Disorders of gait and station
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Disorders of gait and station

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Disorders of gait and station Disorders of gait and station Presentation Transcript

  • Dr. Sumit Kharat
  • Prevalence, Morbidity and Mortality  Gait disorders has been described in 15% individuals     older than age 65 yrs By the age 80 yrs 1 in 4 person will require mechanical aid to assist ambulation. 30 % of those with age >65yr fall every year 8% of those with age >75 yrs suffer serious fall related injury One in five elderly limit activity voluntarily because of fear of falling.
  • Physiology of gait  Station is the way patient stands and gait is the way patient walks.  In human, bipedal gait and erect position over narrow base require more efficient maintenance and control of equilibrium and have more complex mechanism than quadruped animals.  Standing may be considered a postural reflex mechanism mediated through brainstem.
  • Various CNS centres and their role  “Central pattern generators’’ in spinal cord and brainstem found in lower animals.  These are group of interneurons that co-ordinate with motor neurons to produce patterned movements like walking.  Their existence is unproven in human but locomotion likely depends on their activity.  Their activity is modulated by higher centres in subthalamus and mid-brain especially pedunculopontine nucleus through reticular fibres.
  •  Command and control centres in brainstem, cerebellum and forebrain modify action of spinal pattern generators to promote stepping.  Step generation is dependant on locomotor centres in pontine tegmentum, midbrain and sub thalamic regions.  Locomotor synergies are established through reticular formation and descending pathways in ventromedial spinal cord.
  • Cerebral control  Goal and purpose of walking.  Avoidance of obstacles.  Adaption of locomotor programme to context and terrain.
  • Postural control  Maintenance of centre of mass over base of support through the gate cycle.  Unconscious postural adjustments  Vestibular nuclei and midline cerebellum contribute to balance control.
  • Sensory information for postural control primarily generated by Visual system 2. Vestibular system 3. Proprioceptive receptors in muscle spindles and joints 1.
  • Gait  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.  For a single limb it comprises of 4 events  Initial contact>>>Stance phase>>Pre-swing phase >>Swing phase  Periods of single limb support alternates with periods of double limb support.
  •  Various parameters to measure gait are gait velocity,     stride time, stride length and step length. A typical adult walking on a level surface has velocity 80 m/min, 113 steps /min, stride length – 1.41 m. 60% stance phase+ 40% swing phase+ 10%double limb support. Centre of mass of human body is located just anterior to the s2 vertebral body. An effective gait has minimal displacement of centre of mass.
  • Examination of station  Patient asked to stand with feet closely together.  Stand with eyes open and eyes closed.  One foot at a time  On toes and heels  Tandem with one heel in front of other.  Light push.
  •  Cerebellar disease there is broad base and swaying.  Lesion in the vermis – swaying on backward, forward and either side.  Hemispheric lesion / unilateral vestibular diseasepatient sways or falls towards affected side OR  There may be tilting of the head towards the involved side with chin rotated towards sound side.  Patient will lose balance more easily when pushed towards involved side.
  •  Movement disorder may become apparent.  Skeletal abnormality- kyphosis, scoliosis. Lordosis.  Developmental anamolies  Hemiparesis- flexed and pronated upper extremities and extended lower extremity.  Parkinson’s disease- flexed posture, stooped over, with head and shoulder bent forward and arms and knees flexed.
  •  Depressed – stooped and dejected  Manic states- erect, aggressive posture  Schizophrenia- may assume bizarre posture and maintain it for long time.
  • Examination of Gait  Width of the base- normally medial malleoli should     pass within about 2 inches of each other during stride phase. Asymmetry of toe lift- foot drop. Stride length- shortened stride length may be early evidence of bifrontal or extra pyramidal disease. Decreased arm swing on one side may be early indicator of Hemiparesis or hemi parkinsonism. Tandem walking
  •  Movements of hip – excessive in proximal muscle weakness.  Brisk walk with abrupt stop and turn  Walking on heel and toes  To hop on either foot
  • Gait disorders  Neurologic  Non-neurologic  Non-organic
  • Etiology of gait disorders           Sensory deficits 18.3% Myelopathy 16.7% Multiple infarcts 15.0% Parkinsonism 11.7% Cerebellar degeneration 6.7% Hydrocephalus 6.7% Toxic/metabolic 2.5 Psychogenic 3.3% Other 5.0% Unknown cause 14.2%
  • Abnormal gaits 1) Cautious gait 2) Spastic gait 3) Parkinsonian gait 4) Hyperkinetic gait 5) Frontal gait disorders 6) Cerebellar ataxia 7) Sensory ataxia 8) Steppage gait 9) others
  • Cautious gait (senile gait)  Older patients  Non-specific  Abbreviated stride, lowered centre of mass, slow      velocity, short steps, wide base. No difficulty in foot-floor clearance, no shuffle, no difficulty with initiation of gait, no freezing. “walking on icy/ slippery surface” An adaptation to perceived postural threat Age related degeneration of sensory apparatus Physical therapy
  • Spastic gait (stiff legged gait)  A hemiparetic posture with arms flexed, adducted and     internally rotated. Plantar flexion of the foot on the affected side (equinus deformity). Holds arm tightly by side, rigid and flexed while walking. No arm swing. circumduction and hip hike, dragging and shuffling of the feet Upper motor neuron signs in physical examination.
  •  compromise of corticospinal command and overactivity of spinal reflexes. SPINAL CORD CAUSES  Myelopathy from cervical spondylosis  Demyelinating disease and trauma  hereditary spastic paraplegia  structural lesion -tumor or spinal vascular malformation.
  • With cerebral spasticity, asymmetry is common, involvement of the upper extremities is usually observed, and dysarthria is often an associated feature. Common causes include vascular disease (stroke), multiple sclerosis, and perinatal injury to the nervous system (cerebral palsy).
  • Parkinsonian Gait  Akinetic-rigid.  Rigidity, bradykinesia and loss of associated movements.  Stooped with head and neck forward, knees flexed.  Upper extremities usually flexed at shoulder, elbow and wrist. Fingers usually extended.  Slow, stiff and shuffling. Patient walks with small, mincing steps.  Involuntary acceleration (festination), decreased arm swing, en bloc turning, start hesitation, freezing when encountered an obstacle.
  •  Freezing of gait is even more common in some of the Parkinson's-related neurodegenerative disorders.  Progressive supranuclear palsy  multiple-system atrophy  corticobasal degeneration. These patients frequently present with axial stiffness, postural instability, and a shuffling gait while lacking the characteristic pill-rolling tremor of Parkinson's disease. Falls within the first year suggest the possibility of progressive supranuclear palsy.
  • Hyperkinetic movement disorders  Chorea, Huntington’s disease – abnormal movement become more marked when walking.  Huntington’s disease- gait may be grotesque, dancing or prancing with abundant erroneous movements.
  • Frontal gait disorder  "gait apraxia“  a shuffling, freezing gait with imbalance and other signs of     higher cerebral dysfunction. A wide base of support, short stride, shuffling along the floor, and difficulty with starts and turns. difficulty with gait initiation --"slipping clutch" syndrome. lower body parkinsonism- Strength is preserved, patients are able to make stepping movements when not standing and maintaining balance at the same time. a higher level motor control disorder.
  •  most common cause of frontal gait disorder is vascular disease, particularly subcortical small-vessel disease.  Lesions are frequently found in the deep frontal white matter and centrum ovale.  Binswanger’s disease  Communicating hydrocephalus.
  • Cerebellar Ataxias  a wide base of support, lateral instability of the trunk, erratic foot placement, and decompensation of balance when attempting to walk tandem.  Difficulty maintaining balance when turning and sudden stopping.  unable to walk tandem heel to toe.  Truncal sway in narrow-based or tandem stance.
  •  Two types of lesion 1) Lesion in cerebellar vermis – a lurching, staggering gait without laterality. 2) Hemispheric lesion – persistent swaying and deviation towards affected side. “compass deviation” or “star shaped gait” .
  •  Stroke  Trauma  Tumor  neurodegenerative disease- multiple-system atrophy hereditary cerebellar degeneration  fragile X pre-mutation  Alcoholic cerebellar degeneration.
  • Sensory ataxia  balance depends on high-quality afferent information from the visual and the vestibular systems and proprioception.  When this information is lost or degraded, balance during locomotion is impaired and instability results.  Joint position and vibration sense are diminished in the lower limbs. The stance in such patients is destabilized by eye closure; they often look down at their feet when walking and do poorly in the dark  Tabes dorsalis, SACD of spinal cord, sensory peripheral neuropathy.
  • Cerebellar ataxia Sensory ataxia Base of support Wide-based Narrow base, looks Wide-based down Velocity Variable Slow Very slow Stride Irregular, lurching Regular with path deviation Short, shuffling Romberg +/– Unsteady, falls +/– Heel shin Abnormal +/– Normal Initiation Normal Normal Hesitant Turns Unsteady +/– Hesitant, multistep +++ ++++ Postural instability + Frontal gait Poor postural synergies getting up from a chair Falls Late event Frequent Frequent
  • Steppage (equine) gait  Patient lifts one or both legs high during respective     stride phases FOOT DROP : Weakness of dorsiflexors of foot and toe. To prevent tripping patient compensates by lifting the foot as high as possible, hiking the hip and flexing the hip and knee. Double tap sound may be heard. SENSORY ATAXIA : patient lifts up feet then slaps them on the floor to improve proprioceptive feedback.
  •  CAUSES:  Unilateral – peroneal nerve palsy, L5 radiculopathy.  Bilateral- ALS, Charcot-Marie-Tooth disease, peripheral neuropathies and some muscular dystrophies.
  • Myopathic (waddling) gait  Weakness of hip girdle muscle.  Myopathy and muscular dystrophy.  Pronounced lordosis in case of weak hip flexors.  Trendelenberg’s sign - an abnormal drop of pelvis on the side of swing leg due to hip abductor weakness.  Bilateral weakness cause an exaggerated pelvic swing resulting inn waddling gait.
  • Toxic and metabolic disorders  Alcohol intoxication  chronic renal disease  hepatic failure  Sedative drugs, especially neuroleptics and long-acting benzodiazepines
  • Psychogenic Gait Disorder  Some patients with extreme anxiety or phobia walk      with exaggerated caution with abduction of the arms, as if walking on ice. Hysterical gait disordersOdd gyrations of posture wastage of muscular energy (astasia-abasia), extreme slow motion, dramatic fluctuations over time may be observed in patients with somatoform disorders and conversion reaction.
  • Thank you.