Cerebellar Disorders

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 (ponticerebellar 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 fingerhammertip 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 jointmuscular 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 nonlesional 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 Finger-nose test, Diadochokinesis test and diametric test. investigation (Identification ataxia) Heel-knee test. Basic symbols of ataxia

Cerebellar

Abnormal balance, unstableness in walking and in Romberg test. Asynergic Babinsky Misses and intention tremor seen in finger-nose test, dysmetria, disdiadochokinesis. Misses and intentional tremor seen in heel-knee test. Types of ataxia (syndromes) Sensory

Vestibular

Frontal

1. Abnormal 1. Abnormal balance, 1. Abnormal balance, 1. Abnormal balance, unstableness in balance, unstableness in walking unstableness in walking and in unstableness in and in Romberg test. walking and in Romberg test. walking and in 2. Misses in finger-nose Romberg test. 2. Vestibular Romberg test. and heel-knee test 2. Asynergic 2. Symptoms of headache, 3. Abnormal in muscularBabinsky oral nausea, vomit joint sensation, 3. Misses and automatism, 3. Nystagmus grasp reflex and increased in degree of intentional tremor decreased ataxia when eyes are

in finger-nose closed 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 cerebellar pediculus, sensation peripheral apparatus, conducting stract in nerves: posterior root, cochlearvestibular trancus of the brain posterior funiculus, nerve nuclei and tract and spinal cord thalamus, parietal lobe

intellect.

Frontal lobe, frontal-ponscerebellar trac