A 66 Year old man finds that he has more difficulty in moving about for the past one year. he is annoyed by a tremor in his hands , but the tremor goes away when he performs routine tasks using his hands. His friends remark that he does not smile at them , but only stares with a fixed expression on his face. He also complains of difficulty in initiation of movements and had developed an odd gait despite his efforts to correct it. He has not suffered any loss of mental ability. He was diagnosed to have cereballar lesion. He responded well to conservative treatment.
The human cerebellum changes with age. These changes may differ from those of other parts of the brain, for example the gene expression pattern in the human cerebellum shows less age-related alteration than in the cerebral cortex. Some studies have reported reductions in numbers of cells or volume of tissue, but the amount of data relating to this question is not very large.
Difficulty in moving/ Odd Gait
Patients with cerebellar damage, regardless of the causes or location, exhibit persistent errors in movement. These movement errors are always on the same side of the body as the damage to the cerebellum, reflecting the cerebellum’s unusual status as a brain structure in which sensory and motor information is represented ipsilaterally rather than contralaterally. Furthermore, somatic, visual, and other inputs are represented topographically within the cerebellum; as a result, the movement deficits may be quite specific. For example, one of the most common cerebellar syndromes is caused by degeneration in the anterior portion of the cerebellar cortex in patients with a long history of alcohol abuse . Such damage specifically affects movement in the lower limbs, which are represented in the anterior spinocerebellum. The consequences include a wide and staggering gait, with little impairment of arm or hand movements. Thus, the topographical organization of the cerebellum allows cerebellar damage to disrupt the coordination of movements performed by some muscle groups but not others.
The implication of these pathologies is that the cerebellum is normally capable of integrating the moment-to-moment actions of muscles and joints throughout the body to ensure the smooth execution of a full range of motor behaviors. Thus, cerebellar lesions lead first and foremost to a lack of coordination of ongoing movements .. For example, damage to the vestibulocerebellum impairs the ability to stand upright and maintain the direction of gaze. The eyes have difficulty maintaining fixation; they drift from the target and then jump back with a corrective saccade, a phenomenon called nystagmus. Disruption of the pathways to the vestibular nuclei may also result in a loss of muscle tone. In contrast, patients with damage to the spinocerebellum have difficulty controlling walking movements; they have a wide-based gait with small shuffling movements, which represents the inappropriate operation of groups of muscles that normally rely on sensory feedback to produce smooth, concerted actions. The patients also have difficulty performing rapid alternating movements such as the heel-to-shin and/or finger-to-nose tests, a sign referred to as dysdiadochokinesia. Over- and underreaching may also occur (called dysmetria). During the movement, tremors—called action or intention tremors—accompany over- and undershooting of the movement due to disruption of the mechanism for detecting and correcting movement errors. Finally, lesions of the cerebrocerebellum produce impairments in highly skilled sequences of learned movements, such as playing a musical instrument. The common denominator of all of these signs, regardless of the site of the lesion, is the inability to perform smooth, directed movements.
SUMMARY: The cerebellum does not initiate movement, but it contributes to coordination, precision, and accurate timing. It receives input from sensory systems and from other parts of the brain and spinal cord, and integrates these inputs to fine tune motor activity. Because of this fine-tuning function, damage to the cerebellum does not cause paralysis, but instead produces disorders in fine movement, equilibrium, posture, and motor learning.
Cerebellar injury results in movements that are slow and uncoordinated. Individuals with cerebellar lesions tend to sway and stagger when walking.
 Cerebellar Lesion
Damage to the cerebellum can lead to:
1) loss of coordination of motor movement (asynergia),
2) the inability to judge distance and when to stop (dysmetria),
3) the inability to perform rapid alternating movements (adiadochokinesia),
4) movement tremors (intention tremor),
5) staggering, wide based walking (ataxic gait),
6) tendency toward falling,
7) weak muscles (hypotonia),
8) slurred speech (ataxic dysarthria), and
9) abnormal eye movements (nystagmus
 Loss of Expressions:
Cerebellum is also involved in some cognitive functions such as attention and language, and probably in some emotional functions such as regulating fear and pleasure responses
the cerebellum consists of a large number of more or less independent modules, all with the same geometrically regular internal structure, and therefore all, it is presumed, performing the same computation. If the input and output connections of a module are with motor areas (as many are), then the module will be involved in motor behavior; but, if the connections are with areas involved in non-motor cognition, the module will show other types of behavioral correlates. The cerebellum, Doya proposes, is best understood as a device for supervised learning, in contrast to the basal ganglia, which perform reinforcement learning, and the cerebral cortex, which performs unsupervised learning.
 Causes of Lesion:
Signs & Symptoms
PATHOPHYSIOLOGY AND TREATMENT OF ATAXIA:
- Dysfunction of the vestibulocerebellum impairs the balance and the control of eye movements. This presents itself with postural instability, in which the person tends to separate his/her feet upon standing, in order to gain a wider base and to avoid bodily oscillations (especially forward-backward ones). The instability is therefore worsened when standing with the feet together, regardless of whether the eyes are open or closed. This is a negative Romberg’s test, or more accurately, it denotes the individual’s inability to carry out the test, because the individual feels unstable even with open eyes.
- Dysfunction of the spinocerebellum presents itself with a wide-based “drunken sailor” gait, characterised by uncertain starts and stops, lateral deviations, and unequal steps. This part of the cerebellum regulates body and limb movements.
- Dysfunction of the cerebrocerebellum presents with disturbances in carrying out voluntary, planned movements. These include:
- intention tremor (coarse trembling, accentuated over the execution of voluntary movements, possibly involving the head and eyes as well as the limbs and torso);
- peculiar writing abnormalities (large, unequal letters, irregular underlining);
- a peculiar pattern of dysarthria (slurred speech, sometimes characterised by explosive variations in voice intensity despite a regular rhythm).
The term sensory ataxia is employed to indicate ataxia due to loss of proprioception – the loss of sensitivity to the positions of joint and body parts. This is generally caused by dysfunction of the dorsal columns of the spinal cord, because they carry proprioceptive information up to the brain. In some cases, the cause of sensory ataxia may instead be dysfunction of the various parts of the brain which receive positional information, including the cerebellum, thalamus, and parietal lobes Sensory ataxia presents itself with an unsteady “stomping” gait with heavy heel strikes, as well as a postural instability that is usually worsened when the lack of proprioceptive input cannot be compensated for by visual input, such as in poorly lit environments.
Physicians can find evidence of sensory ataxia during physical examination by having the patient stand with his/her feet together and eyes shut. In affected patients, this will cause the instability to worsen markedly, producing wide oscillations and possibly a fall. This is called a positive Romberg’s test. Worsening of the finger-pointing test with the eyes closed is another feature of sensory ataxia. Also, when the patient is standing with arms and hands extended toward the physician, if the eyes are closed, the patient’s finger will tend to “fall down” and then be restored to the horizontal extended position by sudden muscular contractions (the “ataxic hand”).
The term vestibular ataxia is employed to indicate ataxia due to dysfunction of the vestibular system, which in acute and unilateral cases is associated with prominent vertigo, nausea and vomiting. In slow-onset, chronic bilateral cases of vestibular dysfunction, these characteristic manifestations may be absent, and dysequilibrium may be the sole presentation.
The three types of ataxia have overlapping causes, and therefore can either coexist or occur in isolation.
a. Focal lesions
Any type of focal lesion of the central nervous system (such as stroke, brain tumour, multiple sclerosis) will cause the type of ataxia corresponding to the site of the lesion: cerebellar if in the cerebellum, sensory if in the dorsal spinal cord (and rarely in the thalamus or parietal lobe), vestibular if in the vestibular system (including the vestibular areas of the cerebral cortex).
b. Exogenous substances
Exogenous substances that cause ataxia mainly do so because they have a depressant effect on central nervous system function. The most common example is ethanol, which is capable of causing reversible cerebellar and vestibular ataxia. Other examples include various prescription drugs (e.g. most antiepileptic drugs have cerebellar ataxia as a possible adverse effect), Lithium level over 1.5mEq/L, cannabis ingestion and various other recreational drugs (e.g. ketamine, PCP or dextromethorphan, all of which are NMDA receptor antagonists that produce a dissociative state at high doses). Exposure to high levels of methylmercury, through consumption of fish with high mercury concentrations, is also a known cause of ataxia and other neurological disorders
c. Vitamin B12 deficiency
Vitamin B12 deficiency may cause, among several neurological abnormalities, overlapping cerebellar and sensory ataxia.
Causes of isolated sensory ataxia
Peripheral neuropathies may cause generalised or localised sensory ataxia (e.g. a limb only) depending on the extent of the neuropathic involvement. Spinal disorders of various types may cause sensory ataxia from the lesioned level below, when they involve the dorsal columns.
Non-hereditary cerebellar degeneration
Non-hereditary causes of cerebellar degeneration include chronic ethanol abuse, paraneoplastic cerebellar degeneration, high altitude cerebral oedema, coeliac disease, normal pressure hydrocephalus and cerebellitis.
Ataxia may depend on hereditary disorders consisting of degeneration of the cerebellum and/or of the spine; most cases feature both to some extent, and therefore present with overlapping cerebellar and sensory ataxia, even though one is often more evident than the other. Hereditary disorders causing ataxia include autosomal dominant ones such as spinocerebellar ataxia, episodic ataxia, and dentatorubropallidoluysian atrophy, as well as autosomal recessive disorders such as Friedreich’s ataxia (sensory and cerebellar, with the former predominating) and Niemann Pick disease, ataxia-telangiectasia (sensory and cerebellar, with the latter predominating), and abetalipoproteinaemia. An example of X-linked ataxic condition is the rare fragile X-associated tremor/ataxia syndrome.
Arnold-Chiari malformation is a malformation of the brain. It consists of a downward displacement of the cerebellar tonsils and the medulla through the foramen magnum, sometimes causing hydrocephalus as a result of obstruction of cerebrospinal fluid outflow.
The movement disorders related to ataxia are primarily treated with physical therapy. As ataxia involves a loss of coordinated and efficient action of stabilising muscles in the trunk, exercise training typically includes a focus on stability exercise. There is often an array of other motor deficits requiring exercise treatment including weakness, balance impairment and decreased endurance. It is also possible that treatment will include strategies to manage difficulties with everyday activities, such as a cane or walker to decrease the risk of falls associated with a balance impairment, or prescription of a wheelchair.