How are reflexes suppressed?

How are reflexes suppressed?

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What neurophysiological process keeps reflex arcs in check? For example, the withdrawal reflex causes the hand to jerk back when the fingers touch something painfully hot incidentally. However, that reflex can be voluntarily suppressed when one deliberately touches that same hot object on purpose. What neural process is involved in conscious suppression of reflexes?

Short answer
The pain withdrawal reflex can only be suppressed when touching something painful on purpose. Deliberate, conscious contraction of the extensor muscle before reflex initiation can prevent the contraction of the flexor muscles once the reflex is started.

The pain withdrawal reflex arc (Fig. 1) receives input from sensory neurons that enter the dorsal part of the spinal cord via the dorsal root of the spinal nerve and synapse onto interneurons within the spinal gray matter. The interneurons in turn synapse onto motor neurons, which send axons that exit the cord via the ventral root. They conduct information to the muscles. The resulting withdrawal reflex is initiated by activating motor neurons of the flexor muscles (agonist), and simultaneous inhibition of the motor neurons to the extensor muscles (antagonist). This loosening of the antagonist while the agonist is being contracted is referred to as reciprocal inhibition (Crone, 1993). More important to the question is the fact that the motor response is well under way before the signals responsible for the conscious sensation of pain (which exit the reflex pathway in the spinal cord) ever reach the brain (Cornell University).

Fig. 1. Schematic of the pain withdrawal reflex arc. Source: Washington Uni.

Hence, the reflex pathway is initiated even before we are aware of any pain. The only possible way to suppress a reflex that is faster than perception is to start counteracting the agonist (flexor) before the reflex is initiated, i.e., by contracting the antagonist (extensor) before touching the painful object.

- Crone, Dan Med Bull (1993); 40(5): 571-81

Cranial Nerves IX (Glossopharyngeal) and X (Vagus)


The gag, or pharyngeal, reflex is centered in the medulla and consists of the reflexive motor response of pharyngeal elevation and constriction with tongue retraction in response to sensory stimulation of the pharyngeal wall, posterior tongue, tonsils, or faucial pillars. This reflex is examined by touching the posterior pharynx with the soft tip of a cotton applicator and visually inspecting for elevation of the pharynx. Both sides of the pharynx should be examined for both the afferent and the efferent limbs of the reflex by touching one side first and then the other, while watching for symmetry of pharyngeal movement. The normal reflex response varies, and it may be reduced in the elderly or in smokers. Asymmetry of the reflex is the feature most indicative of pathology.

Neural Control of Lower Urinary Tract Function

Functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain and lumbosacral spinal cord that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet via a combination of voluntary and reflex mechanisms. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. During urine storage, spinal sympathetic and somatic reflexes are active to maintain a quiescent bladder and a closed outlet. During micturition, these spinal storage reflexes are suppressed by input from the brain, while parasympathetic pathways in the brain are activated to produce a bladder contraction and relaxation of the urethra. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic pathway that consists of essential relay circuitry in the periaqueductal gray and pontine micturition center. These circuits in the rostral brain stem are, in turn, regulated by inputs from the forebrain that mediate voluntary control of micturition. Thus neural control of micturition is organized as a hierarchical system in which spinal storage reflexes and supraspinal voiding reflexes are regulated voluntarily by higher centers in the brain. In young children the voluntary mechanisms are undeveloped and voiding is purely reflex. Voluntary control emerges during maturation of the nervous system and depends on learned behavior. Diseases or injuries of the nervous system in adults cause re-emergence of involuntary micturition, leading to urinary incontinence.

Behavioural Pattern of Animals | Zoology

The following points highlight the three categories of behavioural pattern of animals. The categories are: 1. Instinctive Behaviours or Fixed Action Pattern (FAP) 2. Learning Behaviour 3. Complex Behaviour.

Category # 1. Instinctive Behaviours or Fixed Action Pattern (FAP):

Instinctive Behaviours are genetically inherited characteristics that impel animals to behave in a certain fixed way. It is also referred to as Fixed Action Pattern (FAP) or Innate Behaviour or Inborn Behaviour or Inherent Behaviour. Instinct is generally described as patterns of inherited pre-set behavioural responses which develop along with the developing nervous system.

It is a familiar behaviour which evolves gradually over the generations by selection, to match an animal’s behaviour to its environment. It may be defined as a behaviour which does not require learning or practice, but which appears spontaneously at the first instance of its need.

Although this definition is of a negative kind, it emphasises the other fami­liar way in which behaviour can become matched to circumstances. In the latter case, animals do not have any present responsive­ness, but are able to modify their behaviour in the light of individual experience. The terms Inherited Adaptations and Acquired Adaptations are sometime used to empha­sise the source.

In the animal kingdom, there are a num­ber of behavioural patterns which are depic­ted in the genes. To name a few — the courtship display and mating in most ani­mals, feeding patterns, nest building, parental care, singing, wings cleaning, terri­toriality and aggression, construction of web by spiders (Fig. 5.2A), construction of nest by birds etc..

A few common examples are:

1. During the breeding season a pea­cock starts dancing as soon as it sees a pea­hen. The dancing act is not learnt by watch­ing.

2. A weaver bird never learns to con­struct a nest (Fig. 5.2B). It simply knows it.

3. A tailor bird brings two leaves together and stiches them with a long flexible grass (Fig. 5.2C) and then cushions the bottom with soft grasses, where it lays her eggs. This vital information were passed on to them through the genes of their parents.

4. Bees do not learn to build their hive, this property is acquired genetically.

Another very interesting example of instinctive behaviour or FAP is provided by the Mason wasp (Manobia sp). A female wasp, after emerging from her cell, has a brief moment of interaction with another wasp when she mates with a male. Later, totally on her own, she selects a hollow stem and builds at its inner end, a partition of mud mixed with her saliva.

Close to this partition she lays an egg. Thereafter, she hunts for caterpillars which she lightly paralyses with her sting. She carries 5-8 of them to the cell which would act as future food supply for the larva when it hatches. After being satis­fied, she builds another partition sealing off the egg with its food supply.

She then lays a second egg beyond the second partition, pro­vides it with future food supply and seals it off. The process continues till 8-10 cells are constructed in line along the cavity of stem, until the female has reached the outside. She then plugs the outside end with mud (Fig. 5.3) and flies off to seek another stem for more construction of cells.

The female wasp carries out this ela­borate series of behaviour patterns in total isolation and that too in her short lifespan of a few weeks. It is, thus, not possible for her to acquire everything from scratch, through trial and error method, and that too in her tight schedule. Thus, she has to rely on preset unlearnt responses.

Cooper (1957), while studying this parti­cular wasp species (Manobia quadridens), made some fascinating observations. While examining a stem, he observed that prior to the emergence into the adult all the pupae were oriented with their heads facing the open end.

Normally, the outermost pupae (although derived from later-layed eggs), emerge out of the stem first breaking through the partition and leaving a clear passage for other siblings, coming from deeper in the stem. Under no condition do they ever make the wrong choice of end.

How does the pupae make the correct choice of end? Cooper observed that there was no possibility that they detected light or used gravity or oxygen concentration as a cue. The emerging pupated adults rely heavily on information left behind by their mother.

While building the partition between the cell the female wasp retreating outwardly, leaves the inner side of the partition as rough mud, whilst the outer side she smooths into a concave form (Fig. 5.3A).

Cooper then made an artificial hollowed stem in which he used glass paper to make partitions. The partitions were reversed in orientation (Fig. 5.3B) and, as a result, emerging adults headed ‘inwards’ towards the blind end. Thus, Cooper was able to show unequivocally that the larvae used just the characteristics of concavity and smoothness versus roughness to orient itself.

Such information is obviously passed from one generation of wasps to its offspring genetically. Under no conditions does neither the mother wasp’s action nor the response of the larvae can rely on experience. Instinct is understood as an innate behaviour mechanism that impel animals to behave in a certain fixed way. The notion of Fixed Action Pattern was formulated by Konrad Lorenz (1958).

Sign stimulus or releaser:

FAP is a specific and stereotyped sequence of acti­vities that are triggered by particular stimulus called sign stimulus or releaser. Definite sign stimulus or releaser works and initiates instinctive acts.

1. The red belly in the males of three-spined stickleback fish is one specific sign stimulus, responsible for releasing territorial defence and other reproductive activities.

2. The red spot present on the bill of herring gull is pecked by its chicks which acts as a sign stimulus. This induces the parent to regurgitate food called crop milk.

3. When the parent of song birds alights on the nest with food in their beak, it creates a jerk. This acts as a sign stimuli for the begging behaviour of the chicks.

Occasionally, when there is total absence of flying insects, insectivorous birds may fly out and go through all the motions of catch­ing, killing and devouring an imaginary insect. Such occasional responses may occur in the absence of appropriate stimulus called vacuum behaviours.

Instinct or Fixed Action Pattern as a rule shows two compo­nents:

(a) Stereotyped or consummatory action, and

(b) Appetitive or searching behaviour.

(a) Stereotyped or consummatory action:

Similar FAP has been found to be exhibited by all individuals of a species (stereotype). A classical example is provided by grey-lag geese in the study of egg-rolling. These birds build their nest on the ground and uses stereotype set of behaviour to bring back eggs that roll out of the nest (Fig. 5.4).

The movements shown in Fig. 5.4 are typical of the species, no matter in which environment or circumstances it may live. This act is performed automatically and needs no prior experience. The sight of an egg outside the nest acts as a stimulus and that instigates the egg rolling behaviour.

(b) Appetitive or searching behaviour:

This behaviour comprises of a longer, more variable sequence of movements that leads to the consummatory action. Appetitive beha­viour may be defined as a behaviour for a particular situation that contains a stimulus that could lead to the performance of the consummatory action.

According to Eckhard Hess (1962), appetitive behaviour can be characterised in two ways:

(i) A motor pattern, generally locomotion, and

(ii) An orientation towards the goal or stimuli to which the animal is receptive (such as smell, sight of food, water and mate).

Both appetitive and consummatory actions are dependent on the level of motiva­tion for that particular behaviour. This can be amply demonstrated in the case of a hungry dog. When the dog is hungry it starts showing searching behaviour.

The motivational level/urge/drive increases for eating, after locating a food. It starts indulging in a consummatory action (that is eating food). As the animal eats, the motivational level of hunger gradually decreases till it gets to almost zero when the animal has eaten its full meal. This stops both consummatory and appetitive behaviours.

Characteristics of Instincts:

1. Instincts are behaviours that are basically determined and transferred through genes.

2. Instincts are similar in all individuals of a species.

3. Instincts involve complex and highly rigid pattern of behaviour involving numerous muscles, muscle groups, organs and systems that function in an entirely coordinated manner.

4. Instinctive actions are specific and stereotyped sequence of activities that are triggered by complex stimuli called sign stimuli.

Conservative nature of FAP:

FAPs are considered to be extremely conservative in the evolution of a species. Once they have appeared in a species, they are resistant to phylogenetic changes. This can be confirmed through the study of behaviour of long-tailed and short-tailed monkeys. When a long tailed monkey runs on a branch its long-tail moves from side to side for balancing the body. It is a fixed action pattern (FAP).

Although short-tailed monkeys had stopped using their tail as a structure of balancing yet they perform similar type of movements of the tail. Short-tail monkeys probably evolved from long-tail ones. The long tail had the important function of balancing and the FAP once evolved persisted even when the morphological structure of long tail had dis­appeared.

Category # 2. Learning Behaviour:

Learning may be defined as a relatively permanent change in behaviour as a result of experience. This definition of learning, how­ever, has a drawback, in that often it is diffi­cult to determine how long a time period con­stitutes “relatively permanent”. In the above definition of learning an interesting relation­ship can be drawn between learning and what evolutionary ecologists refer to as “phenotypic plasticity”.

A phenotype may be defined as the observable characteristics of an organism, while phenotypic plasticity is the ability of an organism to produce different phenotypes depending on environmental con­ditions. A good example of phenotypic plasti­city is provided by the bryozoan, Membranipora membranacea. It lives in colonies and, while doing so, individuals typically lack the spines that are often used as a defence against predators.

In the absence of predators, Membranipora membranacea simply do not grow spines. However, when individuals are exposed to predators they grow spines rela­tively quickly. Such a dramatic change from spineless to spined, as a result of environ­mental changes (addition of predators), con­stitutes a case of phenotypic plasticity.

Now, considering the definition of lear­ning as “a relatively permanent change in behaviour as a result of experience”, it then becomes one type of phenotypic plasticity, if behaviour is considered as a phenotype.

Thus, if “behaviour” is replaced by pheno­type then learning is considered as a form of phenotypic plasticity and it comprises of everything from long-lasting morphological changes to behavioural changes that come about due to experience.

Learning by Animals:

How animals learn or what are the mechanisms for learning, are the questions which has intrigued animal behaviourists. Heyes (1994) has put forward three com­monly recognized types of experience that can lead to learning.

(a) Learning from single-stimulus experience:

The simplest form of learning is a single stimulus which can be of any form. For example, in the cage of a rat, if for nume­rous times each day, a blue coloured stick is placed, then the rats will often take note of such a disturbance. They would turn their heads in that direction.

If the rat pays more attention to the blue stick over time, then sensitisation (sensitive to the stimuli) has occurred. On the other hand, if the rat takes less and less notice of the stick, then habitua­tion is said to have taken place. Thus, sensi­tisation and habituation are two simple forms of single-stimulus learning.

Habituation as a problem:

If animals become habituated quickly to stimuli, then it becomes very difficult to examine certain types of behaviour, particularly in labora­tories. This is amply demonstrated in the case of anti-predatory behaviour. Supposing two aquariums are taken and placed side by side.

In one is placed a predatory fish, while, in the other, some prey fishes are kept. In such a case visual interactions between predatory and prey are possible (Fig. 5.5), but the predator is unable to cause any harm to the prey.

Such experimental protocol spares the life of the potential prey. However, it creates a scenario in which the prey sub­sequently will get habituated to the predator, having learnt that the predator cannot pose any real danger. Ethologists, thus, have to go to great lengths to be certain that habituation has not occurred in their study material at the time of setting up experiments.

Consequences of habituation or sensitisation in learning:

A single-stimulus resulting in habituation or sensitisation may also have other consequences for learning such as:

(i) If an animal gets habituated to a particular stimulus, then it may interfere with later attempts to get the individual to associate that stimulus with another event. For example, in the case of the blue stick experiment with the rat, which has become habituated with it, it would prove more difficult for them to subsequently learn that the blue stick signals the arrival of food or any other event.

(ii) If sensitisation to a single cue has taken place, then it can be utilised for the association of other events.

(b) Stimulus-stimulus (Pavlovian con­ditioning):

In this case, instead of giving a single stimulus like the blue stick, it is paired with a second stimulus, say the odour of a cat (the odour of which the rats have an inherent fear). In this experiment, five seconds after the introduction of the blue stick, the odour of a cat is sprayed at one corner of the cage.

Subsequently, the rat learns to associate stimulus 1 (blue stick) with stimulus 2 (cat odour). It responds by hiding as soon as the blue stick appears and before the odour of the cat is sprayed. Such designed experiment is called Pavlovian or classical conditioning.

Pavlovian conditioning was first deve­loped by Ivan Pavlov (1849-1936) in the late 1800’s. Experiments of Pavlovian condition­ing involve two stimuli-conditioned and unconditioned. A conditioned stimulus (CS) is a stimulus that fails initially to elicit a particular response, but does so when it becomes associated with a second (uncondi­tioned) stimulus.

The blue stick is considered as the conditioned stimulus. Unconditioned stimulus (US) is a stimulus that elicits a vigorous response in the absence of training. The US, thus, is the cat odour. The rat having learnt to hide on seeing the blue stick alone — then, such response is called conditioned response (CR).

In the learning literature, distinction is made between pleasant and unpleasant stimuli. Any stimulus that is considered to be positive, pleasant or rewarding is labeled as appetitive stimulus. It includes food, a safe place to live, presence of potential mate etc. Any stimulus that is associated with some unpleasant event is called aversive stimulus.

Relationships also can be distinguished between positive and negative types. In the above Pavlovian conditioning experiment, when the first event (placement of the blue stick) predicts the occurrence of the second event (cat odour), such relationships are said to be positive.

If the first event predicts that the second event will not occur, then it is a negative relationship. Relationships that are positive produce excitatory conditioning, while those that are negative produce inhibitory conditioning.

When a res­ponse made by an animal is somehow rein­forced, then instrumental conditioning has occurred. It is also known as operant or goal- directed learning. A classical example of instrumental learning is provided in the case of a rat pressing some sort of lever to get food to drop into his cage. Here the rat quick­ly associates itself with an action (pressing a bar) to get a response (food dropping into the cage).

Edward Thorndike (1911), working on instrumental learning, postulated the law of effect. The law of effect states that if a response in the presence of a stimuli is followed by a delightful or satisfying event, then the association between the stimulus and the response will be strengthened. On the contrary, if the response is followed by an adverse or hostile event, then the association will be weakened.

The drawback of instrumental learning is that it ignores the fact that behaviour was a continuous and free-flowing variable. This problem is somewhat rectified by B. F. Skinner (1938), who has devised the Skinner box which allowed a free-operant procedure. Skinner’s idea was to create a continuous measurement of behaviour that would be divided into meaningful units.

Pavlovian conditioning and instrumental learning differs in the basic fact that, in the latter, the animal must undertake some action or response in order for the conditio­ning process to produce learning. However, there is still some doubt over the relative merits of Pavlovian and instrumental learn­ing techniques.

Ability to Learn:

The ability to learn is thought to be under some sort of complex genetic control, but whether this ability is favoured by natural selection is a matter of question. If it is favoured then under what circumstances?

Psychologists, behaviour ecologists and ethologists are of the opinion that the ability to learn should be favoured over the genetic transmission of fixed trait when the environ­ment in which an animal lives changes often, but not too often.

Information is best passed on by genetic transmission when the envi­ronment rarely changes, because such a means of transmission avoids the cost of learning and the environment the offspring encoun­ters is similar to that of their parents.

However, if the environment is constantly changing, there is nothing worth learning as what is learnt is completely irrelevant in the next situation. Past experience, thus, is of no predictive value. Therefore, genetic transmis­sion of a fixed response, rather than a learned response, is favoured.

Somewhere, in between an environment that never changes and “one that always does, learning is favoured over genetic transmission of a fixed response as it is worth paying the cost of learning. In such a case, the environment is stable enough to favour learning, but not so stable as to favour transmission.

David Stephens (1933), while agreeing with the above, has challenged the assump­tions about environmental stability saying that two types of stability need to be sepa­rated.

Stephens has broken environmental predictability into two sections:

(i) Predic­tability within the generation (lifetime) of an individual, and

(ii) Predictability bet­ween the environment of parents and off­spring.

Stephens has put forward a model (Table 5.1) of the evolution of learning. From this model, Stephens has shown that lear­ning is favoured when predictability within the lifetime of an individual is high, but environmental predictability between gene­rations is low (box 3).

In all the other cases (boxes 1, 2 and 4) as learning has a cost asso­ciated with it, fixed genetic transmission is favoured. In box 3, learning is favoured because once an organism learns what to do it can repeat the appropriate behaviour dur­ing its lifetime.

Types of Learnt Behaviour:

Learnt behaviour can be distinguished into eight types:

When a stimulus is repeated frequently with neither reward nor punishment, resulting in a gradual decrease in behavioural responsiveness then it is called habituation. Here the animal learns to ignore insignificant stimuli.

A few examples of habituation are:

(i) Scarecrows erected to drive away birds in crop-fields are effective for a short time. Soon the birds get habitua­ted to this harmless scarecrow.

(ii) Cloud- shadow passing overhead causes escape responses in young birds which gradually diminishes.

(iii) Fishes present in a water body next to a railway track show gradual decrease in behavioural response due to the commotion created by passing trains.

Imprinting cannot be precisely defined. However, it is the imposi­tion of a stable behaviour pattern in a young animal by exposure to particular stimuli during a critical period in the animal’s deve­lopment. Imprinting refers to various beha­vioural changes whereby a young animal becomes attached to a ‘mother figure’ and/or a future mating partner.

Konrad Lorenz (1937) was the one who introduced imprin­ting through his experiments with geese, where he got broods of goslings to follow him and treat him as their mother figure.

Imprinting generally takes place after hatching or birth and often results in a very fixed attachment, which is difficult to change. Such learnings are unique and unlike other forms, is irreversible and restricted to a brief ‘critical period’ just after hatching.

Imprinting occurs before anything else has been acquired by learning. It is often a very clear and identifiable event and this has made it extremely useful for the study of the neural basis of learning and memory.

Imprinting can be measured by the amount of attention paid to the mother, time spent in close association, latency to approach, time spent in following mother if she moves and so on. This type of response to mother figure is generally called ‘filial imprinting’ to contrast it with ‘sexual imprinting’.

Sexual imprinting is not measu­rable at this particular time but only later in life when it can be observed how its early experience affects an animal’s choice of sexual partners at maturity.

The response to mother figure is called filial imprinting. The range of objects which can elicit approach and attachment in young birds is very large. Stimuli for imprinting may be visual, audi­tory or olfactory. There seems to be no limit to the range of visual stimuli. Movements help to catch attention like flashing lights. A stationary object will attract young birds pro­vided it is contrasting with its background.

Auditory stimuli are found to be attractive to many young birds. For example, in mallard ducklings, sound is very important to induce following the mother figure. Wood-ducks nest in holes in trees. The call of the mother from the water outside the nest hole induces the young ones to approach the mother in spite of the fact that they have not seen her properly.

An example of odour stimuli is provided by the 5 to 14 day old baby shrews. These baby shrews become imprinted on the odour of the individual mother that is nursing them. Young shrews form a caravan early in life, having learned the odour of their mother, which they will follow (Fig. 5.6). When 5 or 6 day old shrews are provided with a substitute mother of another species, the odour of this caretaker mother becomes imprinted upon them.

Later, when the shrews are 15 days old, they are returned back to their real mother. It was seen that these siblings do not follow her and do not form the caravan like chain on any siblings that were left with the real mother.

However, they followed a piece of cloth impregnated with the odour of their caretaker mother, a response that demonstrates that young shrews become imprinted with the odour of whoever nurses them when they are young.

According to Lorenz, early experience of young geese and ducks affect their choice of sexual partner when they are mature. In sexual imprinting young individuals “imprint” on what consti­tutes an appropriate mate from observing adults in their population. Like filial imprin­ting, in sexual imprinting also, there is virtu­ally no limit to the range of objects which can provoke attachment.

A complete experimental work of sexual imprinting was performed taking zebra finch and Bengalese finch. These birds were selec­ted, as they readily breed in small cages and have a very rapid life cycle (They become independent at about 5 weeks and starts breeding soon after). Immelmann (1972) placed a single zebra finch egg among a number of Bengalese finch eggs and allowed the Bengalese parents to rear the whole brood.

Later, the fostered zebra finch male was isolated till it attained sexual maturity. A cage was then constructed which was divi­ded into three parts by two transparent parti­tions, but with a continuous perch running through them. In the middle part, the fostered zebra finch male was placed, while on either side compartments the females of Bengalese finch and zebra finch were kept.

The results observed was very interesting. The male finch directed its courtship towards the female Bengalese finch (Fig. 5.7). The female Bengalese finch was neutral and usually showed avoidance as the male approached her. The female zebra finch, on the other hand, responded naturally with all the usual conspecific greeting calls and perched as close to the male as the partition allowed.

The sexu­ally imprinted male zebra finch initially pre­ferred to court with the females of their Bengalese foster-parent species. Immelmann then took such imprinted males and then forced them to pair with the females of zebra finch. Although initially being uninterested they were subsequently forced, in the absence of any choice, to give in and breed with their conspecific partners.

They were allowed to raise one or two broods of young together. The males were then, once again, tested for their preference in the three compartmented cage. If was observed that the foster-parent Bengalese females still remained a strong choice for courtship. Such dramatic results suggest how resistant sexual imprin­ting is to changes.

Imprinting, thus, is a unique form of learning because of 3 factors:

1. It takes place only during a brief sen­sitive period early in the life.

2. It has great stability, often lasting for the rest of the animal’s life.

3. It influences the animal’s adult social and sexual behaviour

When the response is modified by past experience it is called conditioned reflex. These reflexes are coordinated by the brain. The mechanism of conditioned reflex can be best understood through the work of I. P. Pavlov (1901) on dog. A hungry dog was placed on a stand and restrained by a harness.

The dog was then presented with food in powder form at regular intervals. The delivery of the food was preceded with an external stimulus, like the ringing of a bell. The dog began responding to the bell alone by licking its lips and secretion of saliva.

There are many instances of conditioned reflexes from our daily life. An empty hot utensil when touched burns the finger and is dropped down immediately (simple reflex action). On the other hand, an equally hot utensil full of eatables, when touched, is equally painful for the fingers, and is put down quickly but gently without spilling the contents (conditioned reflex). The difference in the degree of response reveals the involve­ment of conditioning and memory, followed by a conscious decision by the brain.

(d) Trial-and-error learning:

Animals through trial-and-error method learn things of day to day happenings. They try various alternatives and gradually learn to solve the problem through failure and success. B. F. Skinner’s (1938) experiment of liver pushing by rat resulting in the dropping of food is an example of trial-and-error learning.

Another experiment conducted by Skinner was with pigeons where it learns to press a lever to open the door of a box to get food grains. In both the cases the experiment was repeated many times. The animals gradually press the bar in less and less time interval and finally in no time.

According to Thorpe (1960), learning also takes place even in those cases where no punishment or reward is associated. Latent learning is the association of different stimuli without any immediate reward or punishment. Animals in their life time are exposed to new experi­ences and are always in the process of lear­ning, which may be utilised in later stages of life (thus the word latent).

A good example of latent learning was provided by Metzgar (1967) working with deer-mouse (Peromyscus leucopus). One group of deer-mice was given exposure to and experience by placing them in an enclosed big hall containing natural things like plants, hay, twigs, logs etc. A second group of mice was kept in laboratory cages without any exposure to the above natural things.

Next, the mice from each group were placed in the enclosed room along with a predatory owl. Metzgar observed that only two of twenty deer-mouse with previous experience of the hall were captured by the owl, while eleven of twenty mice with no prior experience of the habitat were caught. This shows that latent learning apparently provided the experienced deer-mouse to avoid the predator (owl).

Insight is considered as the ability to respond correctly to a situation that is experienced for the first time in life and quite different from any experience encoun­tered previously. Demonstration of insight was provided by W. Kohler (1927) through his experiment on chimpanzee.

Kohler put a chimpanzee in a room where a number of boxes were kept scattered on the ground. He hung a few bananas from the ceiling which were too high for the chimpanzee to reach. At first the chimpanzee tried to reach the bananas by jumping.

On failing to reach it, he sat down pondering. After some time he stood up and stacked the wooden boxes, one above the other and climbed up to get the bananas. This response appeared after a period of apparent thought and is called insight.

Reasoning may be defined as the ability to combine sponta­neously two or more separate experiences to form a new experience which is effective for obtaining a desired goal. Reasoning is a men­tal process which is very evolved form of behaviour, found perhaps only in apes, dolphins, killer whales and human beings. However, much is yet to be learnt about the neural mechanism of reasoning.

Cognition may be defined as the ways by which animals take in information through the senses, process the information and then decide to act on it. Cognitive process such as perception, lear­ning, memory and decision-making play important role in mate choice, foraging and lot of other behaviours. Cognition cannot be observed directly) It is an improvement over insight, where one gains and uses the know­ledge acquired for various things.

Tolman (1886-1959) is regarded as the father of modern cognitive approach to ani­mal behaviour. He pioneered the idea of cognitive maps which is a mental model of the external environment, which may be con­structed following exploratory behaviour. Such cognitive maps are acquired by animals indicating how the relevant spatial or causal features of the environment relate to each other.

Category # 3. Complex Behaviour:

The simplest unit of behaviour is the reflex. Behavioural patterns were initially thought to have been brought about by long and complex chain of reflexes. But behaviour is not all about external stimuli it is also based on internal physiological conditions and spontaneous reactions controlled by nervous, hormonal and muscular systems.

However, one can learn some of the basic features of behavioural mechanisms through the study of properties which reflexes share with more complex patterns and which can be clearly related to the properties of indi­vidual nerve cells. On the operation of the nerve cells, all behaviour depends.

It is difficult to draw a firm line between reflexes and complex behaviour. Complex behaviour can incorporate many reflexes. For example, the swallowing reflex is the culmi­nation of elaborate food-seeking behaviour. Complex behaviour, thus, is the product of an integrated series of changes in cell chem­istry initiated by receptor cells and carried on by sensory interneurons and motor cells and muscles.

For example, singing in a crick­et or a bird, where the body works due to the coordination of nerves, muscles and sense organs. The nervous system is remarkable in the sense that it not only responds to stimuli but also possesses a remarkable ability to preserve the effect of previous stimuli for a shorter or longer period.

Charles Sherrington (1906), the father of modern neurophysiology, considered ways in which reflexes operate and how the central nervous system integrates them into adap­tive behaviour by combining information gathered from different sources, arranging them into sequences of action and allocating priorities.

The properties of reflexes and complex behaviour are:

(a) Latency:

Latency is the delay between giving a stimulus and seeing its effect. Latency in response is exhibited by both reflexes and complex behaviour. When a dog encounter­ing a painful stimulus, the latency between the encountering of the stimulus and showing of flexion reflex (that is, withdrawal of the leg), lies between 60 and 200 milliseconds.

Of this delay, a small fraction of time is taken for nerve impulses to be conducted along axons while the majority of the delay is due to the synapses (the term coined by Sherrington) between one neuron and the next. Thus, the delays between stimulus and response in complex behaviour are due to the fact that, in the chain between receptors and effectors, there are often dozens of synapses to cross.

Another example of latency can be cited from the toad’s tongue flip to the escape of a cockroach. Slowed-down film shows that just before the toad’s tongue flips out of its mouth and strikes, the cockroach can sense it and would run out of reach. The important cue is the tiny gusts of wind produced by the toad’s movement which are picked up by the cock­roach through many tiny wind-sensitive hairs on its cerci.

The critical gust of wind occurred, on average, 41 ms (milliseconds) before the tongue starts emerging from the mouth. The latency period between the puffs of air and the cockroaches reaction (escape behaviour) is 44ms, which is sufficient for it to escape.

It is often difficult to measure latencies for complex behaviour. It has been observed with reflexes that the stronger the stimulus, the shorter the latency. Some evidences sug­gest that the same is true for certain complex behaviour.

Hinde (1960), working on chaffin­ches (Fringilla coelebs), was able to measure the latency between presenting various frightening stimuli and how soon they gave their first alarm calls. He observed that the stimulus which the strongest produced the shortest latency.

(b) Summation:

It has been observed that sometimes individual neurons respond only after they have received several post-synaptic potentials and, thus, are able to summate (add up) excitation coming either at different times (temporal summation) or from different places (spatial summation). An example of summation at the level of reflex is provided by Sherrington (1906), through the scratch reflex of the dog.

When an irritating stimulus is elicited in the dog’s back, the hind leg on the same side is brought forward and is rhythmi­cally scratched at the spot. First, weak stimuli are given singly at two points of the skin (A and B), 8 cm apart. They do not evoke the reflex.

When both the points are stimulated simultaneously the reflex appears with a latency of about 1 second. Thus, neither is strong enough alone to evoke scratching, but are effective when given together. Fig. 5.8 shows the above spatial summation.

Summation in more complex behaviour occurs between stimuli of quite different types, which are perceived by different sense organs. The sight and smell of food plus the sound of utensils summate when we are hungry.

Male rats respond sexually to a combination of visual, olfactory and tactile stimuli from a receptive female. Generally, young male rats do not respond unless any two such sources are available. However, mature males, with previous experience, will respond to one type of stimulus alone (a case of temporal summation).

(c) ‘Warm-up’ or Facilitation or ‘Motor- recruitment’:

At first some reflexes do not appear at full strength. But, when with no change to the stimulus, their intensity increases over a few seconds. Such type of reflexes are said to be ‘Warm-up’, where neurons show synaptic facilitation, each successive postsynaptic potential (PSP) being larger than the previous one.

Hinde (1954) found that when an owl is shown to chaffinches it shows a type of ‘warm-up’ effect. The bird gives out a mob­bing call in response to the owl. The number of calls given by the chaffinch after the owl is shown is counted in successive 10-second periods. It was observed that the bird begins by calling at a relatively low rate and the maximum calling rate is reached at about 2-5 minutes, after which it gradually declines (Fig. 5.9).

Similar type of ‘warm-up’ effect is also exhibited by a pet dog when it encounters an auditory or olfactory stimuli of any unwan­ted trespasser. Initially the dog responds with slow barking, the intensity increases and then gradually declines.

Sherrington showed that such ‘warm-up’ in some reflexes is due to summation of stimuli which evokes a response from more and more nerve fibres, producing stronger concentration. This phenomenon was named by Sherrington ‘motor recruitment’.

Such type probably also occurs with com­plex behaviour, not only in the change of intensity but also in the nature of the behaviour. This was amply exemplified by Sherrington (1917) from what he named as the cat’s ‘pinna reflex’.

At first repeated tac­tile stimulation to the cat’s ear causes it to be laid back. If the stimulation persists, the ear is fluttered, subsequently the cat shakes its head and, when all the above fails to remove the irritation, it brings its hind leg up and scratches. It is clear that here more is involved than the recruitment of a few extra motor neurons.

Recruitments are also made to mechanisms which control patterns of movement such as ear-fluttering, head shak­ing, and scratching. All these mechanisms are probably activated in some way by stim­uli to the ear, but their thresholds are differ­ent, with the laying back on the ear being the lowest threshold. Workers studying complex behaviour generally rank the patterns they observe on an intensity scale of increasing thresholds.

(d) Inhibition:

Within the nervous sys­tem, nerve cells actively inhibit each other’s transmission of information. At the beha­vioural level, prevention of one’s activity occurrence, while another is in progress, con­stitutes inhibition. Muscles are generally arranged in anta­gonistic (a muscle contracts and limits the action of another) pairs, such that, when one flexes, the other extends it.

Sherrington showed that, when in one member of a mus­cle pair, excitation occurs it is accompanied by inhibition of its antagonistic pair. However, such inhibition is not absolute. Once a muscle is stretched by its antagonistic pair, then its own ‘stretch reflex’ will tend to make it contract. Mutual inhibition allows them to take the lead in turn during the limb movements and to alternate flexion and extension of the limbs.

In complex behaviour, the role of inhibi­tion is less obvious than that of excitation. When an animal is stimulated, the obvious result is that the it makes a response. Sherrington showed that the muscles, whose action is common to several different reflexes, compete with each other for the final common pathway.

The different controlling patterns of complex behaviour like fighting, feeding and sleeping compete for the control of the animal’s musculature. However, only one behaviour can occur at a time. The nervous system will allocate priorities since there will often be conflicts as to which stimuli should an animal respond to. Thus, inhibition of action would be as crucial as excitation.

To substantiate the above let us take a very common example where many animals require to take in food and water over the same time in order that digestion can pro­ceed normally. McFarland & Lloyd (1973), experimenting on doves, gave food and water to birds who had previously been deprived of both.

The doves alternated their behaviour between feeding and drinking. Much before satisfying their hunger, the doves abruptly stopped feeding and switched over to drinking.

Shortly after, they switched back to feeding again. They conti­nued in this fashion till they gradually ceased both activities. The thing to be focused in such behaviour is that the birds spent only a few seconds on each (feeding or drinking). Thus, sustained bouts of each activity in turn inhibited the other or, in other words, there was alternate inhibition of one activity by the other.

Sherrington further showed that when inhibition was removed from a reflex, it came back at a higher intensity than it had previ­ously. Sherrington called it ‘reflex rebound’. For example, when courtship was not allowed for some time, it has a lowered threshold and when, at last, it was evoked, it was performed at a much higher intensity.

Another example was provided by Vestergaard (1980), who found that when laying domestic hens were kept on wire, where they had no substrate in which to dust bath and when subsequently they were given access to litter, it was seen that they started dust bathing quickly and dust bathe in very much longer bouts than do hens kept all the time on litter.

Inhibition is, thus, of critical importance in animal behaviour, at all levels. Inhibition at neuronal level means that the firing of one nerve cell is actually suppressed because of the action of another. Inhibition at beha­vioural level means that behaviour which otherwise would have occurred is prevented from occurring by the action of another moti­vational system.

(e) Feedback Control:

Complex beha­viour or reflex generally consists of a steady output of any activity. For example, when we are standing at ease, our full body is evenly balanced over the pelvic girdle. If we receive any slight push or jostling, the body easily corrects it. This is done by the muscles of the legs and back which are held at a constant level of tension and if, shifted from this level, they correct and bring the body upright again.

In another case, animals under normal circumstances maintain a very constant body weight. To maintain it, animals eat and drink sufficiently at regular intervals. In case surplus food is available, they do not overeat. On the other hand, if there is scarcity of food, they spend more time in searching for food and when they get access to it, they consume more to replace any deficit.

In both the above examples, behaviour acts as a homeostatic (meaning ‘same state’) system. It serves to preserve the status quo. In the first example, status quo was achieved through reflex systems controlling the leg and trunk muscles. In the second example, it was achieved through a series of more complex systems regulating the search for food, feeding and satiation.

However, in both cases, the operation requires that the end result (posture and balance in the first case and nutrition in the second) is monitored in the same way. When a reflex deviates from the set value, a signal is sent to the control mechanisms to correct the imbalance and bring the end result back again to the set value. A diagrammatical representation of the above idea is shown in Fig. 5.10.

The homeostatic control of posture can be better understood at a neurophysiological level. Motor neurons have their cell bodies in the ventral horn of the spinal cord that run to the muscle (Fig. 5.11). It is the activity of the motor neurons that determines the tension developed by the muscle. Further, with every skeletal muscle, are muscle spindles that are embedded within its fibres so that they con­tract and relax with it.

These muscle spindles are specialised sense organs for recording the degree of tension in the muscle. Sensory nerves from it run back to the spinal cord. On entering through the dorsal root it synapses with the motor neurons and back to the mus­cle. Thus forming a closed loop, which forms the basis of the stretch reflex.

The feedback control at a reflex level takes place in the following manner:

1. When a muscle is stretched by the contraction of its antagonists, the muscle spindles are also stretched. Their sensory fibres increase their rate of firing, stimulating the motor neurons so that the muscle con­tracts.

2. The state of tension in the muscle (output) is affected by a disturbance (being stretched by other muscles). A feedback mechanism (muscle spindle) records the change. It feeds back to change the motor nerve (input) and restore the original input.

The above feedback control is over­simplified. The real situation includes other regulatory mechanisms that allows control over the muscle contractions involved in the maintenance of posture and also in move­ments.

In many behaviours, however, there is no feedback control. When a movement is made very rapidly, there is simply no time to modify the movement — such as, the tongue flip of the toad towards the cockroach. Such behaviour is said to be under ‘open-loop’ control (Fig. 5.10) where no feedback occurs.

To sum up the complex behaviour, it can be said that despite the many levels at which behaviour of animals is studied, there are certain principles (excitation, inhibition, summation, facilitation and feedback) that appear to be common to many different levels. Different techniques and very diffe­rent concepts are required for studying single neurons and for the behaviour of whole ani­mals.

Nonetheless, it is important to keep these common principles in mind, so as to break-down complex behaviour patterns into smaller units, some of which may be similar to reflexes. However, one cannot always explain behavioural observations using reflex terminology as there are diffe­rences in complexity, which often require different types of approach.

Hering, Ewald


German physiologist Karl Ewald Konstantin Hering (1834–1918) was not only one of the founders of modern visual science but also made significant contributions in many other areas. In 1868, Hering and Josef Breuer reported that sustained distention of the lungs of anesthetized animals decreased the frequency of inspiratory effort or caused transient apnea, a reflex phenomenon designated eponymically as the Hering–Breuer reflex. In 1868, Hering proposed the law of equal innervation, which attributed the conjugacy of eye movements to innate connections in which yoked eye muscles are innervated equally Hering's Law challenged Hermann von Helmholtz's view that each eye is controlled independently and binocular vision is learned. In 1872, Hering similarly challenged the trichromatic color vision theory of Thomas Young and Hermann von Helmholtz, which held that the human eye perceives all colors in terms of three primary colors instead, Hering proposed the opponent process theory, which stated that the visual system operates using a system of color opponency, such that responses to one color of an opponent channel are antagonistic to those to the other color.

Pathophysiology of Spasticity: Implications for Neurorehabilitation

Spasticity is the velocity-dependent increase in muscle tone due to the exaggeration of stretch reflex. It is only one of the several components of the upper motor neuron syndrome (UMNS). The central lesion causing the UMNS disrupts the balance of supraspinal inhibitory and excitatory inputs directed to the spinal cord, leading to a state of disinhibition of the stretch reflex. However, the delay between the acute neurological insult (trauma or stroke) and the appearance of spasticity argues against it simply being a release phenomenon and suggests some sort of plastic changes, occurring in the spinal cord and also in the brain. An important plastic change in the spinal cord could be the progressive reduction of postactivation depression due to limb immobilization. As well as hyperexcitable stretch reflexes, secondary soft tissue changes in the paretic limbs enhance muscle resistance to passive displacements. Therefore, in patients with UMNS, hypertonia can be divided into two components: hypertonia mediated by the stretch reflex, which corresponds to spasticity, and hypertonia due to soft tissue changes, which is often referred as nonreflex hypertonia or intrinsic hypertonia. Compelling evidences state that limb mobilisation in patients with UMNS is essential to prevent and treat both spasticity and intrinsic hypertonia.

1. Introduction

Spasticity is a stretch reflex disorder, manifested clinically as an increase in muscle tone that becomes more apparent with more rapid stretching movement. It is a common consequence of lesions that damage upper motor neurons causing upper motor neuron syndrome (UMNS).

The main objectives of this paper are (1) to describe the clinical features of spasticity as one component of UMNS (2) to describe the mechanisms of muscle tone in normal subjects (3) to show that spasticity is due to an exaggeration of stretch reflexes caused by an abnormal processing of sensory inputs in the spinal cord (4) to show that muscle hypertonia in patients with UMNS is also caused by muscle shortening and fibrosis (intrinsic hypertonia) (5) to show that lesions damaging upper motor neurons disturb the balance of supraspinal inhibitory and excitatory inputs controlling the stretch reflex (6) to describe changes of stretch reflex excitability in the spinal cord triggered by the upper motor neurons dysfunction and (7) to underline that limb mobilisation in patients with UMNS is essential to prevent and treat both spasticity and intrinsic hypertonia.

2. Definition and Clinical Features

The core feature of spasticity is the exaggeration of stretch reflexes. The result is the velocity-dependent increase in resistance of a passively stretched muscle or muscle group. In 1980, Lance published this frequently cited definition: “Spasticity is a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motoneuron syndrome” [1]. This definition emphasizes the fact that spasticity is just one component of UMNS.

Besides the dependence from velocity, spasticity is also a length-dependent phenomenon. In the quadriceps, spasticity is greater when the muscle is short than when it is long [2, 3]. This is probably one of the mechanisms underlying the so-called clasp knife phenomenon. Bending the knee, at first (when the muscle is short) a great resistance is met. Then, when the quadriceps lengthens, the resistance suddenly disappears. Another mechanism underlying the clasp knife phenomenon could be the excitation of higher-threshold muscle receptors (groups III and IV) belonging to the flexor reflex afferents [4]. On the contrary, in the flexor muscles of the upper limb [5] and in the ankle extensors (triceps surae) [3], spasticity is greater when the muscle is long.

Spasticity is more often found in the flexor muscles of the upper limb (fingers, wrist, and elbow flexors) and in the extensor muscles of the lower limb (knee and ankle extensors). However, there are several exceptions. For example, we observed patients in whom spasticity is prevalent in extensor muscles of the forearm.

3. Stretch Reflex and Muscle Tone in Healthy Subjects

In healthy subjects, stretch reflexes are mediated by excitatory connections between Ia afferent fibers from muscle spindles and α-motoneurons innervating the same muscles from which they arise. Passive stretch of the muscle excites the muscle spindles, leading Ia fibers to discharge and send inputs to the α-motoneurons through mainly monosynaptic, but also oligosynaptic pathways. The α-motoneurons in turn send an efferent impulse to the muscle, causing it to contract.

Surface EMG recordings in a normal subject at rest clearly show that passive muscle stretches, performed at the velocities used in the clinical practice to assess muscle tone, do not produce any reflex contraction of the stretched muscle. For instance, recording the EMG of elbow flexors during imposed elbow extension, no stretch reflex appears in the biceps when the passive displacement occurs at the velocities usually used during the clinical examination of muscle tone (60°–180° per second). It is only above 200° per second that a stretch reflex can be usually seen. Therefore, stretch reflex is not the cause of the muscle tone in healthy subjects. The muscle tone in healthy subjects is completely due to biomechanical factors [6].

4. Muscle Tone in Patients with Spasticity: The Exaggerated Stretch Reflex

Differently from healthy subjects, in patients with spasticity evaluated at rest (completely relaxed), a positive linear correlation between EMG activity of the stretched muscle and stretch velocity was found using a range of displacement velocities similar to that used in the clinical practice to evaluate the muscle tone. When the passive stretch is slow, the stretch reflex tends to be small (low amplitude) and the tone may be perceived relatively normal or just increased. When the muscle is stretched faster, stretch reflex increases and the examiner detects an increase in muscle tone. Therefore, spasticity is due to an exaggerated stretch reflex [6].

Although spasticity is velocity-dependent, surface EMG recordings show that in many cases if the stretch is maintained (velocity = 0), the muscle still keeps contracting, at least for a time. So, although spasticity is considered classically dynamic, there is also an isometric tonic muscle contraction after the stretch reflex elicited in a dynamic condition (Figure 1 personal unpublished data).

5. Soft Tissue Changes: Intrinsic Hypertonia

Spasticity is responsible for the velocity-dependence of muscle hypertonia in patients with UMNS. However, it must be stressed that in such patients muscle hypertonia is a complex phenomenon, where spasticity represents only one aspect.

Animal studies show that muscle immobilization at short lengths reduces serial sarcomere number [7] and increases the proportion of connective tissue in the muscle [8]. These changes, which emerge very early during immobilisation [9], enhance muscle resistance to passive displacements [10] and increase the resting discharge of muscle spindles and their sensitivity to stretch [11]. It is likely that muscle contracture in patients with UMNS is produced by similar adaptations.

In patients with UMNS, muscle contracture makes a significant contribution to hypertonia [12–14]. Hypertonia in patients with UMNS, therefore, can be divided into two components: hypertonia mediated by the stretch reflex, which corresponds to spasticity, and hypertonia due to muscle contracture, which is often referred as nonreflex hypertonia or intrinsic hypertonia. In contrast to spasticity, in intrinsic hypertonia resistance to passive displacements is not related to the velocity of the movement. However, in a clinical setting it can be difficult to distinguish reflex and nonreflex contributions to muscle hypertonia [15, 16], especially when muscle fibrosis occurs without shortening of the muscle. Biomechanical measures combined with EMG recordings can be helpful in this attempt [17]. It is important to say, however, that the two components of hypertonia are likely to be intimately connected. The reduced muscle extensibility due to muscle contracture might cause “any pulling force to be transmitted more readily to the spindles,” thus increasing spasticity [18].

6. The Exaggeration of Stretch Reflex in Patients with Spasticity Is due to an Abnormal Processing of Sensory Inputs in the Spinal Cord

Theoretically, the exaggeration of the stretch reflex in patients with spasticity could be produced by two factors. The first is an increased excitability of muscle spindles. In this case, passive muscle stretch in a patient with spasticity would induce a greater activation of spindle afferents with respect to that induced in a normal subject, of course considering a similar velocity and amplitude of passive displacements. The second factor is an abnormal processing of sensory inputs from muscle spindles in the spinal cord, leading to an excessive reflex activation of α-motoneurons.

Classical studies in the decerebrate cat suggest that γ-motoneurons hyperactivity and subsequent muscle spindle hyperexcitability have a role in producing hypertonia [19]. On the contrary, studies in humans suggest that fusimotor dysfunction probably contributes little to exaggerated stretch reflex [20]. The commonly accepted view, therefore, is that spasticity is due to an abnormal processing in the spinal cord of a normal input from the spindles.

The velocity-dependence of spasticity can be attributed to the velocity sensitivity of the Ia afferents. However, several studies suggest that II afferent fibers from muscle spindles are also involved in spasticity activating the α-motoneurons through an oligosynaptic pathway [21, 22]. It has been suggested that II afferent fibers, which are length-dependent, could be responsible for the muscle contraction in isometric conditions often seen after the dynamic phase of the stretch reflex in patients with spasticity [23].

7. Upper Motor Neuron Syndrome: A Complex Picture Where Spasticity Is Only One Component

After a stroke or a trauma damaging upper motor neurons, weakness and loss of dexterity are immediately apparent. Other signs can be hypotonia and loss (or reduction) of deep tendon reflexes. These signs are known as the negative features of the UMNS. Sometime later, other signs appear, characterised by muscle overactivity: spasticity, increased deep tendon reflexes (also called tendon jerks), clonus, extensor spasms, flexor spasms, Babinski sign, positive support reaction, cocontraction, spastic dystonia, and associated reactions. These signs are known as the positive signs of the UMNS. Among them, the only one that tends to appear soon after the lesion, together with the manifestation of the negative signs, is the Babinski sign [24].

The hyperexcitability of the stretch reflex produces spasticity, clonus, and the increase of deep tendon reflexes. Increased excitability of the physiological flexor withdrawal reflex produces flexor spasms of the lower limbs, commonly seen after spinal cord injuries. The release of primitive reflexes (existing at birth but later suppressed during development) is the cause of the Babinski sign and the positive support reaction. The Babinski sign is a cutaneous reflex, while the positive support reaction is a proprioceptive reflex.

On the contrary, cocontraction and associated reactions do not depend on spinal reflexes therefore, they are efferent phenomena. Also spastic dystonia is thought to depend upon an efferent drive.

Cocontraction is the simultaneous contraction of both the agonist and the antagonist muscles around a joint, for example, the wrist flexors and extensors. In healthy subjects, the voluntary output from the motor cortex activates the motoneurons targeting the agonist muscles and, through the Ia interneurons, inhibits those innervating the antagonist muscles (reciprocal inhibition). In the UMNS, cocontraction is due to the loss of reciprocal inhibition during voluntary command [25]. This is likely to be the most disabling form of muscle overactivity in patients with UMNS, as it hampers generation of force or movement.

Associated reactions are involuntary movements due to the activation of paretic muscles which occur during voluntary activation of unaffected muscles or during involuntary events such as yawning, sneezing, and coughing [26]. An example of associated reaction is the elbow flexion and arm elevation often seen in hemiplegic subjects during walking [23].

Spastic dystonia refers to the tonic contraction of a muscle or a muscle group when the subject is at rest. It can be described as a relative inability to relax muscles [18]. Spastic dystonia can alter resting posture contributing to the hemiplegic posture: the upper limb is flexed and adducted the lower limb is extended [23]. Although not induced by muscle stretch, spastic dystonia is sensitive to muscle stretch and length. It can be triggered by muscle stretch, even though prolonged stretch can reduce it [18]. The common view is that spastic dystonia is an efferent phenomenon, mediated by an abnormal pattern of supraspinal descending drive [18]. The inability to relax the muscle (i.e., spastic dystonia) is a central feature in spastic patients and is likely to be connected to the prolonged firing of α-motoneurons, a well-documented phenomenon in patients with UMNS [27]. We think that this inability to relax the muscle is present not only after a voluntary contraction or after an involuntary event (for instance yawning, sneezing, and coughing), but also after a reflex contraction, possibly having a role in the isometric tonic muscle contraction often seen in spastic patients after the dynamic phase of stretch reflex. We do think that this issue warrants further studies.

8. Supraspinal Influences on the Stretch Reflex: Studies in Animals

In 1946, Magoun and Rhines discovered a powerful inhibitory mechanism in the bulbar reticular formation, in an area immediately behind the pyramids (ventromedial bulbar reticular formation). The stimulation of this area can suppress any type of muscle activity, including stretch reflex activity, both in decerebrate and in intact animals. Studies conducted with the local application of strychnine were the first to show that the ventromedial bulbar reticular formation receives facilitatory influences from the premotor cortex [28]. Accordingly, while the destruction of the primary motor cortex [29] or the interruption of its pyramidal projections in the brain stem [30] caused a flaccid weakness, more extensive cortical lesions, involving premotor and supplementary motor areas, were followed by increased activity of the stretch reflex due to the inhibition of the ventromedial bulbar reticular formation [31]. The inhibitory influences from the bulb are conducted down to the spinal cord by the dorsal reticulospinal tract, which runs very close to the lateral corticospinal tract (pyramidal tract) in the dorsal half of the lateral funiculus [32].

In contrast, the stimulation of the reticular formation of the dorsal brain stem from basal diencephalon to the bulb (dorsal reticular formation) can facilitate or exaggerate any type of muscle activity, including stretch reflex activity [28]. The facilitatory effects, unlike the inhibitory effects of the reticular formation, are not controlled by the motor cortex [33]. The facilitatory influences from the dorsal reticular formation are conducted down to the spinal cord by the medial reticulospinal tract in the anterior funiculus, together with the vestibulospinal tract. The latter, important in the cats as far as the development of hypertonia is concerned, seems to be of declining significance in the primates [34].

In conclusion, studies in animals showed that two major balancing descending systems exist, controlling stretch reflex activity: the inhibitory dorsal reticulospinal tract on one hand and the facilitatory medial reticulospinal and vestibulospinal tract on the other. Only the ventromedial bulbar reticular formation, the origin of the dorsal reticulospinal tract, is under cortical control. The prevalence of the facilitatory system on the inhibitory one leads to the exaggeration of the stretch reflex (Figure 2).

9. Supraspinal Influences on the Stretch Reflex: Studies in Humans

These studies provided results in line with those performed in animals. First, spasticity is not related to the pyramidal system. Selective damage to the pyramidal tract at the level of the cerebral peduncle [35] and at the level of the pyramids [36] is not followed by spasticity. Second, spasticity is due to loss or reduction of the inhibitory influences conducted by the dorsal reticulospinal tract. Section of the dorsal half of the lateral funiculus, performed to treat parkinsonism, was followed by spasticity [37]. Third, spasticity is maintained through the facilitatory influences conducted by the medial reticulospinal tract. The vestibulospinal tract plays only a minor role. Section of the vestibulospinal tract in the anterior funiculus of the cord, undertaken by Bucy with the hope of relieving hypertonia, resulted in transient but not permanent reduction in spasticity [38]. In contrast, extensive unilateral or bilateral anterior cordotomy, which is likely to have destroyed both the vestibulospinal tract and the medial reticulospinal tract, was followed by a dramatic reduction of spasticity [39]. Finally, some observations are in line with the finding in animals that the facilitatory corticobulbar system comes from the premotor cortex. Indeed, small capsular lesions in the anterior limb of the internal capsule, where the fibres from the premotor areas are located, tend to be associated with spastic hypertonus, whereas those confined to the posterior limb are not [40].

In conclusion, brain lesions cause spasticity when they disrupt the facilitatory corticobulbar fibers, thus leading to the inhibition of the ventromedial reticular formation, from which the dorsal reticulospinal tract takes its origin. Incomplete spinal cord lesions cause spasticity when they destroy the dorsal reticulospinal tract sparing the medial reticulospinal tract. In the complete spinal cord lesion, both the facilitatory and inhibitory influences on the stretch reflex are lost. As all these tracts inhibit the physiological flexor withdrawal reflex, flexor spasms are predominant [41].

10. Changes in Spinal Neuronal Circuitry in Spasticity

Dorsal reticulospinal tract exerts its inhibitory control over the stretch reflex through the activation of inhibitory circuits in the spinal cord. Some inhibitory circuits reduce the excitability of the stretch reflex acting on the membrane of α-motoneurons. These circuits are globally defined as postsynaptic inhibitory circuits and their effect is called postsynaptic inhibition. They include disynaptic reciprocal Ia inhibition, Ib inhibition, and recurrent inhibition [42]. Moreover, there is a circuit which reduces the excitability of the stretch reflex acting on the presynaptic terminals of Ia afferents through axoaxonal GABAergic synapses. The activation of this presynaptic inhibitory circuit reduces the release of neurotrasmitters in the synaptic cleft between Ia presynaptic terminals and the membrane of α-motoneurons causing presynaptic inhibition [43]. All these postsynaptic and presynaptic circuits can be investigated in humans using neurophysiological techniques based on the H-reflex [44].

Postsynaptic inhibitory circuits have been extensively investigated in patients with spasticity: Ib inhibition [45], disynaptic reciprocal Ia inhibition [46], and recurrent inhibition [47]. In general, all these mechanisms have been found to be decreased in patients with spasticity, supporting the concept that decreased postsynaptic inhibition is involved in the hyperexcitability of the stretch reflex. Also presynaptic inhibition has been found to be depressed in spastic patients with paraplegia [48] and in the upper limb of spastic hemiplegic patients [49].

Besides presynaptic inhibition, postactivation depression is another mechanism reducing the release of neurotransmitters from Ia afferents [50]. Although the molecular mechanisms responsible for postactivation depression are still an open issue [51], it has been shown that postactivation depression reflects an intrinsic neuronal property associated with a decreased probability of transmitter release from the repetitively activated Ia afferents [52]. Therefore, postactivation depression is not mediated by inhibitory spinal circuits and it does not seem to be controlled by descending motor pathways. In comparison to healthy controls, postactivation depression has been found to be lower in patients with spasticity [53]. A positive correlation has been reported between the diminished postactivation depression and the severity of spasticity following stroke [54] and cerebral palsy [55]. Moreover, in subjects with spinal cord injury, postactivation depression is normal in the acute phase and becomes depressed only just before the development of spasticity [56]. Altogether these studies state that postactivation depression plays a pivotal role in the development of spasticity. Compelling evidences in animals [57], healthy subjects [58–60], and spinal cord injured patients [60–63] state that reduction of postactivation depression is mainly caused by limb immobilisation, as that caused by the negative features of the UMN syndrome. We have recently shown that physical exercise can determine a partial normalization of postactivation depression in hemiparetic patients with spasticity following unilateral hemispheric stroke. This partial normalization was accompanied by a decrease of muscle hypertonia in some subjects [64].

11. Brain and Spinal Cord Plasticity

In damage from acute events (such as stroke or trauma), the delay between the neurological insult and the appearance of spasticity argues against it simply being a release phenomenon and suggests some sort of plastic changes, occurring in the spinal cord and also in the brain.

In the central nervous system, hypersensitivity of receptors resulting from partial or complete denervation is well documented [65]. The resulting hyperexcitability of the postsynaptic membrane may be caused by the formation of new receptors or by morphological changes in denervated receptors. This phenomenon (denervation supersensitivity) could be implicated in the increased excitability of α-motoneurons deprived of their regular descending excitation from the corticospinal pathways. Moreover, α-motoneurons after an UMN lesion are known to release growth factors locally [66]. These tend to promote local sprouting from neighbouring interneurons, thus creating conditions for the formation of new abnormal synapses between these interneurons and the somatic membrane of the deprived motor neurons. The new interneuronal endings branch onto the membrane of α-motoneurons and occupy the spaces left empty by the missing descending fibers [67], thus leading to the creation of new abnormal reflex pathways [68].

Furthermore, brainstem descending pathways (reticulospinal, vestibulospinal, tectospinal, and rubrospinal tracts) could be increasingly recruited to take over some of the execution of motor command following disruption of the corticospinal pathways. The excitatory connections to spinal motoneurons of these pathways are likely to be less selective than those of the corticospinal tract, leading to muscle overactivity.

Finally, an important mechanism could be the progressive reduction of postactivation depression due to limb immobilization [56, 57].

12. Pain and Spasticity

Spasticity can be the direct cause of pain [69]. It has been shown in healthy subjects that lengthening a contracted muscle (eccentric contraction) can cause the disruption of some muscle fibers with the release of substances that may excite the muscle nociceptors [70]. The same process is likely to happen when a spastic muscle is stretched. However, it must be said that all the positive and negative features of UMN syndrome along with soft tissue changes perturb body weight distribution, inducing excessive stress on joint structures and causing pain [23]. Sensory disturbances can also play a role. All these components lead to the pain perceived by the patients with UMNS. The relationship between spasticity and pain is made even more strict by the fact that pain increases spasticity, creating a spiralling course of more pain and disability [71].

13. Implications for Neurorehabilitation

This review underlines two aspects of great relevance for rehabilitation. The first point concerns the core feature of spasticity, that is, the exaggeration of stretch reflex. This phenomenon is mediated by several spinal mechanisms ranging from denervation supersensitivity of α-motoneurons to the reduced excitability of both postsynaptic and presynaptic inhibitory circuits which control the stretch reflex. These mechanisms, which reflect an aberrant adaptation of the neural circuitry at the spinal level, are actually the result of the lesion of the upper motor neuron. Postactivation depression, conversely, is a phenomenon that controls the excitability of the stretch reflex acting at the spinal level without depending on supraspinal control. It reflects an intrinsic membrane property of Ia afferent fibers, which appears to be independent of the influences exerted by rostral centres. In patients with UMNS, postactivation depression decreases due to limb immobilization, which in turn is caused by weakness and the other negative signs. This is an issue of fundamental importance as passive limb mobilization can restore postactivation depression reducing and even preventing spasticity, as proved by recent findings in humans [62, 64, 70].

The second point is that spasticity is not the only cause of muscle hypertonia in patients with UMNS. In such subjects, muscle immobilization (especially at short lengths) leads to muscle contracture, which makes a significant contribution to hypertonia [12, 13, 18, 64]. Furthermore, muscle fibrosis and the other components of muscle contracture could even increase spasticity through an overactivation of spindle afferents during muscle lengthening [18]. Muscle contractions may be prevented and treated by prolonged muscle stretching [72].

In conclusion, in patients with UMNS, weakness leaves the affected muscles immobilized. The immobilisation in a shortened position leads to muscle contracture, which is the cause of intrinsic hypertonia. At the same time, muscle immobilisation reduces postactivation depression, which is a pivotal mechanism in the development of spasticity. Therefore, in patients with UMNS, mobilization of the affected limbs and the prevention of prolonged shortened position of the affected muscles are probably the most important things to do in order to prevent and treat muscle hypertonia. In this attempt, physiotherapy has an utmost role providing a regular and individualised stretching program, along with the correct positioning of limbs and the applications of splints and casts.

Conflict of Interests

The authors declare that there is no conflict of interests regarding the publication of this paper.


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Neurology Solved MCQs – Set 2

11. Define a short-acting hypnotic?

A. Thiopentone
B. Phenobarbitone
C. Pentobarbitone
D. Diazepam
E. Suxamethonium
F. None of these
G. both a&b

The amount of ADH that is secreted varies with
(A) blood levels of glucose
(B) blood calcium levels
(C) the oxygen content of blood
(D) blood osmotic pressure
(E) all of the above
(F) Both a&b

Muscles weakness, spasticity, brisk reflexes, Babinsky response develop with damage in

A. upper motor neuron
B. optic tract
C. occipital lobe
D. thalamus optics
E. none of these
F. all of above

14. Select the correct statement regarding Brain functions?

A. Electrical stimulation of the descending reticular formation produces muscular relaxation.
B. Electrical stimulation of the hypothalamus produces anger and rage.
C. Electrical stimulation of the ascending reticular formation produces an increase in arousal.
D. Electrical stimulation of Cranial Nerve X (Vagus nerve) increases heart rate.
E. Electrical stimulation of the ventromedial nucleus of the hypothalamus (VMH) increases feeding.
F. None of these
G. both a&b

15. Define the function of noradrenaline?

A. Are enhanced by conversion into dopamine by dopamine-β-hydroxylase.
B. Are suppressed by inhibitors of monoamine oxidase.
C. Includes vasodilation in some arteriolar beds.
D. Is blocked by cocaine.
E. Are terminated by uptake 1 and 2 transporters.
F. None of these
G. both a&b

16. Define the use of Doxapram ?

A. Can be used to reverse respiratory depressant effects of a barbiturate overdose.
B. Is anticonvulsant at high doses.
C. Decreases heart rate and cardiac output.
D. Is a psychomotor stimulant drug.
E. Is a tricyclic antidepressant (TCA)
F. None of these
G. both a&b

17. What is the common side effect of morphine?

A. Hyperventilation
B. Depression
C. Constipation
D. Coughing
E. Hyperthermia
F. None of these
G. both a&b the drug used for the treatment of constipation?

A. atropine
B. Omeprazole
C. Sorbitol
D. Gaviscon
E. none of these
F. both a&b

19. The mechanism of action of sulfonylureas such as glipizide is

A. stimulation of glucose transporters
B. stimulation of insulin synthesis
C. Blockade of ATP-sensitive potassium channels
D. blockade of calcium channels
E. activation of ATP-sensitive potassium channels
F. None of these
G. both a & b

20. Loss of balance, coordination & decreased muscles tone develop with damage in

A. cerebellar
B. upper motor neuron
C. optic tract
D. occipital lobe
E. thalamus optics
F. None of these
G. All of the above


In the 1980s and 1990s, neurophysiologists Giacomo Rizzolatti, Giuseppe Di Pellegrino, Luciano Fadiga, Leonardo Fogassi, and Vittorio Gallese at the University of Parma placed electrodes in the ventral premotor cortex of the macaque monkey to study neurons specialized in the control of hand and mouth actions for example, taking hold of an object and manipulating it. During each experiment, the researchers allowed the monkey to reach for pieces of food, and recorded from single neurons in the monkey's brain, thus measuring the neuron's response to certain movements. [19] [20] They found that some neurons responded when the monkey observed a person picking up a piece of food, and also when the monkey itself picked up the food. The discovery was initially submitted to Nature, but was rejected for its "lack of general interest" before being published in a less competitive journal. [21]

A few years later, the same group published another empirical paper, discussing the role of the mirror-neuron system in action recognition, and proposing that the human Broca's region was the homologue region of the monkey ventral premotor cortex. [22] While these papers reported the presence of mirror neurons responding to hand actions, a subsequent study by Pier Francesco Ferrari and colleagues [23] described the presence of mirror neurons responding to mouth actions and facial gestures.

Further experiments confirmed that about 10% of neurons in the monkey inferior frontal and inferior parietal cortex have "mirror" properties and give similar responses to performed hand actions and observed actions. In 2002 Christian Keysers and colleagues reported that, in both humans and monkeys, the mirror system also responds to the sound of actions. [3] [24] [25]

Reports on mirror neurons have been widely published [26] and confirmed [27] with mirror neurons found in both inferior frontal and inferior parietal regions of the brain. Recently, evidence from functional neuroimaging strongly suggests that humans have similar mirror neurons systems: researchers have identified brain regions which respond during both action and observation of action. Not surprisingly, these brain regions include those found in the macaque monkey [1] However, functional magnetic resonance imaging (fMRI) can examine the entire brain at once and suggests that a much wider network of brain areas shows mirror properties in humans than previously thought. These additional areas include the somatosensory cortex and are thought to make the observer feel what it feels like to move in the observed way. [28] [29]

Many implicitly assume that the mirrorness of mirror neurons is due primarily to heritable genetic factors and that the genetic predisposition to develop Mirror neuron evolved because they facilitate action understanding. [30] In contrast, a number of theoretical accounts argue that mirror neurons could simply emerge due to learned associations, including the Hebbian Theory, [31] the Associative Learning Theory, [30] Canalization [32] and Exaptation. [ citation needed ]

The first animal in which researchers have studied mirror neurons individually is the macaque monkey. In these monkeys, mirror neurons are found in the inferior frontal gyrus (region F5) and the inferior parietal lobule. [1]

Mirror neurons are believed to mediate the understanding of other animals' behaviour. For example, a mirror neuron which fires when the monkey rips a piece of paper would also fire when the monkey sees a person rip paper, or hears paper ripping (without visual cues). These properties have led researchers to believe that mirror neurons encode abstract concepts of actions like 'ripping paper', whether the action is performed by the monkey or another animal. [1]

The function of mirror neurons in macaques remains unknown. Adult macaques do not seem to learn by imitation. Recent experiments by Ferrari and colleagues suggest that infant macaques can imitate a human's face movements, though only as neonates and during a limited temporal window. [33] Even if it has not yet been empirically demonstrated, it has been proposed that mirror neurons cause this behaviour and other imitative phenomena. [34] Indeed, there is limited understanding of the degree to which monkeys show imitative behaviour. [9]

In adult monkeys, mirror neurons may enable the monkey to understand what another monkey is doing, or to recognize the other monkey's action. [35]

It is not normally possible to study single neurons in the human brain, so most evidence for mirror neurons in humans is indirect. Brain imaging experiments using functional magnetic resonance imaging (fMRI) have shown that the human inferior frontal cortex and superior parietal lobe are active when the person performs an action and also when the person sees another individual performing an action. It has been suggested that these brain regions contain mirror neurons, and they have been defined as the human mirror neuron system. [36] More recent experiments have shown that even at the level of single participants, scanned using fMRI, large areas containing multiple fMRI voxels increase their activity both during the observation and execution of actions. [28]

Neuropsychological studies looking at lesion areas that cause action knowledge, pantomime interpretation, and biological motion perception deficits have pointed to a causal link between the integrity of the inferior frontal gyrus and these behaviours. [37] [38] [39] Transcranial magnetic stimulation studies have confirmed this as well. [40] [41] These results indicate the activation in mirror neuron related areas are unlikely to be just epiphenomenal.

A study published in April 2010 reports recordings from single neurons with mirror properties in the human brain. [42] Mukamel et al. (Current Biology, 2010) recorded from the brains of 21 patients who were being treated at Ronald Reagan UCLA Medical Center for intractable epilepsy. The patients had been implanted with intracranial depth electrodes to identify seizure foci for potential surgical treatment. Electrode location was based solely on clinical criteria the researchers, with the patients' consent, used the same electrodes to "piggyback" their research. The researchers found a small number of neurons that fired or showed their greatest activity both when the individual performed a task and when they observed a task. Other neurons had anti-mirror properties, that is, they responded when the participant performed an action but were inhibited when the participant saw that action.

The mirror neurons found were located in the supplementary motor area and medial temporal cortex (other brain regions were not sampled). For purely practical reasons, these regions are not the same as those in which mirror neurons had been recorded from in the monkey: researchers in Parma were studying the ventral premotor cortex and the associated inferior parietal lobe, two regions in which epilepsy rarely occurs, and hence, single cell recordings in these regions are not usually done in humans. On the other hand, no one has to date looked for mirror neurons in the supplementary motor area or the medial temporal lobe in the monkey. Together, this therefore does not suggest that humans and monkeys have mirror neurons in different locations, but rather that they may have mirror neurons both in the ventral premotor cortex and inferior parietal lobe, where they have been recorded in the monkey, and in the supplementary motor areas and medial temporal lobe, where they have been recorded from in human – especially because detailed human fMRI analyses suggest activity compatible with the presence of mirror neurons in all these regions. [28]

Another study has suggested that human beings don't necessarily have more mirror neurons than monkeys, but instead that there is a core set of mirror neurons used in action observation and execution. However, for other proposed functions of mirror neurons the mirror system may have the ability to recruit other areas of the brain when doing its auditory, somatosensory, and affective components. [43]

A number of studies have shown that rats and mice show signs of distress while witnessing another rodent receive footshocks. [44] The group of Christian Keysers recorded from neurons while rats experienced pain or witnessed the pain of others, and has revealed the presence of pain mirror neurons in the rat's anterior cingulate cortex, i.e. neurons that respond both while an animal experiences pain and while witnessing the pain of others. [45] Deactivating this region of the cingulate cortex led to reduced emotional contagion in the rats, so that observer rats showed reduced distress while witnessing another rat experience pain. [45] The homologous part of the anterior cingulate cortex has been associated with empathy for pain in humans, [46] suggesting a homology between the systems involved in emotional contagion in rodents and empathy for pain in humans.

Although many in the scientific community have expressed excitement about the discovery of mirror neurons, there are scientists who have expressed doubts about both the existence and role of mirror neurons in humans. According to scientists such as Hickok, Pascolo, and Dinstein, it is not clear whether mirror neurons really form a distinct class of cells (as opposed to an occasional phenomenon seen in cells that have other functions), [47] and whether mirror activity is a distinct type of response or simply an artifact of an overall facilitation of the motor system. [10]

In 2008, Ilan Dinstein et al. argued that the original analyses were unconvincing because they were based on qualitative descriptions of individual cell properties, and did not take into account the small number of strongly mirror-selective neurons in motor areas. [9] Other scientists have argued that the measurements of neuron fire delay seem not to be compatible with standard reaction times, [47] and pointed out that nobody has reported that an interruption of the motor areas in F5 would produce a decrease in action recognition. [10] (Critics of this argument have replied that these authors have missed human neuropsychological and TMS studies reporting disruption of these areas do indeed cause action deficits [38] [40] without affecting other kinds of perception.) [39]

In 2009, Lingnau et al. carried out an experiment in which they compared motor acts that were first observed and then executed to motor acts that were first executed and then observed. They concluded that there was a significant asymmetry between the two processes that indicated that mirror neurons do not exist in humans. They stated "Crucially, we found no signs of adaptation for motor acts that were first executed and then observed. Failure to find cross-modal adaptation for executed and observed motor acts is not compatible with the core assumption of mirror neuron theory, which holds that action recognition and understanding are based on motor simulation." [48] However, in the same year, Kilner et al. showed that if goal directed actions are used as stimuli, both IPL and premotor regions show the repetition suppression between observation and execution that is predicted by mirror neurons. [49]

In 2009, Greg Hickok published an extensive argument against the claim that mirror neurons are involved in action-understanding: "Eight Problems for the Mirror Neuron Theory of Action Understanding in Monkeys and Humans." He concluded that "The early hypothesis that these cells underlie action understanding is likewise an interesting and prima facie reasonable idea. However, despite its widespread acceptance, the proposal has never been adequately tested in monkeys, and in humans there is strong empirical evidence, in the form of physiological and neuropsychological (double-) dissociations, against the claim." [10]

Vladimir Kosonogov sees another contradiction. The proponents of mirror neuron theory of action understanding postulate that the mirror neurons code the goals of others' actions because they are activated if the observed action is goal-directed. However, the mirror neurons are activated only when the observed action is goal-directed (object-directed action or a communicative gesture, which certainly has a goal too). How do they "know" that the definite action is goal-directed? At what stage of their activation do they detect a goal of the movement or its absence? In his opinion, the mirror neuron system can be activated only after the goal of the observed action is attributed by some other brain structures. [50]

Neurophilosophers such as Patricia Churchland have expressed both scientific and philosophical objections to the theory that mirror neurons are responsible for understanding the intentions of others. In chapter 5 of her 2011 book, Braintrust, Churchland points out that the claim that mirror neurons are involved in understanding intentions (through simulating observed actions) is based on assumptions that are clouded by unresolved philosophical issues. She makes the argument that intentions are understood (coded) at a more complex level of neural activity than that of individual neurons. Churchland states that "A neuron, though computationally complex, is just a neuron. It is not an intelligent homunculus. If a neural network represents something complex, such as an intention [to insult], it must have the right input and be in the right place in the neural circuitry to do that." [51]

Recently, Cecilia Heyes (Professor of Experimental Psychology, Oxford) has advanced the theory that mirror neurons are the byproduct of associative learning as opposed to evolutionary adaptation. She argues that mirror neurons in humans are the product of social interaction and not an evolutionary adaptation for action-understanding. In particular, Heyes rejects the theory advanced by V.S. Ramachandran that mirror neurons have been "the driving force behind the great leap forward in human evolution." [11] [52]

Development Edit

Human infant data using eye-tracking measures suggest that the mirror neuron system develops before 12 months of age, and that this system may help human infants understand other people's actions. [53] A critical question concerns how mirror neurons acquire mirror properties. Two closely related models postulate that mirror neurons are trained through Hebbian [54] or Associative learning [55] [56] [57] (see Associative Sequence Learning). However, if premotor neurons need to be trained by action in order to acquire mirror properties, it is unclear how newborn babies are able to mimic the facial gestures of another person (imitation of unseen actions), as suggested by the work of Meltzoff and Moore. One possibility is that the sight of tongue protrusion recruits an innate releasing mechanism in neonates. Careful analysis suggests that 'imitation' of this single gesture may account for almost all reports of facial mimicry by new-born infants. [58]

Understanding intentions Edit

Many studies link mirror neurons to understanding goals and intentions. Fogassi et al. (2005) [59] recorded the activity of 41 mirror neurons in the inferior parietal lobe (IPL) of two rhesus macaques. The IPL has long been recognized as an association cortex that integrates sensory information. The monkeys watched an experimenter either grasp an apple and bring it to his mouth or grasp an object and place it in a cup.

  • In total, 15 mirror neurons fired vigorously when the monkey observed the "grasp-to-eat" motion, but registered no activity while exposed to the "grasp-to-place" condition.
  • For 4 other mirror neurons, the reverse held true: they activated in response to the experimenter eventually placing the apple in the cup but not to eating it.

Only the type of action, and not the kinematic force with which models manipulated objects, determined neuron activity. It was also significant that neurons fired before the monkey observed the human model starting the second motor act (bringing the object to the mouth or placing it in a cup). Therefore, IPL neurons "code the same act (grasping) in a different way according to the final goal of the action in which the act is embedded." [59] They may furnish a neural basis for predicting another individual's subsequent actions and inferring intention. [59]

Learning facilitation Edit

Another possible function of mirror neurons would be facilitation of learning. The mirror neurons code the concrete representation of the action, i.e., the representation that would be activated if the observer acted. This would allow us to simulate (to repeat internally) the observed action implicitly (in the brain) to collect our own motor programs of observed actions and to get ready to reproduce the actions later. It is implicit training. Due to this, the observer will produce the action explicitly (in his/her behavior) with agility and finesse. This happens due to associative learning processes. The more frequently a synaptic connection is activated, the stronger it becomes. [50]

Empathy Edit

Stephanie Preston and Frans de Waal, [60] Jean Decety, [61] [62] and Vittorio Gallese [63] [64] and Christian Keysers [3] have independently argued that the mirror neuron system is involved in empathy. A large number of experiments using fMRI, electroencephalography (EEG) and magnetoencephalography (MEG) have shown that certain brain regions (in particular the anterior insula, anterior cingulate cortex, and inferior frontal cortex) are active when people experience an emotion (disgust, happiness, pain, etc.) and when they see another person experiencing an emotion. [65] [66] [67] [68] [69] [70] [71] David Freedberg and Vittorio Gallese have also put forward the idea that this function of the mirror neuron system is crucial for aesthetic experiences. [72] Nevertheless, an experiment aimed at investigating the activity of mirror neurons in empathy conducted by Soukayna Bekkali and Peter Enticott at the University of Deakin yielded a different result. After analyzing the report's data, they came up with two conclusions about motor empathy and emotional empathy. First, there is no relationship between motor empathy and the activity of mirror neurons. Second, there is only weak evidence of these neurons’ activity in the inferior frontal gyrus (IFG), and no evidence of emotional empathy associated with mirror neurons in key brain regions (inferior parietal lobule: IPL). In other words, there has not been an exact conclusion about the role of mirror neurons in empathy and if they are essential for human empathy. [73] However, these brain regions are not quite the same as the ones which mirror hand actions, and mirror neurons for emotional states or empathy have not yet been described in monkeys.

Christian Keysers at the Social Brain Lab and colleagues have shown that people who are more empathic according to self-report questionnaires have stronger activations both in the mirror system for hand actions [74] and the mirror system for emotions, [70] providing more direct support for the idea that the mirror system is linked to empathy. Some researchers observed that the human mirror system does not passively respond to the observation of actions but is influenced by the mindset of the observer. [75] Researchers observed the link of the mirror neurons during empathetic engagement in patient care. [76]

Studies in rats have shown that the anterior cingulate cortex contains mirror neurons for pain, i.e. neurons responding both during the first-hand experience of pain and while witnessing the pain of others, [45] and inhibition of this region leads to reduced emotional contagion in rats [45] and mice, [44] and reduced aversion towards harming others. [77] This provides causal evidence for a link between pain mirror neurons, and emotional contagion and prosocial behavior, two phenomena associated with empathy, in rodents. That brain activity in the homologous brain region is associated with individual variability in empathy in humans [46] suggests that a similar mechanism may be at play across mammals.

Human self awareness Edit

V. S. Ramachandran has speculated that mirror neurons may provide the neurological basis of human self-awareness. [78] In an essay written for the Edge Foundation in 2009 Ramachandran gave the following explanation of his theory: ". I also speculated that these neurons can not only help simulate other people's behavior but can be turned 'inward'—as it were—to create second-order representations or meta-representations of your own earlier brain processes. This could be the neural basis of introspection, and of the reciprocity of self awareness and other awareness. There is obviously a chicken-or-egg question here as to which evolved first, but. The main point is that the two co-evolved, mutually enriching each other to create the mature representation of self that characterizes modern humans." [79]

Language Edit

In humans, functional MRI studies have reported finding areas homologous to the monkey mirror neuron system in the inferior frontal cortex, close to Broca's area, one of the hypothesized language regions of the brain. This has led to suggestions that human language evolved from a gesture performance/understanding system implemented in mirror neurons. Mirror neurons have been said to have the potential to provide a mechanism for action-understanding, imitation-learning, and the simulation of other people's behaviour. [80] This hypothesis is supported by some cytoarchitectonic homologies between monkey premotor area F5 and human Broca's area. [81] Rates of vocabulary expansion link to the ability of children to vocally mirror non-words and so to acquire the new word pronunciations. Such speech repetition occurs automatically, fast [82] and separately in the brain to speech perception. [83] [84] Moreover, such vocal imitation can occur without comprehension such as in speech shadowing [85] and echolalia. [86]

Further evidence for this link comes from a recent study in which the brain activity of two participants was measured using fMRI while they were gesturing words to each other using hand gestures with a game of charades – a modality that some have suggested might represent the evolutionary precursor of human language. Analysis of the data using Granger Causality revealed that the mirror-neuron system of the observer indeed reflects the pattern of activity in the motor system of the sender, supporting the idea that the motor concept associated with the words is indeed transmitted from one brain to another using the mirror system [87]

The mirror neuron system seems to be inherently inadequate to play any role in syntax, given that this definitory property of human languages which is implemented in hierarchical recursive structure is flattened into linear sequences of phonemes making the recursive structure not accessible to sensory detection [88]

Automatic imitation Edit

The term is commonly used to refer to cases in which an individual, having observed a body movement, unintentionally performs a similar body movement or alters the way that a body movement is performed. Automatic imitation rarely involves overt execution of matching responses. Instead the effects typically consist of reaction time, rather than accuracy, differences between compatible and incompatible trials. Research reveals that the existence of automatic imitation, which is a covert form of imitation, is distinct from spatial compatibility. It also indicates that, although automatic imitation is subject to input modulation by attentional processes, and output modulation by inhibitory processes, it is mediated by learned, long-term sensorimotor associations that cannot be altered directly by intentional processes. Many researchers believe that automatic imitation is mediated by the mirror neuron system. [89] Additionally, there are data that demonstrate that our postural control is impaired when people listen to sentences about other actions. For example, if the task is to maintain posture, people do it worse when they listen to sentences like this: "I get up, put on my slippers, go to the bathroom." This phenomenon may be due to the fact that during action perception there is similar motor cortex activation as if a human being performed the same action (mirror neurons system). [90]

Motor mimicry Edit

In contrast with automatic imitation, motor mimicry is observed in (1) naturalistic social situations and (2) via measures of action frequency within a session rather than measures of speed and/or accuracy within trials. [91]

The integration of research on motor mimicry and automatic imitation could reveal plausible indications that these phenomena depend on the same psychological and neural processes. Preliminary evidence however comes from studies showing that social priming has similar effects on motor mimicry. [92] [93]

Nevertheless, the similarities between automatic imitation, mirror effects, and motor mimicry have led some researchers to propose that automatic imitation is mediated by the mirror neuron system and that it is a tightly controlled laboratory equivalent of the motor mimicry observed in naturalistic social contexts. If true, then automatic imitation can be used as a tool to investigate how the mirror neuron system contributes to cognitive functioning and how motor mimicry promotes prosocial attitudes and behavior. [94] [95]

Meta-analysis of imitation studies in humans suggest that there is enough evidence of mirror system activation during imitation that mirror neuron involvement is likely, even though no published studies have recorded the activities of singular neurons. However, it is likely insufficient for motor imitation. Studies show that regions of the frontal and parietal lobes that extend beyond the classical mirror system are equally activated during imitation. This suggests that other areas, along with the mirror system are crucial to imitation behaviors. [7]

Autism Edit

It has also been proposed that problems with the mirror neuron system may underlie cognitive disorders, particularly autism. [96] [97] However the connection between mirror neuron dysfunction and autism is tentative and it remains to be demonstrated how mirror neurons are related to many of the important characteristics of autism. [9]

Some researchers claim there is a link between mirror neuron deficiency and autism. EEG recordings from motor areas are suppressed when someone watches another person move, a signal that may relate to mirror neuron system. This suppression was less in children with autism. [96] Although these findings have been replicated by several groups, [98] [99] other studies have not found evidence of a dysfunctional mirror neuron system in autism. [9] In 2008, Oberman et al. published a research paper that presented conflicting EEG evidence. Oberman and Ramachandran found typical mu-suppression for familiar stimuli, but not for unfamiliar stimuli, leading them to conclude that the mirror neuron system of children with ASD (Autism Spectrum Disorder) was functional, but less sensitive than that of typical children. [100] Based on the conflicting evidence presented by mu-wave suppression experiments, Patricia Churchland has cautioned that mu-wave suppression results cannot be used as a valid index for measuring the performance of mirror neuron systems. [101] Recent research indicates that mirror neurons do not play a role in autism:

. no clear cut evidence emerges for a fundamental mirror system deficit in autism. Behavioural studies have shown that people with autism have a good understanding of action goals. Furthermore, two independent neuroimaging studies have reported that the parietal component of the mirror system is functioning typically in individuals with autism. [102]

Some anatomical differences have been found in the mirror neuron related brain areas in adults with autism spectrum disorders, compared to non-autistic adults. All these cortical areas were thinner and the degree of thinning was correlated with autism symptom severity, a correlation nearly restricted to these brain regions. [103] Based on these results, some researchers claim that autism is caused by impairments in the mirror neuron system, leading to disabilities in social skills, imitation, empathy and theory of mind. [ who? ]

Many researchers have pointed out that the "broken mirrors" theory of autism is overly simplistic, and mirror neurons alone cannot explain the differences found in individuals with autism. First of all, as noted above, none of these studies were direct measures of mirror neuron activity - in other words fMRI activity or EEG rhythm suppression do not unequivocally index mirror neurons. Dinstein and colleagues found normal mirror neuron activity in people with autism using fMRI. [104] In individuals with autism, deficits in intention understanding, action understanding and biological motion perception (the key functions of mirror neurons) are not always found, [105] [106] or are task dependent. [107] [108] Today, very few people believe an all-or-nothing problem with the mirror system can underlie autism. Instead, "additional research needs to be done, and more caution should be used when reaching out to the media." [109]

Research from 2010 [110] concluded that autistic individuals do not exhibit mirror neuron dysfunction, although the small sample size limits the extent to which these results can be generalized.

Theory of mind Edit

In Philosophy of mind, mirror neurons have become the primary rallying call of simulation theorists concerning our "theory of mind." "Theory of mind" refers to our ability to infer another person's mental state (i.e., beliefs and desires) from experiences or their behaviour.

There are several competing models which attempt to account for our theory of mind the most notable in relation to mirror neurons is simulation theory. According to simulation theory, theory of mind is available because we subconsciously empathize with the person we're observing and, accounting for relevant differences, imagine what we would desire and believe in that scenario. [111] [112] Mirror neurons have been interpreted as the mechanism by which we simulate others in order to better understand them, and therefore their discovery has been taken by some as a validation of simulation theory (which appeared a decade before the discovery of mirror neurons). [63] More recently, Theory of Mind and Simulation have been seen as complementary systems, with different developmental time courses. [113] [114] [115]

At the neuronal-level, in a 2015 study by Keren Haroush and Ziv Williams using jointly interacting primates performing an iterated prisoner's dilemma game, the authors identified neurons in the anterior cingulate cortex that selectively predicted an opponent's yet unknown decisions or covert state of mind. These "other-predictive neurons" differentiated between self and other decisions and were uniquely sensitive to social context, but they did not encode the opponent's observed actions or receipt of reward. These cingulate cells may therefore importantly complement the function of mirror neurons by providing additional information about other social agents that is not immediately observable or known. [116]

Sex-Based Differences Edit

A series of recent studies conducted by Yawei Cheng, using a variety of neurophysiological measures, including MEG, [117] spinal reflex excitability, [118] electroencephalography, [119] [120] have documented the presence of a gender difference in the human mirror neuron system, with female participants exhibiting stronger motor resonance than male participants.

In another study, sex-based differences among mirror neuron mechanisms was reinforced in that the data showed enhanced empathetic ability in females relative to males. During an emotional social interaction, females showed a greater ability in emotional perspective taking than did males when interacting with another person face-to-face. However, in the study, data showed that when it came to recognizing the emotions of others, all participants' abilities were very similar and there was no key difference between the male and female subjects. [121]

Sleep paralysis / Ghostly Bedroom Intruders Edit

Baland Jalal and V. S. Ramachandran have hypothesized that the mirror neuron system is important in giving rise to the intruder hallucination and out-of-body experiences during sleep paralysis. [122] According to this theory, sleep paralysis leads to disinhibition of the mirror neuron system, paving the way for hallucinations of human-like shadowy beings. The deafferentation of sensory information during sleep paralysis is proposed as the mechanism for such mirror neuron disinhibition. [122] The authors suggest that their hypothesis on the role of the mirror neuron system could be tested:

"These ideas could be explored using neuroimaging, to examine the selective activation of brain regions associated with mirror neuron activity, when the individual is hallucinating an intruder or having an out-of-body experience during sleep paralysis ." [122]

ICSE Biology Question Paper 2010 Solved for Class 10

SECTION-I (40 Marks)

(Attempt all questions from this Section)

Question 1:
(a) Name the following :
(i) The type of cell division which occurs in the cells of the reproductive organs.
(ii) A plant with sunken stomata.
(iii) A foreign body that induces the formation of antibodies in the body.
(iv) The place where fertilization occurs in the female reproductive system.
(v) An organization that looks after maternal and child welfare centres. [5]

(b) State whether the following statements are true or false. If false, rewrite the correct form of the statement by changing the first or last word only.
(i) Tubectomy is the surgical method of sterilisation in males.
(ii) Mitosis is the type of cell division occurring in the cells of injured parts of the body.
(iii) Photolysis is the process of splitting of water molecules in the presence of grana and temperature.
(iv) Dilation of the pupil is brought about by the sympathetic nervous system.
(v) Chromosomes other than the pair of sex chromosome are called alleles. [5]

(c) Given below are five sets df five terms each. In each case, rewrite the terms in logical sequences as directed at the end of each statement, One has been done for you as an example.
Example : Anaphase, Telophase, Prophase, Metaphase, Interphase.
(sequential order of Karyokinesis)
Answer : Interphase, Prophase, Metaphase, Anaphase, Telophase.
(i) Vagina, Ovary, Uterus, Oviduct, Cervix (pathway of egg after ovulation)
(ii) Motor Neuron, Receptor, Sensory Neuron, Effector, Association Neuron.
(pathway of a nerve impulse)
(iii) Pupil, Yellow Spot, Cornea, Lens, Aqueous humour (path of entry of light into the eye from an object)
(iv) Stoma, Mesophyll cells, Xylem, Substomatal space, Intercellular space, (loss of water due to transpiration)
(v) Cortical cells, root hair, soil, water, endodermis, xylem. (entry of water into the plant from the soil) [5]
(d) There are five sets consisting of five terms given below. In each set there is a word which is an odd one. For each of these sets write down the category of the group having identified the odd one out, as shown in the example :
Example : (0) cell wall, vacuole, centrosome, plastids, mitochondria.

S.No. Category Odd One
1 Organelles of Plant Cell Centrosome

(i) Blinking, Knitting without looking, Smiling, Blushing, Crying.
(ii) Myopia, Cataract, Hypermetropia, Squint, Cretinism.
(iii) Cowper’s gland, Urethral gland, Lachrymal gland, Seminal vesicles, Prostrate gland.
(iv) Vasopressin, Growth hormone, TSH, ACTH, FSH.
(v) Cresol, DDT, Lime, Mercurochrome, Bordeaux mixture. [5]

(e) Choose the correct answer to the following statements out of the three choices given after each statement.
(i) A point of contact between two neurons is termed:
(1) Synapsis (2) Neuro motor junction (3) Synapse
(ii) Loss of wateras droplets from hydathodes is called :
(1) Transpiration (2) Bleeding (3) Guttation
(iii) The technical term for the fertilized egg is:
(1) Placenta (2) Zygote (3) Morula
(iv) The photo receptor cells of the retina sensitive to colour are :
(1) Cones (2) Rods (3) Organ of Corti
(v) Salk’s vaccine is used to build immunity against:
(1) Tuberculosis (2) Poliomyelitis (3) Malaria [5]

(f) The figure below represents an experiment set up to study a physiological process in plants:
(i) Name the physiological process being studied.
(ii) Explain the process.
(iii) What is the aim of the experiment ?
(iv) Give a wall balanced equation to represent the process. [5]

(g) Given below is an example of a certain structure and its special functional activity:
Example : (0) Ribosomes and Protein synthesis. On a similar pattern complete the following:
(i) Hypothalamus and ……… .
(ii) Suspensory ligaments and ……… .
(iii) Semi circular canals and ……… .
(iv) Mitochondria and ……… .
(v) Seminiferous tubules and ……… . [5]

(h) Explain the following terms :
(i) Antibiotics
(ii) Antiseptic
(iii) Hormones
(iv) Diffusion
(v) Destarched plant. [5]

(a) (i) Meiosis
(ii) Nerium
(iii) Antigen
(iv) Fallopian tube
(v) Red Cross

(b) (i) False Vasectomy is the surgical method of sterilisation in males.
(ii) True.
(iii) False Photolysis is the process of splitting of water molecules in the presence of grana and light.
(iv) True.
(v) False Chromosomes other than the pair of sex chromosome are called autosomes.

(c) (i) Ovary, Oviduct, Uterus, Cervix, Vagina.
(ii) Receptor, Sensory Neuron, Association Neuron, Motor-Neuron, Effector.
(iii) Cornea, Aqueous humour, Pupil, Lens, Yellow spot.
(iv) Xylem, Mesophyll cells, Intercellular space, Substomatal space, Stoma.
(v) Soil, Water, Root hair, Cortical cells, Endodermis, Xylem.

S. No. Category Odd One
(i) Simple reflex Knitting without looking
(ii) Eye defects Cretinism
(iii) Male reproductive system Lachrymal gland
(iv) Anterior pituitary secreted Vasopressin
(v) Disinfectants Mercurochrome

(e) (i)—(3) Synapse
(ii)—(3) Guttation
(iii)—(2) Zygote
(iv)—(1) Cones
(v)—(2) Poliomyelitis.

(f) (i) The physiological process being studied is photosynthesis.
(ii) It is the process by which green plants manufacture glucose from carbon dioxide and water which they get from atmosphere and soil respectively.
(iii) The aim of the experiment is to find out that oxygen is given out during photosynthesis.

(g) (i) Hypothalamus and control pituitary function.
(ii) Suspensory ligaments and to held lens in position.
(iii) Semi circular canals and balancing the body.
(iv) Mitochondria and release of energy.
(v) Seminiferous tubules and spermatogenesis.

(h) (i) Antibiotics: The chemical substances which are produced by a micro¬organism, can stop growth of or kill another micro-organism. e.g., Pencillin.
(ii) Antiseptics—These are chemical substances which destroy some bacteria and prevent the growth of others. Antiseptics are used locally in contact of body tissues because they are mild and are harmless to the tissues they work upon.
Examples of antiseptics—Tincture, benzoic acid, boric acid, hydrogen peroxide, dettol and mercurochrome.
(iii) Hormones: According to Selye (1948), “Hormones are the physiological organic compounds produced by certain cells for the sole purpose of directing theractivities to distant parts of the same origins.”
A hormone is defined as “a chemical messenger secreted by an endocrine gland which reaches its destination by the blood stream and which has the power of influencing the activity of other distant target organs.”
(iv) Diffusion: It is the process of movement of molecules of a substance (solid, liquid or gas) from the region of their higher concentration to the region of their lower concentration through the concentration gradient.
Diffusion may be defined as the process of random movement of molecules of a substance from a region of higher concentration to a region of lower concentration.
(v) Destarched plant: The plant which has no starch in the leaves and the leaf remains yellowish brown when the leaf is tested for photosynthesis with iodine solution.

(Attempt any Four questions from this Section.)

Question 2:
(a) Given below is the outline of the male reproductive system :
(i) Name the parts labelled 1 to 5.
(ii) State the functions of the parts labelled 1 and 4.
(iii) Name the cells of part 5 that produce testosterone.
(iv) Why is the structure 5 present outside the body in the scrotal sacs ?
(v) What is semen ? [5]

(b) Given one point of difference between the following on the basis of what is given in the brackets :
(i) Myopia and Hypermetropia. (cause of the defect)
(ii) Cerebrum and Spinal cord. (arrangement ofcytons and axons of neuron)
(iii) Genotype and Phenotype. (definition)
(iv) Karyokinesis and Cytokinesis. (explain the term)
(v) Light reaction and Dark reaction. (site of occurrence) [5]

(a) (i) 1—Seminal vesicle
2—Prostate gland
3— Urethra
4— Sperm duct/vas deferens
(ii) Part 1—Its secretion serves as a medium for the transportation of the sperms.
Part 2—It carry the sperms.
(iii) Leydig cells or interstitial cells of part 5 produces testosterone.
(iv) The structure 5 is present outside the body in the scrotal sac because sperms are produced at 2 to 3°C lower than that of body temperature so, when too hot the skin of scrotal sac looses and testes are away from the body and when it is cold the skin contracts and testis are closer to the body for warmth.
(v) Semen—The mixture of seminal vesicles secretios and sperms produces a milky fluid, which is called semen.

Myopia Hypermetropia
Lengthened of the eyeball from front to back. Shortening of the eyeball from front to back.

Cerebrum Spinal cord
Axons (white matter) on the inner side and cytons (gray matter) on the outer side are present. Cytous (Gray matter) on the inner side and Axons (white matter) on the outer side are present.

Genotype Phepotype
It is the genetic makeup of an organism. It is the physical appearance of an organism.

Karyokinesis Cytokinesis
The division of nucleus during cell division are called karyokine­sis. The division of cytoplasm after karyokinesis is called cytokinesis.

Light Reaction Dark Reaction
It takes place in the grana of chloroplast. It takes place in the stroma of chloroplast.

Question 3:
(a) (i) State Mendel’s Law of Dominance.
(ii) A pure tall plant (TT) is crossed with a pure dwarf plant (tt).
Draw Punnett squares to show (1) F1 generation (2) F2 generation.
(iii) Give the Phenotype of the F2 generation.
(iv) Give the Phenotypic and Genotypic ratio of the F1 and F2 generation.
(v) Name any one X-linked disease found in humans. [5]

(b) Answer the following briefly :
(i) Three functions of WHO.
(ii) Three advantages of a small family.
(iii) Explain the terms :
(1) Population density
(2) Natality. [5]

(a) (i) Mendel’s Law of Dominance: Out of a pair of contrasting characters present together, only one is able to express itself while the other remain suppressed.
(iii) Phenotype of the F2 generation: Pure tall : Hybrid tall : Pure dwarf
(iv) Genotypic ratio of F1 generation: Tt
Phenotype of F1 generation — All tall (Hybrid)
Phenotype ratio of F2 generation = 3 : 1
Genotypic ratio of F2 generation = 1 : 2 : 1
(v) X-linked disease found in human is – Haemophilia.

(b) (i) Three functions of WHO:
(a) To direct and co-ordinate international health projects.
(b) To encourage and conduct scientific research.
(c) To organise international campaigns, to control and eliminate diseases like AIDS.
(ii) Three advantages of a small family:
(a) Children get proper education,
(b) Children can get proper medical facilities.
(c) Children can get proper diet and nutrition.
(iii) (1) Population density: The sum total of individuals in a given geographic region at a specified period is known as the population density. It is the number of individuals in an unit area, such as per square kilometre.
(2) Natality: It is the number of live births per 1000 people of population per year.

Question 4:
(a) Given below is a diagram of a double helical structure of DNA :
(i) Name the four nitrogenous base’s that form a DNA molecule.
(ii) Give the full form of DNA.
(iii) Name the unit of heredity.
(iv) Mention two points of difference between Mitosis and Meiosis. [5]

(b) (i) Draw a well labelled diagram of a Neuron showing the following parts :
Perikaryon, Dendrites, Axon, Node of Ranvier and Myelin sheath.
(ii) State the function of sensory neuron and a motor neuron.
(iii) What is a nerve made up of ? [5]

(a) (i) Adenine, Guanine, Cytocine, Thymine
(ii) De-oxy Ribosenucleic Acid.
(iii) Genes.

Mitosis Meiosis
(1) Occurs in somatic cells. (1) Occurs in reproductive cells.
(2) Produces two daughter cells. (2) Produces four daughter cells

(b) (i)

(ii) Sensory Neuron: It brings the impulse from the receptor to the brain or spinal cord.
Motor Neuron: It brings the impulse from the brain or spinal cord to all effector.
(iii) A nerve is made up of a bundle of nerve fibres or axons.

Question 5:
(a) Given below is the diagram of an apparatus set up to study a very important physiological process:
(i) Name the process being studied.
(ii) Explain the process.
(iii) What change would you observe in the thistle funnel containing sugar solution after about 10 minutes ?
(iv) Is sugar solution hypertonic or hypotonic ?
(v) Name the part of the plant cell which is represented by the sugar solution.
(vi) Explain why much salt is added to pickles. [5]

(b) Explain the following terms :
(i) Reflex action
(ii) Vaccination
(iii) Turgidity
(iv) Bleeding in plants
(v) Cataract. [5]

(a) (i) Osmosis.
(ii) The diffusion of water molecules through a semipermeable membrane from a dilute solution to concentrated solution.
(iii) After about 10 minutes the sugar solution in the thistle funnel rises up.
(iv) Hypotonic.
(v) Cell sap of the root hair.
(vi) The addition of much salt to pickle, the water molecule drawn out of the germ cell by plasmolysis. Thus pickle can be preserved for long duration.

(b) (i) Reflex Action: Reflex action is an automatic, quick and involuntary action in the body brought about by a stimulus. Reflexes are of two types :
(1) Simple (natural) reflexes and.
(2) Conditioned (acquired) reflexes.
(ii) Vaccination: Vaccination is the practice of artificially injecting mild form of the germs Weakened (attenuated) germs, killed germs or the toxins produced by the germs into the body for the development of resistance to diseases.
(iii) Turgidity: The state in which the cell wall is fully stretched and cannot accommodate any more water.
(iv) Bleeding in plants: In plants direct flowing out of plant sap from any cut surface or from an injured part.
(v) Cataract: The eye condition in which the lens turns opaque and vision is cut down even to total blindness.

Question 6:
(a) Given below is an outline of the human body showing the important glands.
(i) Name the glands marked 1 to 5.
(ii) Name the hormone secreted by 2. Give one important function of this hormone.
(iii) Name the endocrine cells present in part 3.
(iv) Name the hormone secreted by part 4.
Give one important function of this hormone. [5]

(b) Give the biological / technical term for the following :
(i) Cessation of menstruation in females.
(ii) An eye defect in which the cornea becomes uneven.
(iii) The period of complete intrauterine development of the embryo.
(iv) Inflammation of meninges.
(v) Non identical twins produced by the fertilization of two eggs.
(vi) Membrane that protects the foetus and secretes a protective fluid.
(vii) Process of conversion of several molecules of glucose to one molecule of starch.
(viii) The photosensitive pigment present in the cone cells of the retina.
(ix) The fluid present in the anterior part in front of the eye lens.
(x) Extracts of toxins secreted by bacteria. [5]

(a) (i) 1—Pituitary gland
2— Thyroid gland
3— Pancreas
4— Adrenal gland
5— Ovary.
(ii) The hormone secreted by part 2 is thyroxine.
Function: Regulates the basal metabolism.
(iii) The endocrine cells present in part 3 is Islets of Langerhans.
(iv) The hormone secreted by part 4 are adrenaline.
Function: Prepares body for any emergency situation.

(b) (i) Menopause.
(ii) Astigmatism.
(iii) Gestation.
(iv) Meningitis
(v) Fraternal twins.
(vi) Amnion
(vii) Polymerisation
(viii) Iodopsin
(ix) Aqueous humour
(x) Toxoids

Question 7:
(a) Given below is a diagram representing a stage during mitotic cell division in an animal cell:
(i) Identify the above stage. Give a reason to support your answer.
(ii) Name the parts labelled 1, 2, 3 and 4.
(iii) What is the function of part 3 ?
(iv) Name the stage that comes just after the stage shown in the diagram. Draw a well labelled diagram of this stage. [5]

(b) Account for the following :
(i) Wilted lettuce leaves become crisp /firm when placed in cold water for a while.
(ii) One feels blinded for a short time while coming out of a dark room.
(iii) The leaves of certain plants roll up on a bright sunny day.
(iv) An alcoholic person walks unsteadily when drunk.
(v) Sleeping under a tree at night is not advisable. [5]

(a) (i) The given stage is prophase of mitosis cell division. In this nuclear membrane and nucleolus disappear sister chromatids attached to centromere. The chromosomes starts moving towards equator.
(ii) (1) Aster
(2) Chromatids
(3) Centromere
(4) Spindle fibres
(iii) Function of Part 3—It is the point of attachment to the Structure that pulls the chromatids to opposite ends of the cell during cell division.
(iv) The stage that comes just after the shown stage is metaphase.

(b) (i) Wilted lettuce leaves when placed in cold water for a while absorb water through endosmosis, the cells of leaves became turgid and thus become crisp/firm.
(ii) When we come out from a dark room we feel dazzling effect for a very short period. It is called light adaptation. In this case the diameter of pupil is reduced to allow less fight to enter the eyes.
(iii) On a bright sunny day, due to transpiration the cells of the leaves loss water and thus cells loses their turgidity and so the leaves roll up.
(iv) The cerebellum, due to the effect of alcohol is unable to co-ordinate muscular movements properly.
(v) During night plants only respire, i.e., taking in oxygen giving out carbon dioxide. The concentration of CO2 increases, plant’s surrounding atmos-phere, which is harmful. Thus, sleeping under a tree at night is not advisable.

Tech Sphere Feats

Mobile Drone

Prerequisites: Tech sphere, Drone.

Benefit: Drones you create gain the Athletics sphere as a bonus talent. If the drone already possess the Athletics sphere, they instead gain a bonus talent from the Athletics sphere. In addition, each drone is created with Acrobatics, Climb, Fly, and Swim as class skills.

Special: This feat may be taken multiple times, each time granting an additional talent from the Athletics sphere.

Receptive to Grafts

Benefit: Your body is more capable of handling a larger amount of cybertech, grafts, and other implants. When determining your maximum implantation value, increase it by 1 for every 2 Hit Dice you possess (minimum 1).

Reckless Drone

Prerequisites: Tech sphere, Drone.

Benefit: Drones you create add twice their base attack bonus to their maximum hit points. In addition, drones you create gain the Berserker sphere or Brute sphere as a bonus talent. If the drone already possess the sphere, they instead gain a bonus talent from either sphere.

Special: This feat may be taken multiple times, each time granting an additional talent from the Berserker or Brute sphere.

Recon Drone

Prerequisites: Tech sphere, Drone.

Benefit: Drones you create gain the Scout sphere as a bonus talent. If the drone already possess the Scout sphere, they instead gain a bonus talent from the Scout sphere. In addition, each drone is created with Perception, Sense Motive, and Stealth as class skills.

Special: This feat may be taken multiple times, each time granting an additional talent form the Scout sphere.

Remote Hacking

Prerequisites: Tech sphere (Remote Control).

Benefit: Your remote control can be used to override signals that don’t belong to you. Locating foreign signals with the remote control requires a Craft (mechanical) check opposed by their sphere DC. Each time you spend an action to control their gadgets you musts make a craft Craft (mechanical) check opposed by their sphere DC +5.

In place of an activation check or Craft (mechanical) check, each time you spend an action to control a foreign gadget, it gets to attempt a Will saving throw opposed by your Tech sphere DC.

Sacrificial Augment (combat)

Prerequisite: Guardian sphere.

Benefit: When your delayed damage pool empties, you may as an immediate action redirect the damage you would take to augment or implant on your person or an innate gadget. The damage redirected this way is treated as untyped lethal damage, bypassing any damage reduction or hardness the augment or implant would possess otherwise.

Special: This overrides the normal rules for the delayed damage pool which states that you cannot further redirect damage from the delayed damage pool.

Shield Drone

Prerequisites: Tech sphere, Drone.

Benefit: Drones you create are proficient with all shields (including tower shields). In addition, drones you create gain the Guardian sphere or Shield sphere as a bonus talent. If the drone already possess the sphere, they instead gain a bonus talent from either sphere.

Special: This feat may be taken multiple times, each time granting an additional talent from the Guardian or Shield sphere.

Technical Compatibility

Prerequisites: Independent Invention, Tech sphere, Drone.

Benefit: Your independent inventions are considered drones for purposes from benefiting from effects that affect drones, and vice versa. In addition as independent inventions you can select Drones as a base form (these independent inventions don’t count towards the maximum number of Hit Dice of drones you may maintain). Your independent inventions can be activated or deactivated as if they where drones.

You may also apply improvements and technical insights to your drones (1 improvement for every 10 levels of technician you possess (minimum 0)).

Technologically Alchemical Ammo (dual sphere)

Prerequisites: Tech sphere, Ammo Spitter, Alchemy sphere (formulae) package.

Benefit: Your ammo spitter may create alchemical or complex ammunition (such as alchemical cartridges and vial bolts) costing 50 gp or less. This alchemical ammunition doesn’t have to be made exclusively for firearms but the weapon firing it must still meet all the prerequisites (such as having the scatter quality).

Undetectable Hacking

Prerequisites: Tech sphere (Remote Control), Remote Hacking.

When you attempt to control a foreign gadget, whether it succeeds or fails on its Will save it must immediately succeed at a second Will save. If it fails this second save, it does not realize it it was subject to a hack attempt (including knowing if any routines were transferred).