Detection of symptoms –  Rapid 360 turn on the spot-Evoked FOG in PD and atypical parkinsonism  Walking rapidly with short steps -Evoked FOG in PD and atypical parkinsonism  Pull test or push and release test –patients with postural instability responds with more than two steps
  65. The Romberg Sign  When proprioception is disturbed, the patient may be able to stand with eyes open but sways or falls with eyes closed (Romberg sign)  Turning the head side to side eliminates vestibular clues and increases the reliance on proprioception (Ropper’s refined Romberg test)  Some histrionic patients will sway with eyes closed in the absence of any organic neurologic impairment (false Romberg sign). The swaying is usually from the hips and may be exaggerated. If the patient takes a step, the eyes may remain closed, which never happens with a bona fide Romberg  The toes of the patient with histrionic sway are often extended; the patient with organic imbalance flexes the toes strongly and tries to grip the floor.
  66. Standardized Rating Scales Generic  Tinetti Mobility Index -Includes an evaluation of gait features and balance under challenging conditions ,Poor performance is associated with an increased risk of falls  Gait and Balance Scale  Berg Balance Scale Disease-specific  Eg, Freezing of Gait Questionnaire
  67. The Parkinsonian Gait  Rigidity, bradykinesia, and loss of associated movements  The patient is stooped, with head and neck forward and knees flexed; the upper extremities are flexed at the shoulders, elbows, and wrists, but the fingers are usually extended  The gait is slow, stiff, and shuffling; the patient walks with small, mincing steps  Other features include involuntary acceleration (festination), decreased arm swing, en bloc turning, start hesitation, and freezing when encountering obstacles such as doorways
  68. PD
  69. The highest-level disorders  Malfunction of the cerebral hemispheres  Include disorders arising from psychiatric origin, including cautious gait and psychogenic gait  These disorders are not completely distinct from each other; patients may have characteristics of more than one or may progress from one to another (Jankovic et al., 2001; Nutt, 2001; Thompson, 2001).
  70. Highest-level disorders  Cautious gait  Subcortical disequilibrium  Isolated gait ignition failure  Frontal gait disorder  Psychogenic gait disorder (PGD)
  71. Proposed terminology Previous terms Lesions Cautious Elderly and senile gait Musculoskeletal ,PNS,CNS Subcortical disequilibrium Tottering Astasia-abasia Thalamic astasia Midbrain Basal ganglia Thalamus Frontal disequilibrium Gait apraxia Frontal ataxia Astasia-abasia Frontal lobe and white matter connections Isolated gait ignition failure Gait apraxia Magnetic gait Slipping clutch gait Lower half parkinsonism Arteriosclerotic parkinsonism Trepidant abasia (Petren’s gait) Frontal lobe, white matter connections and basal ganglia Frontal gait disorder March A petits pas Magnetic gait apraxia Arteriosclerotic parkinsonism Parkinsonian ataxia Lower half Lower body parkinsonism Parkinsonism Frontal lobe and white matter lesions J.G. Nutt, MD; C.D. Marsden, DSc; and P.D. Thompson, MD
  72. Subcortical Disequilibrium  Severe impairment of balance (Masdeu, 2001)  Dysfunction at midbrain,basal ganglia,thalamic level  Often a feature of parkinsonism plus disorder  Also know as thalmic astasia
  73. frontal disequilibrium, isolated gait ignition failure, and frontal gait disorder, are frequently difficult to separate from each other
  74. Frontal Disequilibrium/Frontal Apraxic Gait /Bruns Ataxia  B/L frontal lobe disorders  Difficulty in stepping  Due to damage to front-pontocerebellar tract  The concept of apraxia comes from the observation that leg movements unrelated to walking seem reasonably good  Frontal lobe signs +
  75. Isolated Gait Ignition Failure  Difficulty in initiating and sustaining locomotion  The patient has freezing ,while initiating steps  The term Primary Progressive Freezing Gait has also been used (Factor et al., 2002)  Walk normally once they get started
  76. Frontal gait disorder  Short, shuffling steps, poor balance, initiation failure, and hesitations on turns  Differentiating features are a more upright stance, lack of tremor, frontal lobe signs, and apparent involvement of only the lower part of the body (Thompson, 2001)  This last feature gives rise to the term “lower half parkinsonism” or “lower body parkinsonism.”
  77. Etiologies -  Subcortical arteriosclerotic encephalopathy (Binswanger disease)  Multi-infarct state  Anterior cerebral artery stroke  Normal pressure hydrocephalus  Pick disease  Alzheimer disease, frontotemporal dementia  Subdural hematoma, brain tumors, multiple sclerosis,  Progressive supranuclear palsy (PSP), and corticobasal degeneration (Thompson, 2001).
  78. NPH Gait  Short stride length  Reduced foot clearance  Freezing  Gait apraxia
  79. Cautious gait/ “space phobia”  Walking on ice  There is a wide base with slow, short steps; turns are en bloc. Arms are tense  With support there is marked improvement
  80. Psychogenic gait  Astasia–abasia or Acrobatic gait  Unusual patterns of stance and gait  often dramatic, with lurching  falls are rare  Sudden knee buckling without falling is a common pattern  A suffering or strained facial expression, with moaning and hyperventilation (Lempert et al., 1991)
  81. Marché à petit pas  Walking with very short, often shuffling, steps  This is most typical of a multi-infarct state, but can be seen with parkinsonism
  82. HLGD  Anterior (frontal) and Posterior (Parietotemporo-occipital), a division that may have pathophysiological implications  Frontal or anterior HLGD is the most common form of HLGD  This pattern of HLGD is characterized by freezing of gait (FOG), small steps, and disequilibrium  Frontal HLGD, arose from dysfunction in the cortical basal ganglia loop
  83.  This frontal or anterior HLGD category encompasses gait disorders associated with the various parkinsonian syndromes, multi-infarct and subcortical small- vessel disease, normal-pressure hydrocephalus, and a multitude of other frontal lobe pathologies  Instead of the 5 categories originally proposed,2 clinical subcategories of anterior HLGD have been suggested, a predominantly disequilibrium subtype and a predominantly locomotor subtype
  84.  Predominantly locomotor problems are manifest as start and turn hesitation and FOG. If no etiology is apparent, this gait pattern is sometimes termed primary progressive FOG  Predominant disequilibrium as can occur in patients with progressive supranuclear palsy or frontal lesions
  85. Posterior HLGD  Are characterized by abnormalities in which the sense of postural vertical may be disturbed or other distortions of environment and body maps are present  This syndrome has been associated with parietal and thalamic strokes.
  86. Therapeutic considerations  Etiologic considerations  Symptomatic treatments  Physical therapy can help with strengthening exercises or practice with elemental coordination  Walking aids from canes to walkers
  87. Medical  Anti spasticity drugs -Baclofen, dantrolene, and tizanidine  focal spasticity-BoNT  Anticholinergics, baclofen, and BoNT can be used to treat dystonia  Antiepileptics and clonazepam for the treatment of paroxysmal dyskinesias and myoclonus
  88. Medical  Dopaminergic drugs-hypokinetic gait including freezing  Levodopa resistant FOG –Methylphenidate through noradrenergic mechanism  Improvement in PPFOG-Duloxetin(SNRI),high dose selegiline  Donepezil can be used in levodopa resistant FOG  The extended-release formulation of 4-AP (dalfampridine) dosed at 10 mg twice daily – improves walking in people with multiple sclerosis
  89. Treatment of falls  PD-Levodopa  Vestibular disease-Vestibular sedatives  Episodic ataxia-Acetazolamide  Fall associated with executive dysfunction-Methylphenidate, donepezil
  90. Surgical  DBS OF GPi is good alternative  VP Shunt for NPH patients  Dorsal rhizotomy for spasticity  Subthalamic nucleus stimulation improves off periods of freezing
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