Skip to main content

Ataxic gait

This type of gait can be seen in cases of cerebellar or sensory ataxia.

Cerebellar ataxia and gait:

The problem here lies with the coordinating mechanisms in the cerebellum and its connecting systems. The gait is a clumsy, staggering, unsteady, irregular, lurching, titubating and wide-based. The patient may sway to either side, back or forward. Leg movements are erratic, and step length varies unpredictably.
The patient is unable to follow a straight line on the floor (to walk tandem).

With a lesion of the cerebellar vermis, the patient will exhibit a lurching, staggering gait but without laterality, the ataxia will be as marked toward one side as the other.
Cerebellar ataxia is present with eyes both open and closed; it may increase slightly with eyes closed but not so markedly as in sensory ataxia.

A gait resembling cerebellar ataxia is seen in acute alcohol intoxication.

With a hemispheric lesion the patient will stagger and deviate toward the involved side. In disease localized to one cerebellar hemisphere or in unilateral vestibular disease, there is persistent swaying or deviation toward the abnormal side. As the patient attempts to walk a straight line or to walk tandem he deviates toward the side of the lesion.
A patient with acute vestibulopathy will drift toward the involved side walking forward, and continue to drift during the backward phase. The resulting path traces out a multipointed star pattern. Walking a few steps backward and forward with eyes closed may bring out “compass deviation” or a “star-shaped gait”.
When attempting to walk a fixed circle around a chair, clockwise then counterclockwise, the patient will tend to fall toward the chair if it is on the side of the lesion, or to spiral out away from the chair if on the opposite side.

Either unilateral cerebellar or vestibular disease may cause turning toward the side of the lesion on the Fukuda stepping test. For all the tests that bring out deviation in one direction, other findings must be used to differentiate between vestibulopathy and a cerebellar hemispheric lesion. Unilateral ataxia may be demonstrated by having the patient attempt to jump on one foot, with the eyes either open or closed. The patient with bilateral vestibular disease may seek to minimize head movement during walking, holding the head stiff and rigid; having the patient turn the head back and forth during walking may bring out ataxia.

Sensory ataxia and gait:

The patient in this condition is extremely dependent on visual input for coordination. When deprived of visual input, as with eyes closed or in the dark, the gait deteriorates markedly. The difference in walking ability with and without visual input is the key feature of sensory ataxia. If the condition is mild, locomotion may appear normal when the patient walks eyes open. More commonly it is wide based, and poorly coordinated.

The term “steppage gait” refers to a manner of walking in which the patient takes unusually high steps. Sensory ataxia is one of the causes of a 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.” An additional sound effect may be the tapping of a cane, creating a “slam,slam, tap” cadence. The sound effects may be so characteristic that the trained observer can make the diagnosis by listening to the footfalls.

The patient with sensory ataxia watches her feet and keeps her eyes on the floor while walking. With eyes closed, the feet seem to shoot out, the staggering and unsteadiness are increased, and the patient may be unable to walk. There is less reeling and lurching in sensory ataxia than with a comparable degree of cerebellar ataxia. The difficulty is even worse walking backward, since the patient cannot see where she is going. The patient with bilateral foot drops, however, also has a steppage gait and a double tapping sound striking.

In all of these tests, sensory ataxia can be differentiated from predominantly cerebellar ataxia by accentuation of the difficulty with eyes closed; and unilateral cerebellar or vestibular disease from vermis involvement by laterality of unsteadiness.


Comments

Popular posts from this blog

Hypokalemia - Potassium replacement calculation

 DEFINITION  Hypokalemia is defined as a serum potassium level of less than 3.5 mmol/L. Normal level= 3.5-5.5 mmol/L. It is encountered in >20% of patients. Patients are usually asymptomatic but severe arrhythmias and rhabdomyolysis can occur. Non-specific complaints include easy fatiguability and skeletal muscle weakness. The preferred method of replacement is via the oral route but at times this is not possible. The article below will give you an idea about how to calculate the amount of KCl to be given I.V. 1) Potassium deficit in mmol is calculated as given below: K deficit  (mmol) = (K normal lower limit  - K measured ) x kg body weight x 0.4 2) Daily potassium requirement is around 1 mmol/Kg body weight. 3) 13.4 mmol of potassium found in 1 g KCl . ( molecular weight KCl = 39.1 + 35.5 = 74.6) Suppose we get an asymptomatic patient of  70 Kg with a serum potassium level of 3.0 mmol/L and he is on nil by mouth but having an adequate diuresis, w

The plantar reflex - Babinski's sign

The plantar response is an important test to identify an upper motor neuron lesion.  PROCEDURE  To elicit it, the muscles of the lower limbs must be relaxed. The outer edge of the sole of the foot is stimulated by firmly scratching a blunt object like a key or a stick along it from the heel towards the little toe. This is what  Joseph Babinski did in the year 1896. He described the 'great toe sign' that year and then in 1903 the 'toe abduction or fan sign'. Nowadays, a final medial movement across the sole of the metatarsus is also done. i.e. we start at the heel to the little toe and finally arcing to the big toe. The final arcing movement is absent in the original Babinski plantar response test. Babinski sign refers to a combination of 'the great toe sign' and the 'fan sign'.  SIGNIFICANCE  The normal response is plantar flexion of the toes (down going) and they are drawn together. More precisely, there is flexion of the big toe and addu

Differences between hyperemia and congestion

Hyperemia and congestion both indicate a local increased volume of blood in a particular tissue. Hyperemia is an active process that result from augmented blood flow due to arteriolar dilation (e.g. at sites of inflammation or in skeletal muscle during exercise). The affected tissue is redder than normal because of engorgement with oxygenated blood. Congestion, on the other hand, is a passive process resulting from impaired venous return out of a tissue. It may occur due to systemic causes like cardiac failure or a local cause like isolated venous obstruction. The tissue is cyanosed because the worsening congestion leads to accumulation of deoxygenated hemoglobin in the affected tissues. 

Apgar scoring - table, mnemonic

 INTRODUCTION  The  Apgar score  was devised in 1952 by Dr Virginia Apgar (anesthesiologist) as a simple and repeatable method to quickly and summarily assess the health of newborn children immediately after birth.  This helps to identify those requiring resuscitation and can also be used to predict survival in the neonatal period.   MNEMONIC  A mnemonic for learning purposes includes: A - Appearance (skin colour) P - Pulse (heart rate) G - Grimace (reflex irritability) A - Activity (muscle tone) R - Respiration  Another mnemonic is also useful:  How -   Heart rate Ready - Respiration Is -        Irritability This -    Tone Child -   Colour Apgar scoring is divided into 1 and 5-min scores.  1-MIN SCORE    Sixty seconds after complete birth, the five parameters specified in the table above must be evaluated and scored. A total score of 10 indicates that the baby is in the best possible condition. A score between 0-3 me

Chickenpox - dew on rose petal appearance

Definition: Chickenpox is a benign viral disease of childhood, characterized by an exanthematous vesicular rash. It is an extremely common and contagious condition. It is caused by the varicella-zoster virus which is a herpes virus and contains a double stranded DNA in its center. Epidemiology: Age group affected- 5 to 9 years. The infection can be there at other ages too but it is less frequent. It is highly contagious and it affects all races and both sexes equally. The attack rate is around 90% among seronegative persons. Pathogenesis: Incubation period- 10 to 21 days but is usually 14 to 17 days. Patients are infectious around 48 hours from onset of vesicular rash, during the period of vesicular formation (around 4-5 days) and until all vesicles are crusted. Transmission occurs by respiratory route. The virus is believed to be localized in the nasopharynx, in the reticulo-endothelial system. It then enters the blood. This stage of viremia is characterized by diffused ski