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Function of the Cerebellum in Overall Motor Control

The nervous system uses the cerebellum to coordinate motor control functions at three levels, as follows:
1. The vestibulocerebellum. This consists principally of the small flocculonodular cerebellar lobes (that lie under the posterior cerebellum) and adjacent portions of the vermis. It provides neural circuits for most of the body’s equilibrium movements.

2. The spinocerebellum. This consists of most of the vermis of the posterior and anterior cerebellum plus the adjacent intermediate zones on both sides of the vermis. It provides the circuitry for coordinating mainly movements of the distal portions of the limbs, especially the hands and fingers.
3. The cerebrocerebellum. This consists of the large lateral zones of the cerebellar hemispheres, lateral to the intermediate zones. It receives virtually all its input from the cerebral motor cortex and adjacent premotor and somatosensory cortices of the cerebrum. It transmits its output information in the upward direction back to the brain, functioning in a feedback manner with the cerebral cortical sensorimotor system to plan sequential voluntary body and limb movements, planning these as much as tenths of a second in advance of the actual movements. This is called development of “motor imagery” of movements to be performed.

Coordination and control of voluntary movement.

Associated Signs and Symptoms:-

  • Tremors.
  • Nystagmus (Involuntary movement of the eye).
  • Ataxia, lack of coordination.

Vestibulocerebellum—Its Function in Association with the Brain Stem and Spinal Cord to Control Equilibrium and Postural Movements

The vestibulocerebellum originated phylogenetically at about the same time that the vestibular apparatus in the inner ear developed. loss of the flocculonodular lobes and adjacent portions of the vermis of the cerebellum, which constitute the vestibulocerebellum, causes extreme disturbance of equilibrium and postural movements. We still must ask the question, what role does the vestibulocerebellum play in equilibrium that cannot be provided by other neuronal machinery of the brain stem? A clue is the fact that in people with vestibulocerebellar
dysfunction, equilibrium is far more disturbed during performance of rapid motions than
during stasis, especially so when these movements involve changes in direction of movement and stimulate the semicircular ducts. This suggests that the vestibulocerebellum is especially important in controlling balance between agonist and antagonist muscle contractions of the spine, hips, and shoulders during rapid changes in body positions as required by the vestibular apparatus. One of the major problems in controlling balance is the amount of time required to transmit position signals and velocity of movement signals from the different
parts of the body to the brain. Even when the most rapidly conducting sensory pathways are used, up to 120 m/sec in the spinocerebellar afferent tracts, the delay for transmission from the feet to the brain is still 15 to 20 milliseconds. The feet of a person running rapidly can move as much as 10 inches during that time. Therefore, it is never possible for return signals
from the peripheral parts of the body to reach the brain at the same time that the movements actually occur. How, then, is it possible for the brain to know when to stop a movement and to perform the next sequential act, especially when the movements are performed rapidly? The answer is that the signals from the periphery tell the brain how rapidly and in which
directions the body parts are moving. It is then the function of the vestibulocerebellum to calculate in advance from these rates and directions where the different parts will be during the next few milliseconds. The results of these calculations are the key to the
brain’s progression to the next sequential movement. Thus, during control of equilibrium, it is presumed that information from both the body periphery and the vestibular apparatus is used in a typical feedback control circuit to provide anticipatory correction of postural motor signals necessary for maintaining equilibrium even during extremely rapid motion, including
rapidly changing directions of motion.

Cerebellum and Its Motor Functions

The cerebellum, has long been called a silent area of the brain, principally because electrical excitation of the cerebellum does not cause any conscious sensation and rarely causes any motor movement. Removal of the cerebellum, however, does cause body movements to
become highly abnormal. The cerebellum is especially vital during rapid muscular
activities such as running, typing, playing the piano, and even talking. Loss
of this area of the brain can cause almost total incoordination of these activities
even though its loss causes paralysis of no muscles.
But how is it that the cerebellum can be so important when it has no direct
ability to cause muscle contraction? The answer is that it helps to sequence
the motor activities and also monitors and makes corrective adjustments in the
body’s motor activities while they are being executed so that they will conform to
the motor signals directed by the cerebral motor cortex and other parts of the
The cerebellum receives continuously updated information about the desired
sequence of muscle contractions from the brain motor control areas; it also
receives continuous sensory information from the peripheral parts of the body,
giving sequential changes in the status of each part of the body—its position,
rate of movement, forces acting on it, and so forth. The cerebellum then compares
the actual movements as depicted by the peripheral sensory feedback
information with the movements intended by the motor system. If the two do
not compare favorably, then instantaneous subconscious corrective signals are
transmitted back into the motor system to increase or decrease the levels of
activation of specific muscles.
The cerebellum also aids the cerebral cortex in planning the next sequential
movement a fraction of a second in advance while the current movement is still
being executed, thus helping the person to progress smoothly from one movement to the next. Also, it learns by its mistakes—that is, if a movement does not occur exactly as intended, the cerebellar circuit learns to make a stronger or weaker movement the next time. To do this, changes occur in the excitability of appropriate cerebellar neurons, thus bringing subsequent
muscle contractions into better correspondence with the intended movements.

Inferior colliculus

The inferior colliculi (Latin, lower hills) together with the superior colliculi form the eminences of the corpora quadrigemina, and also part of the tectal region of the midbrain. The inferior colliculus lies caudal to its counterpart - the superior colliculus - above the trochlear nerve, and at the base of the projection of the medial geniculate nucleus (MGN) and the lateral geniculate nucleus (LGN).
The inferior colliculus is the principal midbrain nucleus of the auditory pathway and receives input from several more peripheral brainstem nuclei in the auditory pathway, as well as inputs from the auditory cortex. The inferior colliculus has three subnuclei.

Relationship to auditory system

The inferior colliculi of the midbrain are located just below the visual processing centers known as the superior colliculi. The inferior colliculus is the first place where vertically orienting data from the fusiform cells in the dorsal cochlear nucleus can finally synapse with horizontally orienting data. This homecoming of the aural dimensions puts these dual mesencephalic bumps in the position to fully integrate all the sound location data.
The inferior colliculus function as a master computer both in regard to its hardware (complex connections) and its software (internal organization). IC are large auditory nuclei on the right and left sides of the midbrain. It is divided into three parts, the Central Nucleus of IC (CNIC), dorsal cortex and lateral cortex; however, CNIC is the principal way station for ascending auditory information in the IC.
1. Input and Output Connection of IC
The input connections to the inferior colliculus are composed of many brainstem nuclei. All nuclei except the contralateral ventral nucleus of the lateral lemniscus (LL) send projections to the central nucleus (CNIC) bilaterally. It has been shown that great majority of auditory fibers ascending in the lateral lemniscus terminate in the CNIC. In addition, the IC receives descending inputs from the auditory cortex, medial geniculate body (MGB), and superior colliculus (SC).
The inferior colliculus receives input from both the ipsilateral and contralateral cochlear nucleus and respectively the corresponding ears. Of course, there is some lateralization, the dorsal projections (containing vertical data) only project to the contralateral inferior colliculus. This inferior colliculus contralateral to the ear it is receiving the most information from, then projects to its ipsilateral medial geniculate nucleus.
The medial geniculate body (MGB) is the output connection from interior colliculus and the last subcortical way station. The MGB is composed of ventral, dorsal, and medial divisions, which are relatively similar in humans and other mammals. The ventral division receives auditory signals from the central nucleus of the IC (1).
CNIC: Central Nucleus of IC
AVCN: Anterior Ventral Cochlear Nucleus
PVCN: Posterior Ventral Cochlear Nucleus
SCN: Superior Colliculus Nucleus
LSO: Lateral Superior Olive
MSO: Medial Superior Olive
DNLL: Dorsal Nucleus of the Lateral Lemniscus
MGB: Medial Geniculate Body
SC: Superior Colliculus
TB: Trapezoid Body.......................................................................................

Superior colliculus

The optic tectum or simply tectum is a paired structure that forms a major component of the vertebrate midbrain. In mammals this structure is more commonly called the superior colliculus (Latin, higher hill), but even in mammals, the adjective tectal is commonly used. The tectum is a layered structure, with a number of layers that varies by species. The superficial layers are sensory-related, and receive input from the eyes as well as other sensory systems. The deep layers are motor-related, capable of activating eye movements as well as other responses. There are also intermediate layers, with multi-sensory cells and motor properties.
The general function of the tectal system is to direct behavioral responses toward specific points in egocentric ("body-centered") space. Each layer of the tectum contains a topographic map of the surrounding world in retinotopic coordinates, and activation of neurons at a particular point in the map evokes a response directed toward the corresponding point in space. In primates, the tectum ("superior colliculus") has been studied mainly with respect to its role in directing eye movements. Visual input from the retina, or "command" input from the cerebral cortex, create a "bump" of activity in the tectal map, which if strong enough induces a saccadic eye movement. Even in primates, however, the tectum is also involved in generating spatially directed head turns, arm-reaching movements, and shifts in attention that do not involve any overt movements. In other species, the tectum is involved in a wide range of responses, including whole-body turns in walking rats, swimming fishes, or flying birds; tongue-strikes toward prey in frogs; fang-strikes in snakes; etc.
In some non-mammal species, including fish and birds, the tectum is one of the largest components of the brain. In mammals, and especially primates, the massive expansion of the cerebral cortex reduces the tectum ("superior colliculus") to a much smaller fraction of the whole brain. Even there, though, it remains functionally very important as the primary integrating center for eye movements.


Cerebrospinal fluid (CSF), Liquor cerebrospinalis, is a clear bodily fluid that occupies the subarachnoid space and the ventricular system around and inside the brain. In essence, the brain "floats" in it.
The CSF occupies the space between the arachnoid mater (the middle layer of the brain cover, meninges), and the pia mater (the layer of the meninges closest to the brain). It constitutes the content of all intra-cerebral (inside the brain, cerebrum) ventricles, cisterns, and sulci (singular sulcus), as well as the central canal of the spinal cord.
It acts as a "cushion" or buffer for the cortex, providing a basic mechanical and immunological protection to the brain inside the skull.
It is produced in the choroid plexus.
It is produced in the brain by modified ependymal cells in the choroid plexus (approx. 50-70%), and the remainder is formed around blood vessels and along ventricular walls. It circulates from the choroid plexus through the interventricular foramina (foramen of Monro) into the third ventricle, and then through the cerebral aqueduct (aqueduct of Sylvius) into the fourth ventricle, where it exits through two lateral apertures (foramina of Luschka) and one median aperture (foramen of Magendie). It then flows through the cerebellomedullary cistern down the spinal cord and over the cerebral hemispheres.
It had been thought that CSF returns to the vascular system by entering the dural venous sinuses via the arachnoid granulations or villi. However, some[1] have suggested that CSF flow along the cranial nerves and spinal nerve roots allow it into the lymphatic channels; this flow may play a substantial role in CSF reabsorbtion, in particular in the neonate, in which arachnoid granulations are sparsely distributed. The flow of CSF to the nasal submucosal lymphatic channels through the cribiform plaque seems to be specially important.


CSF has many putative roles, including mechanical protection of the brain, distribution of neuroendocrine factors, and prevention of brain ischemia. The actual mass of the human brain is about 1400 grams; however the net weight of the brain suspended in the CSF is equivalent to a mass of 25 grams.[5] The prevention of brain ischemia is made by decreasing the amount of CSF in the limited space inside the skull. This decreases total intracranial pressure and facilitates blood perfusion. It also cushions the spinal cord against jarring shock.


The blood-brain barrier (BBB) is a separation of circulating blood and cerebrospinal fluid (CSF) maintained by the choroid plexus in the central nervous system (CNS). Endothelial cells restrict the diffusion of microscopic objects (e.g. bacteria) and large or hydrophilic molecules into the CSF, while allowing the diffusion of small hydrophobic molecules (O2, hormones, CO2). Cells of the barrier actively transport metabolic products such as glucose across the barrier with specific proteins.

This "barrier" results from the selectivity of the tight junctions between endothelial cells in CNS vessels that restricts the passage of solutes. At the interface between blood and brain, endothelial cells and associated astrocytes are stitched together by these tight junctions, which are composed of smaller subunits, frequently dimers, that are transmembrane proteins such as occludin, claudins, junctional adhesion molecule (JAM), ESAM and others. Each of these transmembrane proteins is anchored into the endothelial cells by another protein complex that includes zo-1 and associated proteins.
The blood-brain barrier composed of high density cells restricting passage of substances from the bloodstream much more than endothelial cells in capillaries elsewhere in the body. Astrocyte cell projections called astrocytic feet (also known as "glia limitans") surround the endothelial cells of the BBB, providing biochemical support to those cells. The BBB is distinct from the similar blood-cerebrospinal fluid barrier, a function of the choroidal cells of the choroid plexus, and from the blood-retinal barrier, which can be considered a part of the whole.[1]
Several areas of the brain are not "behind" the BBB. One example is the pineal gland, which secretes the hormone melatonin "directly into the systemic circulation.

What is Redout?

A redout occurs when the body experiences a negative g-force sufficient to cause a blood flow from the lower parts of the body to the head. It is the inverse effect of a brownout or greyout, where blood flows away from the head to the lower parts of the body. Redouts are potentially dangerous and can cause retinal damage and hemorrhagic stroke.

Multiple personality disorder (MPD)

Multiple personality disorder is now more usually termed dissociated identity disorder. It is one of the more misunderstood types of mental illness, frequently capturing the interest of writers and filmmakers, who tend to portray it in its most exaggerated form. What is most important to understand is the multiple personality disorder is not schizophrenia. The two are often confused. However, in very rare cases, a personality, or alter, as it is sometimes termed, suffers from schizophrenia.
Multiple personality disorder is almost always caused by persistent trauma, or past trauma such as early childhood sexual or physical abuse. When trauma occurs over a long period of time, the affected person may begin to cope by completely disassociating from the events that cause the trauma. This can lead to “alters,” separate personalities within the same person who either are aware of, or are unaware of the abuse. Alters can be childlike, strong, male, or female, and often emerge as a coping device.
Psychiatrists make the distinction between a person having several personalities, and believing they have several personalities. In general, multiple personality disorder is the belief on the part of the patient that several personalities seem to exist within the self.
One of the main characteristics of multiple personality disorder is that people seem to “lose” time. They seem unaware that time has passed; yet someone observing them may see them acting in many different ways. The afflicted however, tends to have no idea what has occurred. This generally central personality seems most likely to dissociate if the person is exposed to situations which can evoke earlier traumas, or if the person is still enmeshed in a traumatic situation.

Signs and symptoms

Individuals diagnosed with MPD demonstrate a variety of symptoms with wide fluctuations across time; functioning can vary from severe impairment in daily functioning to normal or high abilities. Symptoms can include:----
Patients may experience an extremely broad array of other symptoms that resemble epilepsy, schizophrenia, anxiety disorders, mood disorders, post traumatic stress disorder, personality disorders, and eating disorders.

Multiple sclerosis

Multiple sclerosis is an autoimmune disease that affects the brain and spinal cord (central nervous system).
Symptoms vary, because the location and severity of each attack can be different. Episodes can last for days, weeks, or months. These episodes alternate with periods of reduced or no symptoms (remissions).
Fever, hot baths, sun exposure, and stress can trigger or worsen attacks.
It is common for the disease to return (relapse). However, the disease may continue to get worse without periods of remission.
Because nerves in any part of the brain or spinal cord may be damaged, patients with multiple sclerosis can have symptoms in many parts of the body.
Muscle symptoms:
Loss of balance
Numbness or abnormal sensation in any area
Pain because of muscle spasms
Pain in the arms or legs
Problems moving arms or legs
Problems walking
Problems with coordination and making small movements
Slurred or difficult-to-understand speech
Tremor in one or more arms or legs
Uncontrollable spasm of muscle groups (muscle spasticity)
Weakness in one or more arms or legs
Eye symptoms:
Double vision
Eye discomfort
Uncontrollable rapid eye movements
Vision loss (usually affects one eye at a time)
Other brain and nerve symptoms:
Decreased attention span
Decreased judgment
Decreased memory
Depression or feelings of sadness
Dizziness and balance problems
Facial pain
Hearing loss
Bowel and bladder symptoms:
Difficulty beginning urinating
Frequent need to urinate
Stool leakage
Strong urge to urinate
Urine leakage (incontinence)
There is no known cure for multiple sclerosis at this time. However, there are therapies that may slow the disease. The goal of treatment is to control symptoms and help you maintain a normal quality of life.
Medications used to slow the progression of multiple sclerosis may include:
Immune modulators to help control the immune system, including interferons (Avonex, Betaseron, or Rebif), monoclonal antibodies (Tysabri), glatiramer acetate (Copaxone), mitoxantrone (Novantrone), methotrexate, azathioprine (Imuran), cyclophosphamide (Cytoxan), and natalizumab (Tysabri)
Steroids may be used to decrease the severity of attacks
Medications to control symptoms may include:
Medicines to reduce muscle spasms such as Lioresal (Baclofen), tizanidine (Zanaflex), or a benzodiazepine
Cholinergic medications to reduce urinary problems
Antidepressants for mood or behavior symptoms
Amantadine for fatigue
The following may help MS patients:
Physical therapy, speech therapy, occupational therapy, and support groups
Assistive devices, such as wheelchairs, bed lifts, shower chairs, walkers, and wall bars
A planned exercise program early in the course of the disorder
A healthy lifestyle, with good nutrition and enough rest and relaxation
Avoiding fatigue, stress, temperature extremes, and illness
Multiple sclerosis (MS) affects woman more than men. The disorder most commonly begins between ages 20 and 40, but can be seen at any age.
MS is caused by damage to the myelin sheath, the protective covering that surrounds nerve cells. When this nerve covering is damaged, nerve impulses are slowed down or stopped.
MS is a progressive disease, meaning the nerve damage (neurodegeneration) gets worse over time. How quickly MS gets worse varies from person to person.
The nerve damage is caused by inflammation. Inflammation occurs when the body's own immune cells attack the nervous system. Repeated episodes of inflammation can occur along any area of the brain and spinal cord.
Researchers are not sure what triggers the inflammation. The most common theories point to a virus or genetic defect, or a combination of both.
MS is more likely to occur in northern Europe, the northern United States, southern Australia, and New Zealand than in other areas. Geographic studies indicate there may be an environmental factor involved.
People with a family history of MS and those who live in a geographical area with a higher incidence rate for MS have a higher risk of the disease.
Tests & diagnosis
Symptoms of MS may mimic those of many other nervous system disorders. The disease is diagnosed by ruling out other conditions.
People who have a form of MS called relapsing-remitting may have a history of at least two attacks, separated by a period of reduced or no symptoms.
The health care provider may suspect MS if there are decreases in the function of two different parts of the central nervous system (such as abnormal reflexes) at two different times.
A neurological exam may show reduced nerve function in one area of the body, or spread over many parts of the body. This may include:
Abnormal nerve reflexes
Decreased ability to move a part of the body
Decreased or abnormal sensation
Other loss of nervous system functions
An eye examination may show:
Abnormal pupil responses
Changes in the visual fields or eye movements
Decreased visual acuity
Problems with the inside parts of the eye
Rapid eye movements triggered when the eye moves
Tests to diagnose multiple sclerosis include:
Cerebrospinal fluid tests, including CSF oligoclonal banding
Head MRI scan
Lumbar puncture (spinal tap)
Nerve function study (evoked potential test)
Spine MRI
The outcome varies, and is unpredictable. Although the disorder is chronic and incurable, life expectancy can be normal or almost normal. Most people with MS continue to walk and function at work with minimal disability for 20 or more years.
The following typically have the best outlook:
People who were young (less than 30 years) when the disease started
People with infrequent attacks
People with a relapsing-remitting pattern
People who have limited disease on imaging studies
The amount of disability and discomfort depends on:
How often you have attacks
How severe they are
The part of the central nervous system that is affected by each attack
Most people return to normal or near-normal function between attacks. As the disorder gets worse, there is greater loss of function with less improvement between attacks.
Difficulty swallowing
Difficulty thinking
Less and less ability to care for self
Need for indwelling catheter
Osteoporosis or thinning of the bones
Pressure sores
Side effects of medications used to treat the disorder
Urinary tract infections
When to contact a doctor
Call your health care provider if:
You develop any symptoms of MS
Symptoms get worse, even with treatment
The condition deteriorates to the point where home care is no longer possible

Central Nervous System Synapses

Every medical student is aware that information is transmitted in the central nervous system mainly in the form of nerve action potentials, called simply “nerve impulses,” through a succession of neurons, one after another. However, in addition, each impulse (1) may be blocked in its transmission from one neuron to the next, (2) may be changed from a single impulse into repetitive impulses, or (3) may be integrated with impulses from other neurons to cause highly intricate patterns of impulses in successive neurons. All these functions can be classified as synaptic functions of neurons.
Types of Synapses—Chemical and Electrical
There are two major types of synapses: (1) the chemical synapse and (2) the electrical synapse.
Almost all the synapses used for signal transmission in the central nervous system of the human being are chemical synapses. In these, the first neuron secretes at its nerve ending synapse a chemical substance called a neurotransmitter (or often called simply transmitter substance), and this transmitter in turn acts on receptor proteins in the membrane of the next neuron to excite the neuron, inhibit it, or modify its sensitivity in some other way. More than 40 important transmitter substances have been discovered thus far. Some of the best known are acetylcholine, norepinephrine, epinephrine, histamine, gamma-aminobutyric acid (GABA), glycine, serotonin, and glutamate. Electrical synapses, in contrast, are characterized by direct open fluid channels that conduct electricity from one cell to the next. Most of these consist of small protein tubular structures called gap junctions that allow free movement of ions from the interior of one cell to the interior of the next. Such junctions . Only a few examples of gap junctions have been found in the central nervous system. However, it is by way of gap junctions and other similar junctions that action potentials are transmitted from one smooth muscle fiber to the next in visceral
smooth muscle and from one cardiac muscle cell to the next in cardiac muscle......