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MOVEMENT COORDINATION AND ITS DISORDERS

Accuracy and smooth flow of arbitrary movement in achieved due to the interaction of
the cerebellum, basal ganglia and the cerebral cortex. However, in maintaining the
body balance and proper walking, one must not forget about the in lance of the
labyrinth, proprioceptor muscles and the sight. In case of lesion in any pad of nervous
system, it will lead to the disorder of movement coordination. The cerebellar and its
certain degree can be considered as center coordination impairment.

In the cerebellar there are 2 parts of hemisphere and vermis. Each hemisphere has the
cortex and in the depth of it, there are a couple of nuclei. There are fastigigian,
globules, emboliform, and dentate nucleus. All of the incoming impulses into the
cerebellar end in the cerebellar cortex.
Purkinje Cells of the cerebellar cortex sends afferent impulses from the cortex to the
deep nucleus. The cerebellar adjoins with the brain stem by its pair of the 3 pedicles:
superior cerebellar pedicles lie on the mid brain, middle at the level of pons ; inferior at
the level of medulla oblongata. Inferior of cerebellar penducles composed of fibres in
which the impulse pass thru to the cerebellum or exits from it.

There are 3 impulses pass into the cerebellum. From the vestibular nucleus of the
brain stem thru the cerebellar pediculus in which the afferent impulses goes to the
vestibulocerebellar (especially early in the philogenetics in relation with the cerebellar
parts) for balancing.
From the proprioreceptor of muscle and tendon, the afferentation of impulses in
spinocerebellar
tracts throught lower and upper pediculus in front part ofvermis and into
itsspinocerebellar zone, in which to provide posture (body position), regulation of the
muscular tones, and also accuracy of extremities movement.

From the cerebral cortex (especially the frontal lobe) thru cortico-pontinus tract and
also thru the middle part of cerebellum pediculus, the impulses in the middle part of
vermis and the hemisphere of cerebellum –neocerebellum, in which the coordination of
the movement start at the level of the cortex of the hemisphere.

Motor tract originates from the cerebellar cortex (main form if purkinje cells) goes
towards the deep nucleus and from them to the brain and some to thenuleus of brain
stem. The twice crossing over of the motor tract leads to, cerebellum affecting on the
motor function of the unilateral ends (the first
cross pass the fibre, going from cerebellum to the nucleus of the trunk and the cortex
of the cerebrum, and the Second crossroads is in the descending fibers from the
nucleus of the trunk and
cortex of the cerebrum to the spinal motor neurons).

Basic motor tract of the cerebellum consists of :


1. Crossing of dento-rubro-thalamic and dento-thalmic tract, going from the
superior pedicures and ending in the ventrolateral nucleus of the thalamus,
where it originates-from and goes to pre- and postcentral gyrus of the cortex.
2. Vestibular tract pass from lower pediculus to the vestibular nuclei and reticular
formation of the cerebral. In consequent to that, the cerebellum will affect the
motor neuron of the SC via descending tract of the motor cortex of the cerebral
hemisphere (cortico -spinocerebral tract) and nuclear trunk (rubro-spinocerebral
tract, vestibulo-spinocerebral and reticulo-spinocerebral tract).
To maintain the cerebellar coordination for movement, the whole things depends on
the returning between the cerebellum and the cortex of the cerebal hemisphere:
cortex of hemisphere of cerebrum(cortico -ponticular tract) -> nucleus of pons (ponti-
cerebellar tract) -> cortex of cerebellar (dentorubronucleo-thalamic tract) -> thalamus
(thalamo-corticocal tract) -> cerebral cortex hemisphere.
In that form, cerebellar receives info from different part of nervous system
(proprioceptor muscles and tendons , vestibular apparatus, cortex of the cerebrem)
and analyzes the system, modulate efferentation of impusle and heading to spinal
motor neuron throught the descending tract from the motor cortex of big hemisphere
and nucleuns . Cerebellum maintains balance, muscle tones, and the ability to
maintains accuracy.

Investigation of patients coordination.

1. To investigate the walking condition: request the patient to walk straight with

eyes opened and then followed by closing the eyes .


2. Patient to walk in single Iine, but the heels need to touch the toes closely until
the end. This investigation is called Tandem walking.
3. Also we can investigate by using the flank test - walking side by side and walk in
circles
Diagnose of gait by straight line and flank test.
a. On straight line, with eye closed, does five steps in straight line forward
and, without turning, five steps back. In vestibular analyzer disturbance,
patient fall from a direct line at the side defects.
b. Flank gait: patient puts aside the right leg to the right, then left and does
the same in five steps, and then the same in five steps on the left side. In
vestibular analyzer disturbance, flank gait well carried out in both side, at
cerebellar defect - cannot execute it at side defect (because of falling).

1. Romberg test- it is to check the stability of the patient.


Request the patient to put the feet together, lift the head up a bit, extend the
arms till its on the horizontal level by just standing with the eyes opened and
then with closed eyes.
To check for minimal disorder, one can use a more complicated form of
Romberg in which the patient needs to put one heel in front of the toes of the
other leg in a straight line.

2. Babinsky best: from lying position on the sofa or bed, the patient needs to get
up with arms crooks on the chest and the knees should not flex.
3. Finger nose test - request the patient to extend the arms forward. Then, the
index finger of one hand should touch the tip of the nose and followed by the
other hand. Begin with the eyes opened and only then the patient should do it
with eyes closed.
There are other types which is similar to the finger-nose. They are finger-
hammertip or finger to finger test.
4. To check for diadochokinesis, request the patient to bend hand at the elbow
level like at the
angle of 90 degrees. And then the patient has to do the pronation and
supination of both
hands as quickly as possible.
5. To check for any dysmetria or symmetrical movement, there are several tests
needed to be done.
a. Extend hand forward with the palm of the hand facing upwards and the
patient has to change the palms upward or downward according to the
instruction from the doctor.
b. Extend hands forward, eyes closed, and then raise arms upwards and
drop them to the
horizontal level.
c. Request the patient to take the hammer and take turn to squeeze the
wide part and the narrow part with both the index fingering the thumb.
6. Heel-knee test: in Iylng position on supine, ask the patient to lift one leg up and
put the heel on the knee of the other leg and slide it downwards and vice versa
with the other leg.

Symptoms of coordination disorder.

Abnormal in accuracy, smooth flow, and symmetrical movement, which is NOT DUE to
the decrease of
muscle strength (paresis). It is graded through the types of ataxia and discoordination.

Ataxia is manifested by walking disturbance (usually tandemic and phalangeal


walking), balance
disorders in standing position (Romberg test) and sitting, loss of accuracy, smooth
flow, and harmony in upper and Iower limbs, appearance of diadiadochokinesis and
symmetry and failing in finger-nose or
heel-knee tests.

Degree of ataxia varies from the slightest form as seen in the form of minimal
infringement at performance of special tests up to significant expressiveness that is in
the case of patients with loss of ability to walk, stand and do elemental stuff by
himself.

Types of ataxia (syndrome):


1. Cerebellar
2. Sensory
3. Frontal
4. Vestibular

Cerebellar Ataxia

Developed due to lesion in the cerebellum and its conducting pathways.


Basic manifestation:
1. abnormal coordination in limb movements
2. Balance and gait disorders (truncal ataxia)
3. Muscular hypotonic, dysarthria, and nystagmus.

Ataxia due to cerebellar lesion is express in forms of disorder in the smoothness,


accuracy, and symmetrical movements in the upon and lower extremities.

Patients usually find it hard to eat, write or put on clothes despite of still having normal
muscle strengh in the extremities. The slight degree of ataxia becomes more obvious
in fast-alternating movements.

1. Intentional tremor - Characteristics attribute to the cereballar lesion could be


seen relatively trough rhythmical fluctuation (tremor) of the fingers or legs
especially when they get closer to target objects, as had been observed in
finger-nose/finger-hammer/finger-finger and heel-knee test.
2. Rubral tremors - In any random movement of extremities and in during special
tests, we could observe thigh amplitude tremor in the proximal end because of
distinctive differences in the tremor intensity.
3. Dysdiadochokinesis - slow in dysdiadochokinesis test where the patient could
not alter-between supinating and pronation rapidly.
4. Dysmetria - Patient is unable to move as fast as before and the movements are
not sym trio
i. Fast and accurately to turn palm downwards and upwards while the whale
arms are stretched forward.
ii.The hand is lowered to the horizontal level accordingly, and then lifted
upwards c) Thumb and index finger of the hands takes turn in squeezing the
wide and narrow part of the hammer accordingly.

Discoordination leads to the jagged or crooked handwritings and sometimes the letters
are written
largely (macrography).

In the expressed degree of ataxia, the patient is unable to walk stand or sometimes
even-sit down without the help of others. In moderate ataxia the patient is unstable in
sitting and standing position, walking, and legs are set wide against is noticed that the
steps are not uniformed in length and direction (drunken style of walking). In unilateral
lesion, we can observe the declining condition in be same side of lesion of the
cerebellar hemisphere. In Romberg test, there is instability with eyes opened and it
gets worse with closed eyes but not so remarkable.In Babinsky test, patient is unable
to sit from lying position without using his hands to help himself because the legs will
rise above and makes it difficult - Babinsky asynergia.

In cerebellar lesion, we can observe speech disorder in patients in the form of


dysathria in the type of slow and mumbled speech or ''scanning speech'' or ''staccato
speech”. Scanning form of speech is the pathognomonic for cerebellar lesion.
Scanning speech – syllable of words are separated by noticeable pause
Staccato speech - each syllable is uttered separately.

In lesion of the midbrain, there might be rhythmical tremor of the head and trunk with
the frequency of 3-4 cycles per second/Hz (Titubation -. a tremor of the head and
sometimes trunk, commonly seen in cerebellum disease, slavering or stumbling gait
that is characteristic of certain nervous disorders.)

In cerebellar lesion, usually there is non arbitrary rhythmical movement of the eyeball -
nystagmus which can be graded like the peculiarities of intentional tremor of the eye
muscles. The nystagmus is usually horizontal when the eyes are looking toward one
side and its vertical nystagmus when the eyes look upward.

Sensory Ataxia

Developed due to lesion in conducting tract of muscular-joint sensation (peripheral


nerves, posterior root, posterior funiculus of spinal brad, thalamus, parietal lobe).
In sensitive ataxia:
• Abnormal balance
• Abnormal in accuracy of free limb movements
• Abnormal in muscular

Loss of sensation usually leads to hypotonic muscle and hyperreflexia and


subsequently will lead the disruption of peripheral or central segmental reflex. In full
loss of muscular-joint sensation, maintenance of balance control and walking becomes
impossible. In its partial loss, patient needs to set the legs wide apart, long steps that
are non uniformed has been observed, strong pressure on the surface of each step
taken, mismatch long steps and high lifting of the legs, usually noticeable loud tapping
footsteps. Coordination of movement is influenced by the vision control, that's why the
patient will concentrate hard on his legs movement.

The ataxia becomes worse in closed eye or in the dark. The patient may feel steadier
in walking and Romberg test with eyes open or sufficient lighting. However, the is
finger-nose and heel-knee test may not be obvius to show the sensory disorder and its
dependence on sight control but it surely does if you do the pointing test. To
differentiate between cerebellar ataxia and sensory ataxia, take note that there won't
be any intentional tremor in finger-nose test and heel-knee test, no dysathria and
nystagmus (in sensitive ataxia- presence)

Vestibular Ataxia

This ataxia arises due to lesion in the peripheral vestibular apparatus,


cochleavestibular nerve, vestibular nucleus or trade in the brain stem. Manifestations
include:
• headache,
• balancing disorder during walking, sitting (Romberg test) and walking
In case of moving or shaking of the head, this might lead to nausea and vomiting and
worsening of headache and instability. Patient will walk carefully, feels swaying
especially when the head is moving or shaking or walking on slippery or bumpy roads;
coordination of movement actually depends on the sight control.
In vestibular ataxia, the patient does not have any abnormalities during extremities
coordination tests, preserved joint-muscular sensation, and no disarthria and muscular
hypotonic and hyporeflexia (those are things that differ vestibular ataxia from
cerebellar and sensitive ataxia)

Frontal Ataxia (Gait Apraxia)

This type of gait arises in lesion of be frontal lot of the brain due to lesion of the
frontal-pontino-cerebellar connection. Its manifestation included balance disorder in
walking and standing, sometimes decreased in critical thinking and also intellectuals
might also be observed (dementia). In standing and walking it is quite usual to observe
the flexion posture, the basis of a support at standing and walking has a little bit
widened or expanded, patient walks at a very slow pace, small shuffling steps. In
moderate stage of the gait abnormalities might be improved, when patients walk
together with a healthy person, which allows the patient to walk with his legs with
help. (As opposed to cerebellar ataxia, frontal ataxia does not call the patient to have
intentional tremor (as seen in finger- nose test and heel- knee test), no nystagmus and
dysathria). Compared to sensory ataxia, frontal ataxia does not have abnormalities in
join-muscular sensation, the degree of abnormalities is strongly depends upon the
vision control.

In progressive frontal ataxia, the patient starts to suffer from difficulty of walking in the
beginning, and towards the end of walking, patient digs: lose the ability to stand
(astasia) and walking (abasia), sitting and furtherturns on the bed. Frontal ataxia
usually begins with the demyelination and other symptoms of lesion in the frontal lobe
(symptom of oral reflex/jaw reflex, grasping reflex, anti counter resistance and others).

In certain cases, it is possible to have mixed ataxia, for example in cerebellar and
sensitive ataxia simultaneously. The patient is actually having lesions in the area of
cerebellar and posterior funiculus of the spinal cord. In that case, the typical
manifestations of cerebellar ataxia, eg. intentional tremor originated from the joint-
muscular sensation abnormalities, significant deterioration on coordination in closed
eyes which is a real character for sensitive ataxia.

Localization of Lesion in Ataxia (Topical Diagnosis)

Cerebellar ataxia may be observed in cerebellar lesion and in any of its afferent and
efferent trade. Due to lesion of to hemisphere, cerebellar ataxia might be developed in
the extremities in the same lesion sides (ipsilateral/ homolateral). Therefore, unilateral
cerebellar ataxia shows the homolateral lesion on the hemisphere of the cerebellum or
efferent tracts from it. During walking or standing (Romberg test) the trunk: may
deviate towards the side of hemisphere with lesion. Lesion in the pediculus also leads
to the same symptoms, which developed when the lesion in the hemisphere of the
cerebellum is more extensive. It is important to take note that lesion in signicficant/
large parts in the hemisphere of the cerebellum may proceed without noticeable
movement abnormalities because of the great compensatory abilities held by the non-
lesional parts
High amplitude ‘rubral’ tremor shows the vision on the red nucleus or the superior
pediculus of the cerebellum where all of the locomotor cerebellar passes thru. Lesion in
the spinocerebellar tract as opposed to the cerebellar lesion and its Iocomotor tract
usually DOES NOT HAVE any symptoms of NYSTAGMUS and DYSARTHRIA.

In case of the lesion of vermis of the cerebellar, we may observe only balance disorder
and gait, dysathria and nystagmus without ataxia of the extremities .

Analysis of Iocalization of the lesion of the nervous system in cerebellar, vestibular and
frontal ataxia discussed in this theme are somehow connected in chapter 1- sensory
disorders, chap 6- vestibular
disorder and chap 10 lesion in the root of cerebral.
causes of cerebellar ataxia. Acute development of ataxia could be due to abnormal
circulation in the . cerebellar or the brain stem (hemorrhagic or infarct), alcohol
intoxication, barbiturates or antiepileptic substances (carbamezaplne, phenytoin etc),
encephalitis with cerebellar lesion.

Fast-developing ataxia is usually due to diffused sclerosis, tumor of the brain,


chronic alcohol intoxication. Slow-progressing ataxia was observed in hereditary and
idiopathic degenerative disease with cerebellar lesion, and also in diffused sclerosis
and polyneuropathy. In case of suspicion on hereditary character ataxia, a genetic
investigation should be done.

Treatment of ataxia:
Treat the underlying disease. If it is hereditary or idiopathic - there area effective
treatments available. The medical gymnastics and social adaptation of the patient
have great value in improving the ataxia.

Ataxia

Method of Normal gait, pandemic and phalangial Romberg test Babinsky test
investigation Finger-nose test, Diadochokinesis test and diametric test.
(Identification ataxia) Heel-knee test.

Abnormal balance, unstableness in walking and in Romberg test.


Basic symbols of Asynergic Babinsky
ataxia Misses and intention tremor seen in finger-nose test, dysmetria,
disdiadochokinesis.
Misses and intentional tremor seen in heel-knee test.
Types of ataxia (syndromes)

Cerebellar Sensory Vestibular Frontal

1. Abnormal 1. Abnormal balance, 1. Abnormal balance, 1. Abnormal


balance, unstableness in walking unstableness in balance,
unstableness in and in Romberg test. walking and in unstableness in
walking and in Romberg test. walking and in
2. Misses in finger-nose
Romberg test. 2. Vestibular Romberg test.
2. Asynergic and heel-knee test 2. Symptoms of
headache,
Babinsky 3. Abnormal in muscular- oral
nausea, vomit
3. Misses and joint sensation, automatism,
3. Nystagmus
intentional tremor increased in degree of grasp reflex and
ataxia when eyes are decreased
in finger-nose closed intellect.
and heel-knee 4. Muscle hypotonia
test dysmetria, hyporeflexia
dysathria,
dysdiachokinesis
4. Nystagmus.
Muscle Hypotonia

Localization of lesion
Cerebellum, Conductor of muscular-joint Peripheral vestibular Frontal lobe,
cerebellar pediculus, sensation peripheral apparatus, frontal-pons-
conducting stract in nerves: posterior root, cochlearvestibular cerebellar trac
trancus of the brain posterior funiculus, nerve nuclei and tract
and spinal cord thalamus, parietal lobe