India had been the end destination for the people from all over the world till Moughals. After that Indians started migrating all over the world! I think I am not exaggerating. For a country with a complicated and eventful past things like movement of population should not be a problem. It was not there till 1970 when because of weak ecntral leadership, the local leaders started raising their heads. Otherwise before that we have recieved large scale migration from Pakistan, Bangladesh, Sri Lanka and movement of people inside our own country like movement of Tamilnadu Brahmins . . .
Recently, due to 15 years of ignorant leadership back home, Biharis had UP people have become unwanted. Not only mavericks like Thakareys, responsible people and authorities also have started talking on the isuue in the same tune. although everytime there has been some discussion and an unsuccessful effort to retract the statement "I did not mean so" style.
If we see the whole issue at larger scale, all these cheap slogans cant be seperated from deterioration in the quality of the central leadership. The fact is that slowly it has become weak and from other form of But one wonders, why the elite in this country is
Can Chidambaram say how many of his family members stay where all in this world? What if the criminals do not belong to the migrant population are they are the JAAT born and broughtup in Delhi (which is more likely given the nature of the crime)?. We all know what a migrant in Delhi or Mumbai can do. They can do theft, they can do robbery or murder, they can even rape, but surley only inside some house, not in a moving car . . . Chidambaram may need a coaching on this. More than that I feel some of his advisers or might be even some of the ill oriented intelligence agency members might have misguided him. I am realy pained by his comment. It was not expected out of him.
Well, now that he has retracted the statement, we should forgive him. But like a stubborn he is still saying that he was talking about "behaviour"! I think 1000 PhEd degrees can be awarded in this country on studies related to the behaviour of the people of India and its reason and demography, dynamics and eitiologies! Man, this chap ...should go to north Chennai where people from Madurai keep abusing the local population and then he should come to south Chennai where the locals keep mocking the "migrants" from southern Tamilnadu. And you know what, he is from south Tamilnadu which is supposed to be the house of rogues (according to Tamilnadu level) including Azhagiri. He cant open any end of his body in Chennai, and he is talking in Delhi about "behaviour".
Mr. Rahul, thats the shame on our polics. They can hold their pant properly and they blame the road and traffic when the criminal escapes. In addition to that all the police people are buisy taking the girls to the politicians and to their other bosses. How will they work. For that no one should blame any particular community - thats what Chidambaram meant and thats what most of us have disliked. More over "migrant" word cant be used for people in one's own country. Please go and read because you need to compete with Biharis . . .
So, now people from Haryana will be called an immigrant in Delhi. Tell me who is a Delhite then? Or you promise me that you will read the geography at least of Delhi and area around and meaning of MIGRANT and report to me.
Monday, December 27, 2010
Thursday, December 23, 2010
Kama Sutra
At the close of the Kama Sutra this is what Vatsyayan writes about himself and about the purpose of Kamasutra:
“After reading and considering the works of Babhravya and other ancient authors, and thinking over the meaning of the rules given by them, this treatise was composed, according to the precepts of the Holy Writ, for the benefit of the world, by Vatsyayana, while leading the life of a religious student at Benares, and wholly engaged in the contemplation of the Deity. This work is not to be used merely as an instrument for satisfying our desires. A person acquainted with the true principles of this science, who preserves his Dharma (virtue or religious merit), his Artha (worldly wealth) and his Kama (pleasure or sensual gratification), and who has regard to the customs of the people, is sure to obtain the mastery over his senses. In short, an intelligent and knowing person attending to Dharma and Artha and also to Kama, without becoming the slave of his passions, will obtain success in everything that he may do.”
“After reading and considering the works of Babhravya and other ancient authors, and thinking over the meaning of the rules given by them, this treatise was composed, according to the precepts of the Holy Writ, for the benefit of the world, by Vatsyayana, while leading the life of a religious student at Benares, and wholly engaged in the contemplation of the Deity. This work is not to be used merely as an instrument for satisfying our desires. A person acquainted with the true principles of this science, who preserves his Dharma (virtue or religious merit), his Artha (worldly wealth) and his Kama (pleasure or sensual gratification), and who has regard to the customs of the people, is sure to obtain the mastery over his senses. In short, an intelligent and knowing person attending to Dharma and Artha and also to Kama, without becoming the slave of his passions, will obtain success in everything that he may do.”
Wednesday, December 22, 2010
Spasticity after spinal cord injury
Introduction
Unequivocally, 'spasticity' is understood to be among the symptoms resulting from injury to the upper motor neurons within the central nervous system (CNS) and is a common but not an inevitable sequelae of spinal cord injury (SCI).1, 2, 3 The most commonly cited definition for spasticity is that published by Lance in 1980:4 'Spasticity is a motor disorder characterized 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'. There remains, however, discrepancy in the literature about the definition of spasticity; whereas some authors include symptoms such as clonus, hyperactive tendon reflexes, and spasms within the umbrella term 'spasticity',1, 5, 6, 7 others discuss these same symptoms as related to but separate from spasticity, which is defined by these authors as increased muscle tone.3, 8, 9, 10, 11 Decq2 recently has suggested the use of a modified definition, whereby spasticity, in general, is defined as a symptom of the upper motor neuron syndrome characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes. He follows by separating the various components of spasticity into sub-definitions: (1) intrinsic tonic spasticity: exaggeration of the tonic component of the stretch reflex (manifesting as increased tone), (2) intrinsic phasic spasticity: exaggeration of the phasic component of the stretch reflex (manifesting as tendon hyper-reflexia and clonus), and (3) extrinsic spasticity: exaggeration of extrinsic flexion or extension spinal reflexes. Throughout the discussion to follow, the modified definition of spasticity suggested by Decq2 will be utilized in order to clearly differentiate between the various spasticity-related symptoms that are experienced by individuals with SCI.
The literature has shown that 65–78% of sample populations of individuals with chronic SCI (1 year postinjury) have symptoms of spasticity.6, 12 Although unclear, it has been suggested that the American Spinal Injury Association (ASIA) classification of SCI (severity) and level of injury may predict the likelihood of developing spasticity; for example, in individuals with cervical SCI, 93% of those diagnosed as ASIA A and 78% of those diagnosed as ASIA B–D reported having symptoms of spasticity, whereas in individuals with thoracic SCI, 72% of those diagnosed as ASIA A and 73% of those diagnosed as ASIA B–D reported symptoms of spasticity.6 The greater incidence of lower motor neuron injury associated with lower-level injuries results in a reduced tendency for spasticity development in these individuals.6, 12 Whereas the resolution of spinal shock may coincide with an increase in spasticity symptoms,12 there is no clear relationship between the presence of spasticity symptoms and time since injury beyond the spinal shock period.6
Spasticity has the potential to negatively influence quality of life (QOL) through restricting activities of daily living (ADL), inhibiting effective walking and self-care, causing pain and fatigue, disturbing sleep, compromising safety, contributing to the development of contractures, pressure ulcers, infections, negative self-image, complicating the role of the caretaker, and impeding rehabilitation efforts.3, 6, 7, 13, 14, 15, 16, 17 Reports of problematic spasticity 1, 3, and 5 years following SCI occurred in 35, 31, and 27% of a sample of a population-based cohort of SCI survivors reported to the Colorado Spinal Cord Injury Early Notification System.18 Similarly, of those individuals reporting spasticity in the Stockholm Spinal Cord Injury Study, 40% reported their spasticity to be problematic, in that ADL were restricted and/or the spasticity caused pain.19 In a study by Sköld et al,6 20 and 4% of their total sample perceived their spasticity to restrict ADL and cause pain, respectively. Although Krawetz and Nance20 have identified that severity of spasticity is among the factors that can reduce the degree to which walking is effective in functional ambulators after SCI, Norman et al21 have emphasized that, despite the common association between spasticity and clinical signs of abnormal gait, the nature of this relationship remains unclear. Furthermore, it must be noted that, although spasticity can have a negative impact on QOL, it has been suggested that symptoms of spasticity may increase stability in sitting and standing, facilitate the performance of some ADL and transfers, increase muscle bulk and strength of spastic muscles (thereby helping prevent osteopenia), and increase venous return (possibly diminishing the incidence of deep vein thrombosis).10, 14, 15, 16 This potential for a beneficial effect of spasticity on QOL has a large impact upon decisions regarding its management.7, 16
The use of varied definitions of spasticity complicate its valid and reliable assessment.14, 22 While the Ashworth and modified Ashworth scales14, 15, 23 are commonly used to assess the severity of spasticity, there is some question about their validity in the lower limbs of persons with SCI.24 As spasticity outcomes vary between clinical patient groups and depend on a variety of factors within each individual, a battery of assessment tools is recommended, incorporating clinical, electrophysiologic, neurophysiological,25 and/or biomechanical techniques.14, 26, 27 It is important to note that there are generally poor correlations among clinical scales and, further, reductions in spasticity are not necessarily correlated with improvement in function.27, 28, 29 The lack of agreed-upon measures of spasticity as a whole or of the various 'components of spasticity' limits the quantification of physical status and the study of effectiveness of management strategies.27 The ideal scale should not only quantify the degree and nature of the spasticity, but patient satisfaction, global function, and technological assessment should be considered.29
Pathophysiology of spasticity in SCI
In general, spasticity is classified as a symptom of the upper motor neuron syndrome, characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes.2 Upper motor neurons originate in the brain and brain stem and project to lower motor neurons within the brain stem and spinal cord.11 The lower motor neurons are of two types, both of which originate in the ventral horn of the spinal cord: (1) alpha motor neurons project to extrafusal skeletal fibers and (2) gamma motor neurons project to intrafusal muscle fibers within the muscle spindle.11 With a lesion of the CNS comes interruption of the signals sent via the upper motor neurons to the lower motor neurons or related interneurons. Immediately following SCI, a period exists whereby the individual presents with flaccid muscle paralysis and loss of tendon reflexes below the level of the lesion.5 This period was first described in 1750, with the term 'spinal shock' introduced by Marshall Hall in 1850.30 Spinal shock has been reported to end from 1 to 3 days31 to a few weeks postinjury, with the gradual development of exaggerated tendon reflexes, increased muscle tone, and involuntary muscle spasms:5 the symptoms of spasticity. Recent animal research suggested that a recovery of relatively normal motor neuron excitability and plateau potential behavior (sustained depolarizations), in the absence of normal inhibitory control to turn off plateaus and associated sustained firing, may be implicated in the recovery of spinal shock following SCI.32
Intrinsic tonic spasticity
Decq2 has differentiated intrinsic tonic spasticity (increased muscle tone) as that component of spasticity resulting from an exaggeration of the tonic component of the stretch reflex. Briefly, the stretch reflex is a monosynaptic reflex pathway that originates in the muscle spindles embedded parallel to the muscle fibers and travels via a Ia afferent to the spinal cord, where it synapses either first with interneurons or directly with an alpha motor neuron innervating the muscle from which the stimulus originated.11 The tonic component of the stretch reflex associated with increased muscle tone results from a maintained stretch of the central region of the muscle fibers and the reflex is polysynaptic.11 Upon a sustained stretch, both type Ia and type II afferents (from secondary spindle endings) synapse with interneurons within the ventral horn of the spinal cord. Synapses of the interneurons with alpha motor neurons facilitate contraction in the muscle being stretched.11
It is the hyperexcitability of this tonic stretch reflex that is commonly thought to result in increased muscle tone in response to passive stretch following SCI.3 This hypertonia is velocity-dependent, with faster stretching velocities being associated with greater amounts of reflex activity.3 The development of tonic stretch reflex hyperexcitability could be due to a lower threshold, an increased gain of the stretch reflex, or a combination of the two.22 The resultant increase in muscle tone is thought to be due to a combination of increased denervation hypersensitivity2, 3, 5, 9, 33 and changed muscle properties.11, 13, 22, 34, 35 Denervation leads to an initial downregulation of neuronal membrane receptors, followed by an upregulation, with enhanced sensitivity to neurotransmitters.2 Gradual changes in muscle properties also occur following SCI, such as fibrosis, atrophy of muscle fibers, decrease in the elastic properties, decrease in the number of sarcomeres, accumulation of connective tissue, and alteration of contractile properties toward tonic muscle characteristics, which likely contribute to the increased passive tension.11, 13, 22, 34, 35, 36
Intrinsic phasic spasticity
Intrinsic phasic spasticity encapsulates symptoms such as tendon hyper-reflexia and clonus, and is due to exaggeration of the phasic component of the stretch reflex.2 Tendon hyper-reflexia is identified as an exaggerated muscle response to an externally applied tap of deep tendons.7 Reduced presynaptic Ia inhibition is thought to play an important role in this hyper-reflexia, as the occurrence of reduced presynaptic inhibition of group Ia fibers appears to correlate with the excitability of tendon reflexes.36
Clonus has been defined as 'involuntary rhythmic muscle contraction that can result in distal joint oscillation'37 and most often occurs at the ankle.2, 7, 9 Clonus is elicited by a sudden rapid stretch of a muscle.38 The prevailing theory explaining the underlying mechanism responsible for clonus is that of recurrent activation of stretch reflexes.11, 37, 38 According to this theory, dorsiflexing the ankle causes activation of the Ia muscle spindle afferents and induces a reflex of the triceps surae, resulting in plantar flexion of the ankle.11, 37, 38 This reflex contraction is brief, essentially phasic, and ceases rapidly.2 The muscle then relaxes, causing the ankle to be dorsiflexed once again, due either gravity or the stretch being sustained by an examiner.2 The result is a new stretch reflex, etc.2, 37 Ultimately, it is the disinhibition of the stretch reflex due to interruption of descending influences with SCI, that is thought to cause exaggeration of the phasic stretch reflex pathway and, hence, clonus.3
The second theory is that clonus is the result of activity of a central oscillator or generator within the spinal cord, which rhythmically activates alpha motor neurons in response to peripheral events.37, 38 Beres-Jones et al37 outline observations that they feel support such a hypothesis: (1) reports of similar frequencies of clonus among ankle, knee, and wrist muscles, (2) observations that the clonus frequency is not entrained by the input frequency, suggesting that clonus cannot be solely stretch-mediated, (3) the finding that stimuli other than stretch evoke clonus, and (4) the observation of a refractory period following the clonic EMG burst where tendon tap, H-reflex stimulation, and vibration fail to elicit an efferent response. Therefore, whereas reduced presynaptic inhibition of group Ia fibers appears to be among the contributing factors to tendon hyper-reflexia, the underlying mechanism of clonus has not been clearly elucidated.
Extrinsic spasticity
In addition to the various intrinsic factors that contribute to symptoms of spasticity, involuntary muscle spasms can also occur in response to a perceived noxious stimulus originating extrinsic to the muscle: extrinsic spasticity.2, 3, 7 Flexion spasms are the most common form of extrinsic spasticity, triggered by afferent input from skin, muscle, subcutaneous tissues, and joints (collectively referred to as 'flexor reflex afferents'). These flexor reflex afferents mediate the polysynaptic reflexes involved in the flexion withdrawal reflex.3, 35, 39 SCI can interrupt the inhibition of these reflexes by supraspinal pathways, making them hyperexcitable.2, 3, 40 In other words, whereas flexor withdrawal reflexes occur normally in individuals without SCI, upon disruption of normal descending influences, the threshold for the flexor withdrawal reflex may become lowered, the gain of the system may become raised, or both may occur together.3 A recent study has provided evidence to implicate plateau potentials in the spinal interneuronal and motoneuronal circuitry in the hyperexcitability of flexion withdrawal reflexes in individuals with chronic SCI.41 Intrasegmental polysynaptic connections cause the flexor reflex initiated by a localized stimulus to generate a widespread flexor spasm, which can appear as a coordinated flexion of all joints of the leg.35, 39
Management of spasticity following SCI
In contrast to the general lack of agreement within the literature about the definition and evaluation of spasticity, there appears to be widespread agreement that decisions regarding the management of spasticity must be based on the goal of achieving balance between the useful and detrimental effects of spasticity on an individual's QOL.2, 10, 16, 34 The management of spasticity may be desired for the reduction of 'passive problems', such as preventing contracture, reducing pain, facilitating splint wearing, easing positioning and hygiene, and preventing contractures, or of 'functional problems', including the individual's reduced ability to perform useful work with the motor system.9
In general, no one treatment option will successfully manage spasticity in all individuals; the most conservative tactics are utilized first, with a progression from physical rehabilitation modalities, pharmacologic interventions, injection techniques, intrathecal baclofen, and lastly, surgery.15 In general, local treatments are used primarily by individuals with spasticity predominating in only certain muscle groups, such as which occurs mainly in individuals with stroke or traumatic brain injury.42 In the case of SCI, the distribution of spasticity tends to be more diffuse, making regional or systemic treatment preferable.34 The decision whether or not to treat spasticity and, if so, in what manner, is summarized nicely in a flow chart by Parziale et al (Figure 116).
Unequivocally, 'spasticity' is understood to be among the symptoms resulting from injury to the upper motor neurons within the central nervous system (CNS) and is a common but not an inevitable sequelae of spinal cord injury (SCI).1, 2, 3 The most commonly cited definition for spasticity is that published by Lance in 1980:4 'Spasticity is a motor disorder characterized 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'. There remains, however, discrepancy in the literature about the definition of spasticity; whereas some authors include symptoms such as clonus, hyperactive tendon reflexes, and spasms within the umbrella term 'spasticity',1, 5, 6, 7 others discuss these same symptoms as related to but separate from spasticity, which is defined by these authors as increased muscle tone.3, 8, 9, 10, 11 Decq2 recently has suggested the use of a modified definition, whereby spasticity, in general, is defined as a symptom of the upper motor neuron syndrome characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes. He follows by separating the various components of spasticity into sub-definitions: (1) intrinsic tonic spasticity: exaggeration of the tonic component of the stretch reflex (manifesting as increased tone), (2) intrinsic phasic spasticity: exaggeration of the phasic component of the stretch reflex (manifesting as tendon hyper-reflexia and clonus), and (3) extrinsic spasticity: exaggeration of extrinsic flexion or extension spinal reflexes. Throughout the discussion to follow, the modified definition of spasticity suggested by Decq2 will be utilized in order to clearly differentiate between the various spasticity-related symptoms that are experienced by individuals with SCI.
The literature has shown that 65–78% of sample populations of individuals with chronic SCI (1 year postinjury) have symptoms of spasticity.6, 12 Although unclear, it has been suggested that the American Spinal Injury Association (ASIA) classification of SCI (severity) and level of injury may predict the likelihood of developing spasticity; for example, in individuals with cervical SCI, 93% of those diagnosed as ASIA A and 78% of those diagnosed as ASIA B–D reported having symptoms of spasticity, whereas in individuals with thoracic SCI, 72% of those diagnosed as ASIA A and 73% of those diagnosed as ASIA B–D reported symptoms of spasticity.6 The greater incidence of lower motor neuron injury associated with lower-level injuries results in a reduced tendency for spasticity development in these individuals.6, 12 Whereas the resolution of spinal shock may coincide with an increase in spasticity symptoms,12 there is no clear relationship between the presence of spasticity symptoms and time since injury beyond the spinal shock period.6
Spasticity has the potential to negatively influence quality of life (QOL) through restricting activities of daily living (ADL), inhibiting effective walking and self-care, causing pain and fatigue, disturbing sleep, compromising safety, contributing to the development of contractures, pressure ulcers, infections, negative self-image, complicating the role of the caretaker, and impeding rehabilitation efforts.3, 6, 7, 13, 14, 15, 16, 17 Reports of problematic spasticity 1, 3, and 5 years following SCI occurred in 35, 31, and 27% of a sample of a population-based cohort of SCI survivors reported to the Colorado Spinal Cord Injury Early Notification System.18 Similarly, of those individuals reporting spasticity in the Stockholm Spinal Cord Injury Study, 40% reported their spasticity to be problematic, in that ADL were restricted and/or the spasticity caused pain.19 In a study by Sköld et al,6 20 and 4% of their total sample perceived their spasticity to restrict ADL and cause pain, respectively. Although Krawetz and Nance20 have identified that severity of spasticity is among the factors that can reduce the degree to which walking is effective in functional ambulators after SCI, Norman et al21 have emphasized that, despite the common association between spasticity and clinical signs of abnormal gait, the nature of this relationship remains unclear. Furthermore, it must be noted that, although spasticity can have a negative impact on QOL, it has been suggested that symptoms of spasticity may increase stability in sitting and standing, facilitate the performance of some ADL and transfers, increase muscle bulk and strength of spastic muscles (thereby helping prevent osteopenia), and increase venous return (possibly diminishing the incidence of deep vein thrombosis).10, 14, 15, 16 This potential for a beneficial effect of spasticity on QOL has a large impact upon decisions regarding its management.7, 16
The use of varied definitions of spasticity complicate its valid and reliable assessment.14, 22 While the Ashworth and modified Ashworth scales14, 15, 23 are commonly used to assess the severity of spasticity, there is some question about their validity in the lower limbs of persons with SCI.24 As spasticity outcomes vary between clinical patient groups and depend on a variety of factors within each individual, a battery of assessment tools is recommended, incorporating clinical, electrophysiologic, neurophysiological,25 and/or biomechanical techniques.14, 26, 27 It is important to note that there are generally poor correlations among clinical scales and, further, reductions in spasticity are not necessarily correlated with improvement in function.27, 28, 29 The lack of agreed-upon measures of spasticity as a whole or of the various 'components of spasticity' limits the quantification of physical status and the study of effectiveness of management strategies.27 The ideal scale should not only quantify the degree and nature of the spasticity, but patient satisfaction, global function, and technological assessment should be considered.29
Pathophysiology of spasticity in SCI
In general, spasticity is classified as a symptom of the upper motor neuron syndrome, characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes.2 Upper motor neurons originate in the brain and brain stem and project to lower motor neurons within the brain stem and spinal cord.11 The lower motor neurons are of two types, both of which originate in the ventral horn of the spinal cord: (1) alpha motor neurons project to extrafusal skeletal fibers and (2) gamma motor neurons project to intrafusal muscle fibers within the muscle spindle.11 With a lesion of the CNS comes interruption of the signals sent via the upper motor neurons to the lower motor neurons or related interneurons. Immediately following SCI, a period exists whereby the individual presents with flaccid muscle paralysis and loss of tendon reflexes below the level of the lesion.5 This period was first described in 1750, with the term 'spinal shock' introduced by Marshall Hall in 1850.30 Spinal shock has been reported to end from 1 to 3 days31 to a few weeks postinjury, with the gradual development of exaggerated tendon reflexes, increased muscle tone, and involuntary muscle spasms:5 the symptoms of spasticity. Recent animal research suggested that a recovery of relatively normal motor neuron excitability and plateau potential behavior (sustained depolarizations), in the absence of normal inhibitory control to turn off plateaus and associated sustained firing, may be implicated in the recovery of spinal shock following SCI.32
Intrinsic tonic spasticity
Decq2 has differentiated intrinsic tonic spasticity (increased muscle tone) as that component of spasticity resulting from an exaggeration of the tonic component of the stretch reflex. Briefly, the stretch reflex is a monosynaptic reflex pathway that originates in the muscle spindles embedded parallel to the muscle fibers and travels via a Ia afferent to the spinal cord, where it synapses either first with interneurons or directly with an alpha motor neuron innervating the muscle from which the stimulus originated.11 The tonic component of the stretch reflex associated with increased muscle tone results from a maintained stretch of the central region of the muscle fibers and the reflex is polysynaptic.11 Upon a sustained stretch, both type Ia and type II afferents (from secondary spindle endings) synapse with interneurons within the ventral horn of the spinal cord. Synapses of the interneurons with alpha motor neurons facilitate contraction in the muscle being stretched.11
It is the hyperexcitability of this tonic stretch reflex that is commonly thought to result in increased muscle tone in response to passive stretch following SCI.3 This hypertonia is velocity-dependent, with faster stretching velocities being associated with greater amounts of reflex activity.3 The development of tonic stretch reflex hyperexcitability could be due to a lower threshold, an increased gain of the stretch reflex, or a combination of the two.22 The resultant increase in muscle tone is thought to be due to a combination of increased denervation hypersensitivity2, 3, 5, 9, 33 and changed muscle properties.11, 13, 22, 34, 35 Denervation leads to an initial downregulation of neuronal membrane receptors, followed by an upregulation, with enhanced sensitivity to neurotransmitters.2 Gradual changes in muscle properties also occur following SCI, such as fibrosis, atrophy of muscle fibers, decrease in the elastic properties, decrease in the number of sarcomeres, accumulation of connective tissue, and alteration of contractile properties toward tonic muscle characteristics, which likely contribute to the increased passive tension.11, 13, 22, 34, 35, 36
Intrinsic phasic spasticity
Intrinsic phasic spasticity encapsulates symptoms such as tendon hyper-reflexia and clonus, and is due to exaggeration of the phasic component of the stretch reflex.2 Tendon hyper-reflexia is identified as an exaggerated muscle response to an externally applied tap of deep tendons.7 Reduced presynaptic Ia inhibition is thought to play an important role in this hyper-reflexia, as the occurrence of reduced presynaptic inhibition of group Ia fibers appears to correlate with the excitability of tendon reflexes.36
Clonus has been defined as 'involuntary rhythmic muscle contraction that can result in distal joint oscillation'37 and most often occurs at the ankle.2, 7, 9 Clonus is elicited by a sudden rapid stretch of a muscle.38 The prevailing theory explaining the underlying mechanism responsible for clonus is that of recurrent activation of stretch reflexes.11, 37, 38 According to this theory, dorsiflexing the ankle causes activation of the Ia muscle spindle afferents and induces a reflex of the triceps surae, resulting in plantar flexion of the ankle.11, 37, 38 This reflex contraction is brief, essentially phasic, and ceases rapidly.2 The muscle then relaxes, causing the ankle to be dorsiflexed once again, due either gravity or the stretch being sustained by an examiner.2 The result is a new stretch reflex, etc.2, 37 Ultimately, it is the disinhibition of the stretch reflex due to interruption of descending influences with SCI, that is thought to cause exaggeration of the phasic stretch reflex pathway and, hence, clonus.3
The second theory is that clonus is the result of activity of a central oscillator or generator within the spinal cord, which rhythmically activates alpha motor neurons in response to peripheral events.37, 38 Beres-Jones et al37 outline observations that they feel support such a hypothesis: (1) reports of similar frequencies of clonus among ankle, knee, and wrist muscles, (2) observations that the clonus frequency is not entrained by the input frequency, suggesting that clonus cannot be solely stretch-mediated, (3) the finding that stimuli other than stretch evoke clonus, and (4) the observation of a refractory period following the clonic EMG burst where tendon tap, H-reflex stimulation, and vibration fail to elicit an efferent response. Therefore, whereas reduced presynaptic inhibition of group Ia fibers appears to be among the contributing factors to tendon hyper-reflexia, the underlying mechanism of clonus has not been clearly elucidated.
Extrinsic spasticity
In addition to the various intrinsic factors that contribute to symptoms of spasticity, involuntary muscle spasms can also occur in response to a perceived noxious stimulus originating extrinsic to the muscle: extrinsic spasticity.2, 3, 7 Flexion spasms are the most common form of extrinsic spasticity, triggered by afferent input from skin, muscle, subcutaneous tissues, and joints (collectively referred to as 'flexor reflex afferents'). These flexor reflex afferents mediate the polysynaptic reflexes involved in the flexion withdrawal reflex.3, 35, 39 SCI can interrupt the inhibition of these reflexes by supraspinal pathways, making them hyperexcitable.2, 3, 40 In other words, whereas flexor withdrawal reflexes occur normally in individuals without SCI, upon disruption of normal descending influences, the threshold for the flexor withdrawal reflex may become lowered, the gain of the system may become raised, or both may occur together.3 A recent study has provided evidence to implicate plateau potentials in the spinal interneuronal and motoneuronal circuitry in the hyperexcitability of flexion withdrawal reflexes in individuals with chronic SCI.41 Intrasegmental polysynaptic connections cause the flexor reflex initiated by a localized stimulus to generate a widespread flexor spasm, which can appear as a coordinated flexion of all joints of the leg.35, 39
Management of spasticity following SCI
In contrast to the general lack of agreement within the literature about the definition and evaluation of spasticity, there appears to be widespread agreement that decisions regarding the management of spasticity must be based on the goal of achieving balance between the useful and detrimental effects of spasticity on an individual's QOL.2, 10, 16, 34 The management of spasticity may be desired for the reduction of 'passive problems', such as preventing contracture, reducing pain, facilitating splint wearing, easing positioning and hygiene, and preventing contractures, or of 'functional problems', including the individual's reduced ability to perform useful work with the motor system.9
In general, no one treatment option will successfully manage spasticity in all individuals; the most conservative tactics are utilized first, with a progression from physical rehabilitation modalities, pharmacologic interventions, injection techniques, intrathecal baclofen, and lastly, surgery.15 In general, local treatments are used primarily by individuals with spasticity predominating in only certain muscle groups, such as which occurs mainly in individuals with stroke or traumatic brain injury.42 In the case of SCI, the distribution of spasticity tends to be more diffuse, making regional or systemic treatment preferable.34 The decision whether or not to treat spasticity and, if so, in what manner, is summarized nicely in a flow chart by Parziale et al (Figure 116).
Spasticity
If you dont understand please ask me without hesitation
Spasticity is a frequent and often disabling disease, resulting in loss of mobility and pain from spasms. The core feature of the spastic state is
the exaggeration of stretch reflexes manifesting as hypertonia. The stretch reflex threshold is reduced, and its gain may be increased. The result is the velocity-dependent increase in resistance of a passively stretched muscle or muscle group is detectable clinically. Often, this is associated with a sudden melting of resistance during stretch, the clasp-knife phenomenon. In addition, there may be other related signs, such as weakness, impairment of fine movements of the digits, hyperreflexia, loss of cutaneous reflexes, Babinski's sign, clonus, spasms and changes in
posture.
Spasticity is traditionally ascribed to damage to the pyramidal tract. Work, however, particularly in animals, clearly implicates additional motor tracts in the pathophysiology of the spastic syndrome.
Inhibitory supraspinal influences
Pyramidal tract lesions have not led to spasticity in the hands of many experimenters. Destruction of the primary motor cortex in area 4,9-11 section of the medullary pyramids," or lateral corticospinal tract have lead to weakness (particularly involving fine movements of the digits), hypotonia and hyporeflexia in monkeys and apes observed for up to several months following lesioning.
Flaccid weakness may be present for up to six weeks before spasticity
develops after cerebral and spinal lesions.
Flaccid hemiparesis has been reported after infarcts involving the basis pontis and medullary pyramid but tone was examined just days after the stroke. Other cases have been reported in whom spasticity has supervened, but infarction extended beyond the pyramids.
Hypertonus is conspicuously absent in limited cordotomies involving the lateral pyramidal tracts. It is unlikely that damage to the pyramidal tract alone plays a major role in the production of spasticity. This is in contrast to weakness and loss of superficial reflexes, such as the abdominal reflexes, which are common accompaniments of isolated lesions of the
pyramidal tract.
The association between corticospinal tract damage, and tendon hyperreflexia and the Babinski response is less clear cut. This does not mean, however, that the motor cortex cannot influence tone. Perhaps the most tangible proof of this is the common clinical observation that capsular lesions often lead to more striking spasticity than cortical
lesions. The implication must be that such lesions interrupt fibres originating in cortical areas other than the primary motor cortex (area 4), and that these fibres form part of a motor system influencing tone separate from the corticospinal tract. Extensive cortical lesions, involving
premotor and supplementary motor areas, add spasticity to the paralysis seen with focal lesions of area 4 in monkeys. Forester reported an epileptic patient with a mild hemiparesis due to traumatic injury of the precentral gyrus who developed a spastic hemiplegia following
excision of the premotor cortex. In animal experiments, spasticity is more marked if such lesions are bilateral, suggesting that these non-pyramidal projections can have bilateral effects. The fibres influencing spasticity run with the corticospinal tract as far as the cerebral peduncles. In the cat they lie in the medial portion of the peduncle and in the area just dorsal to this, before ending in the bulbar reticular formation dorsal to the medullary pyramids.
Within the internal capsule there may be some
separation of the pathways, with axons from the primary motor cortex, premotor cortex, and supplementary area passing through the posterior limb, genu, and anterior limb of the internal capsule respectively. This may explain why small capsular lesions in the anterior limb tend to be associated with spastic hypertonus, whereas those involving the posterior limb are not. Large infarctions in the middle cerebral artery territory and subcortical infarcts undercutting most of the descending fibres in the corona radiata lead, in time, to a spastic hemiplegia as they involve both corticospinal and corticoreticular projections.
Although the available evidence suggests that isolated lesions of the pyramidal tract do not cause spasticity, this, of course, need not mean that the pyramidal tract has no influence over tone under normal circumstances.
This point is admirably illustrated by Bucy's analogy that removal of one kidney has little effect on homeostasis. This does not mean that the excised kidney was without effect, only that the remaining kidney has assumed the entire load. Similarly, ipsilateral supplementary motor
and premotor areas, or contralateral motor cortex may assume some of the functions of the destroyed corticospinal fibres from the precentral gyrus. This has been increasingly recognised as underlying the return of power following pyramidal lesions; but its role in tone has not been addressed.
The influence of cortical motor areas over tone is principally mediated by a powerful inhibitory mechanism in the bulbar reticular formation. Electrical stimulation of the ventromedial reticular formation dorsal to the pyramids inhibits the patellar reflex and gastrocnemiussoleus
tonic vibration reflex in intact cats, and abolishes extensor tone in decerebrate preparations and in cats rendered spastic by chronic cerebral lesions. The inhibitory effects in intact animals are potentiated by simultaneous stimulation of the premotor cortex or internal capsule. The anterior and paramedian cerebellar cortex and fastigial nucleus may also modulate the inhibitory actions of the reticular formation, at least in
the cat.
Inhibitory influences survive section of the pyramidal tract in the medulla and are conducted in the cord by the dorsal reticulospinal tract in the dorsal half of the lateral funiculus. The available evidence suggests that the tract occupies a similar position in humans in close relationship
with the lateral corticospinal tract. It is the loss of the cortical drive to the bulbar inhibitory centre which is principally responsible for the spastic hypertonus following lesions of the frontal cortex or internal capsule. In contrast, spasticity is not often a striking feature of human bulbar lesions, perhaps because lesions in the
region of the inhibitory centre also involve respiratory and vasomotor centres and are usually incompatible with life.
The inhibitory centre in the caudal brainstem and the dorsal reticulospinal pathway tonically inhibit flexor reflex afferents as well as spinal stretch reflexes. Thus damage to this system in the lateral funiculus releases flexor reflexes in animals. Shahani and Young have
pointed out that flexor spasms are qualitatively no different to the flexor reflexes recorded in patients with spinal transections and normal subjects, raising the possibility that flexor spasms are a release phenomenon consequent to damage to the dorsal reticulospinal pathway. In addition, it is now believed that the clasp-knife phenomenon is caused by the inhibitory effects of flexor reflex afferents, and lesions involving different levels of the dorsal reticulospinal system release the clasp-knife phenomenon in cats.
Excitatory supraspinal influences
Vestibulospinal activity is important in maintaining decerebrate rigidity, but may have a lesser role in supporting tone in spasticity. Injury to the vestibular nuclei alone has little effect on spasticity in the spastic cat. In contrast, transection of the bulbopontine tegmentum leads to a marked reduction in spasticity. Electrical stimulation of the reticular formation of the dorsal brainstem facilitates the patellar reflex in the intact
animal, and increases hyperreflexia, hypertonus, and clonus in the cat made chronically spastic by previous extirpation of the motor cortex. The facilitatory effects, unlike the inhibitory effects of the reticular formation, are not affected by stimulation of the motor cortex or internal capsule. Thus the reticular formation gives rise to both inhibitory and excitatory systems influencing spasticity. The latter originates in a diffuse area extending from the basal diencephalon, central grey and tegmentum
of the midbrain, the pontine tegmentum, and the lateral bulbar reticular formation, outside of the inhibitory field. The spinal projections of this system involve the ventral half of the cord. This facilitatory
reticulospinal system is central to the state of spasticity, although vestibulospinal influences may make some contribution as lesions of the vestibular nuclei and bulbopontine
tegmentum have a greater effect on spasticity in the cat than tegmental lesions alone. Damage to vestibulospinal and facilitatory reticulospinal pathways in the anterior funiculus of the cord may also contribute to
the release of flexor reflexes and spasms.
Descending spinal pathways
The lesions of the spinal cord affecting tone have been carefully documented in the monkey. Lesions of the ventral funiculus lead to hyperreflexia in the setting of essentially normal tone, while those confined to the lateral corticospinal tract in the lateral funiculus lead to
hypotonia, hyporeflexia and loss of cutaneous reflexes. In contrast, extensive lesions of the lateral funiculus (that include the dorsal reticulospinal tract) are followed by spasticity and hyperreflexia, as is severing of the lateral funiculus in animals with a previously disrupted corticospinal tract. Spasticity is less marked if the vestibulospinal
tracts are also cut. The distribution of hypertonia following the disruption of the dorsal reticulospinal fibres in the lateral funiculus is identical to that following frontal lobe lesions.
Information about the distribution of pathways influencing stretch reflexes and tone in humans comes from cordotomies. Putnam performing this operation for parkinsonism, observed that unilateral section of the dorsal half of the lateral funiculus was followed by a severe
initially flaccid paralysis. As power returned spasticity, hyperreflexia, and clonus appeared. Hyndman, treating intractable pain, cut the intermediate portion of the lateral funiculus bilaterally at the thoracic level, and found that hyperactive knee and ankle jerks, ankle clonus and
Babinski's sign appeared immediately, but spastic hypertonus only developed in one out of six patients, and then was only mild. Histological confirmation of the extent of the lesions, however, was absent in these cases. Spasticity did not develop after bilateral anterolateral cordotomies,
in some cases extending posteriorly to involve the lateral corticospinal tracts. Cordotomies have also been used in the treatment of spasticity. Bucy observed that unilateral or bilateral section of the vestibulospinal tract in the anterior funiculus of patients with congenital spastic paraplegia or quadriplegia only caused a transient reduction in extensor tone in the lower limbs. He concluded that the vestibulospinal tract contributes to the maintenance of human spasticity, but other descending pathways are capable of maintaining spasticity at its full intensity in the absence of vestibulospinal influences. The cordotomies performed
by Bucy were said to spare the deeper sulcal regions of the anterior funiculi, but there was no histological confirmation of this. In contrast, extensive unilateral or bilateral anterior cordotomy (which included the deeper sulcal areas) was followed, after a transient period of flaccidity,
by the loss or considerable reduction of extensor tone in the legs, despite the reappearance of hyperreflexia, adductor spasm, and clonus. On the strength of these findings it seems that lesions must involve the dorsal half of the lateral funiculus to produce spastic hypertonus in man. Presumably lesions here interrupt the inhibitory dorsal reticulospinal tract to cause spasticity. In patients already spastic, extensive anterior cordotomy, but not partial anterior cordotomy, abolishes extensor tone. This, like the results of animal experiments, suggests that the medial reticulospinal tract originating in the excitatory areas of the brainstem
reticular formation5' is more important than the vestibulospinal
tract in maintaining spastic extensor tone. The human medial reticulospinal tract runs in the sulcomarginal territory, in association with the median longitudinal bundles, and is likely to have been spared by Bucy's limited incisions.
In summary, two major balancing descending systems exist controlling tone in humans: on the one hand, the inhibitory dorsal reticulospinal tract; and, on the other, the facilitatory medial reticulospinal and vestibulospinal tracts.
Propriospinal and segmental influences
The striking feature of the hypertonicity and hyperreflexia that develops following complete transection of the spinal cord is the variable period of spinal shock that precedes the tone changes. During this period, which
may last several weeks, muscles are toneless and areflexic below the level of transection, as might be expected following the simultaneous loss of inhibitory and excitatory supraspinal influences on segmental and propriospinal reflexes. The delayed appearance of tone and reflexes has
lead to the suggestion that plasticity within the spinal cord, namely receptor hypersensitivity and sprouting of axon terminals, is responsible for hypertonicity in complete spinal cord lesions. This hypertonicity, may differ from the velocity dependent spasticity seen in partial cord lesions, and result from virtually continuous flexor spasms. Loss or reduction of knee and ankle jerks, paraplegia in flexion, and mass reflexes (exaggerated flexor spasms which also involve bowel and bladder contraction) are common in this situation.
Peripheral effects
Recent studies have challenged the classic view that exaggerated
stretch reflexes are the major cause of established spasticity. In the swing phase of gait, the tibialis anterior shows abnormally high levels of activity, despite the lack of any EMG activity in its antagonist, the triceps surae muscle. This suggests that mechanical changes in the extensor apparatus of the ankle, rather than muscle activity in the triceps surae itself, lead to increased resistance to dorsiflexion movements. Direct measurement of the resistance of the relaxed ankle to slow displacement in hemiparetic subjects has confirmed the importance of mechanical factors.2 Factors that might contribute to the increased mechanical resistance to movement are alterations in tendon compliance2 and physiological, morphometric, and histochemical changes in muscle fibres.
Given the velocity dependence of the stretch reflex, these mechanical factors may be particularly important during functional movements of the leg, which occur at low angular velocities. How the influence of central and mechanical factors on tone and function change with time is, as yet, unclear.
There is limited evidence to suggest that stretch reflex gain reduces over the months to years following the initial lesion. Conversely, if we are to assume that contractures represent the extreme end of the mechanical factors resisting limb movement, then there is reason to believe
that their development is delayed. The issue of the natural history of central and mechanical factors is an important one, as early treatment of hypertonia may avert mechanical changes. This has been the finding in
an animal model of spasticity, and has prompted an investigation of the disease modifying effects of botulinum toxin in spastic cerebral palsy.
Conclusion
Normal tone consists of a balance between inhibitory effects on stretch reflexes mediated by the dorsal reticulospinal tract and facilitatory effects on extensor tone, mediated by the medial reticulospinal tract, and, to a lesser extent in humans, by the vestibulospinal tract. In cortical and capsular lesions some of the drive on the inhibitory centre in the caudal brainstem is lost resulting in a spastic hemiplegia, in which antigravity posture predominates, but flexor spasms are unusual. In practice
partial spinal lesions usually involve the lateral corticospinal and dorsal reticulospinal tract, as most commonly seen in multiple sclerosis where demyelinating lesions have a predeliction for the lateral funiculi. Damage to the corticospinal tract leads to paresis, while loss of inhibitory influences from the dorsal reticulospinal tract, leaves the effects of the medial reticulospinal and Vestibulospinal tracts unopposed. In this situation there is often severe spasticity with tone being greatest in the
antigravity muscles, so that paraplegia in extension may be seen. Extensor and flexor spasms are common, although the former tend to predominate. This is the clinical picture of multiple sclerosis relatively early in its course.
The present hypothesis may also explain the marked spasticity in the legs in the presence of spasms, but little or no weakness in many patients with hereditary spastic paraparesis. Here, there is involvement of the dorsal
reticulospinal tract in the thoracolumbar cord with a degree of sparing of the corticospinal tracts. Support for this comes from pathological reports and from the relative normality of electromyographic responses in leg
muscles to electrical stimulation of the motor cortex in patients with this condition.
In severe or complete cord lesions there is loss of all supraspinal influence on the cord. Hypertonicity is not as marked as in some cases of incomplete cord lesions, as the descending excitatory systems are no longer acting unopposed. Flexion spasms are very prominent, however,
as flexor reflexes are released from the inhibitory influences of the dorsal reticulospinal, vestibulospinal and medial reticulospinal tracts. Paraplegia in flexion may then supervene. This is often the clinical picture of advanced multiple sclerosis, when lesions have also interrupted
function in the descending tracts of the anterior funniculus.
Of course the pattern of spasticity is not fixed and solely determined by the degree of damage to different descending pathways. Stimulation of flexor reflex afferents-for example, by pressure sores, can transform
paraplegia in extension into paraplegia in flexion. Conversely, standing reduces flexor tone and favours extensor tone, a phenomenon that is readily used to advantage in physiotherapy. An additional factor in complete transection is the delayed reorganisation within the isolated cord, which may underline the change in balance from flexor to extensor spasms sometimes seen a year or more after division of the cord.
Acquired pathology rarely respects neuroanatomical boundaries and it may be that further investigation in humans requires the technique of lesion superimposition that has proven so useful in other contexts.
References:-
1.
doi: 10.1136/jnnp.57.7.773
J Neurol Neurosurg Psychiatry 1994 57: 773-777
P Brown
Editorial
2.
Spasticity is a frequent and often disabling disease, resulting in loss of mobility and pain from spasms. The core feature of the spastic state is
the exaggeration of stretch reflexes manifesting as hypertonia. The stretch reflex threshold is reduced, and its gain may be increased. The result is the velocity-dependent increase in resistance of a passively stretched muscle or muscle group is detectable clinically. Often, this is associated with a sudden melting of resistance during stretch, the clasp-knife phenomenon. In addition, there may be other related signs, such as weakness, impairment of fine movements of the digits, hyperreflexia, loss of cutaneous reflexes, Babinski's sign, clonus, spasms and changes in
posture.
Spasticity is traditionally ascribed to damage to the pyramidal tract. Work, however, particularly in animals, clearly implicates additional motor tracts in the pathophysiology of the spastic syndrome.
Inhibitory supraspinal influences
Pyramidal tract lesions have not led to spasticity in the hands of many experimenters. Destruction of the primary motor cortex in area 4,9-11 section of the medullary pyramids," or lateral corticospinal tract have lead to weakness (particularly involving fine movements of the digits), hypotonia and hyporeflexia in monkeys and apes observed for up to several months following lesioning.
Flaccid weakness may be present for up to six weeks before spasticity
develops after cerebral and spinal lesions.
Flaccid hemiparesis has been reported after infarcts involving the basis pontis and medullary pyramid but tone was examined just days after the stroke. Other cases have been reported in whom spasticity has supervened, but infarction extended beyond the pyramids.
Hypertonus is conspicuously absent in limited cordotomies involving the lateral pyramidal tracts. It is unlikely that damage to the pyramidal tract alone plays a major role in the production of spasticity. This is in contrast to weakness and loss of superficial reflexes, such as the abdominal reflexes, which are common accompaniments of isolated lesions of the
pyramidal tract.
The association between corticospinal tract damage, and tendon hyperreflexia and the Babinski response is less clear cut. This does not mean, however, that the motor cortex cannot influence tone. Perhaps the most tangible proof of this is the common clinical observation that capsular lesions often lead to more striking spasticity than cortical
lesions. The implication must be that such lesions interrupt fibres originating in cortical areas other than the primary motor cortex (area 4), and that these fibres form part of a motor system influencing tone separate from the corticospinal tract. Extensive cortical lesions, involving
premotor and supplementary motor areas, add spasticity to the paralysis seen with focal lesions of area 4 in monkeys. Forester reported an epileptic patient with a mild hemiparesis due to traumatic injury of the precentral gyrus who developed a spastic hemiplegia following
excision of the premotor cortex. In animal experiments, spasticity is more marked if such lesions are bilateral, suggesting that these non-pyramidal projections can have bilateral effects. The fibres influencing spasticity run with the corticospinal tract as far as the cerebral peduncles. In the cat they lie in the medial portion of the peduncle and in the area just dorsal to this, before ending in the bulbar reticular formation dorsal to the medullary pyramids.
Within the internal capsule there may be some
separation of the pathways, with axons from the primary motor cortex, premotor cortex, and supplementary area passing through the posterior limb, genu, and anterior limb of the internal capsule respectively. This may explain why small capsular lesions in the anterior limb tend to be associated with spastic hypertonus, whereas those involving the posterior limb are not. Large infarctions in the middle cerebral artery territory and subcortical infarcts undercutting most of the descending fibres in the corona radiata lead, in time, to a spastic hemiplegia as they involve both corticospinal and corticoreticular projections.
Although the available evidence suggests that isolated lesions of the pyramidal tract do not cause spasticity, this, of course, need not mean that the pyramidal tract has no influence over tone under normal circumstances.
This point is admirably illustrated by Bucy's analogy that removal of one kidney has little effect on homeostasis. This does not mean that the excised kidney was without effect, only that the remaining kidney has assumed the entire load. Similarly, ipsilateral supplementary motor
and premotor areas, or contralateral motor cortex may assume some of the functions of the destroyed corticospinal fibres from the precentral gyrus. This has been increasingly recognised as underlying the return of power following pyramidal lesions; but its role in tone has not been addressed.
The influence of cortical motor areas over tone is principally mediated by a powerful inhibitory mechanism in the bulbar reticular formation. Electrical stimulation of the ventromedial reticular formation dorsal to the pyramids inhibits the patellar reflex and gastrocnemiussoleus
tonic vibration reflex in intact cats, and abolishes extensor tone in decerebrate preparations and in cats rendered spastic by chronic cerebral lesions. The inhibitory effects in intact animals are potentiated by simultaneous stimulation of the premotor cortex or internal capsule. The anterior and paramedian cerebellar cortex and fastigial nucleus may also modulate the inhibitory actions of the reticular formation, at least in
the cat.
Inhibitory influences survive section of the pyramidal tract in the medulla and are conducted in the cord by the dorsal reticulospinal tract in the dorsal half of the lateral funiculus. The available evidence suggests that the tract occupies a similar position in humans in close relationship
with the lateral corticospinal tract. It is the loss of the cortical drive to the bulbar inhibitory centre which is principally responsible for the spastic hypertonus following lesions of the frontal cortex or internal capsule. In contrast, spasticity is not often a striking feature of human bulbar lesions, perhaps because lesions in the
region of the inhibitory centre also involve respiratory and vasomotor centres and are usually incompatible with life.
The inhibitory centre in the caudal brainstem and the dorsal reticulospinal pathway tonically inhibit flexor reflex afferents as well as spinal stretch reflexes. Thus damage to this system in the lateral funiculus releases flexor reflexes in animals. Shahani and Young have
pointed out that flexor spasms are qualitatively no different to the flexor reflexes recorded in patients with spinal transections and normal subjects, raising the possibility that flexor spasms are a release phenomenon consequent to damage to the dorsal reticulospinal pathway. In addition, it is now believed that the clasp-knife phenomenon is caused by the inhibitory effects of flexor reflex afferents, and lesions involving different levels of the dorsal reticulospinal system release the clasp-knife phenomenon in cats.
Excitatory supraspinal influences
Vestibulospinal activity is important in maintaining decerebrate rigidity, but may have a lesser role in supporting tone in spasticity. Injury to the vestibular nuclei alone has little effect on spasticity in the spastic cat. In contrast, transection of the bulbopontine tegmentum leads to a marked reduction in spasticity. Electrical stimulation of the reticular formation of the dorsal brainstem facilitates the patellar reflex in the intact
animal, and increases hyperreflexia, hypertonus, and clonus in the cat made chronically spastic by previous extirpation of the motor cortex. The facilitatory effects, unlike the inhibitory effects of the reticular formation, are not affected by stimulation of the motor cortex or internal capsule. Thus the reticular formation gives rise to both inhibitory and excitatory systems influencing spasticity. The latter originates in a diffuse area extending from the basal diencephalon, central grey and tegmentum
of the midbrain, the pontine tegmentum, and the lateral bulbar reticular formation, outside of the inhibitory field. The spinal projections of this system involve the ventral half of the cord. This facilitatory
reticulospinal system is central to the state of spasticity, although vestibulospinal influences may make some contribution as lesions of the vestibular nuclei and bulbopontine
tegmentum have a greater effect on spasticity in the cat than tegmental lesions alone. Damage to vestibulospinal and facilitatory reticulospinal pathways in the anterior funiculus of the cord may also contribute to
the release of flexor reflexes and spasms.
Descending spinal pathways
The lesions of the spinal cord affecting tone have been carefully documented in the monkey. Lesions of the ventral funiculus lead to hyperreflexia in the setting of essentially normal tone, while those confined to the lateral corticospinal tract in the lateral funiculus lead to
hypotonia, hyporeflexia and loss of cutaneous reflexes. In contrast, extensive lesions of the lateral funiculus (that include the dorsal reticulospinal tract) are followed by spasticity and hyperreflexia, as is severing of the lateral funiculus in animals with a previously disrupted corticospinal tract. Spasticity is less marked if the vestibulospinal
tracts are also cut. The distribution of hypertonia following the disruption of the dorsal reticulospinal fibres in the lateral funiculus is identical to that following frontal lobe lesions.
Information about the distribution of pathways influencing stretch reflexes and tone in humans comes from cordotomies. Putnam performing this operation for parkinsonism, observed that unilateral section of the dorsal half of the lateral funiculus was followed by a severe
initially flaccid paralysis. As power returned spasticity, hyperreflexia, and clonus appeared. Hyndman, treating intractable pain, cut the intermediate portion of the lateral funiculus bilaterally at the thoracic level, and found that hyperactive knee and ankle jerks, ankle clonus and
Babinski's sign appeared immediately, but spastic hypertonus only developed in one out of six patients, and then was only mild. Histological confirmation of the extent of the lesions, however, was absent in these cases. Spasticity did not develop after bilateral anterolateral cordotomies,
in some cases extending posteriorly to involve the lateral corticospinal tracts. Cordotomies have also been used in the treatment of spasticity. Bucy observed that unilateral or bilateral section of the vestibulospinal tract in the anterior funiculus of patients with congenital spastic paraplegia or quadriplegia only caused a transient reduction in extensor tone in the lower limbs. He concluded that the vestibulospinal tract contributes to the maintenance of human spasticity, but other descending pathways are capable of maintaining spasticity at its full intensity in the absence of vestibulospinal influences. The cordotomies performed
by Bucy were said to spare the deeper sulcal regions of the anterior funiculi, but there was no histological confirmation of this. In contrast, extensive unilateral or bilateral anterior cordotomy (which included the deeper sulcal areas) was followed, after a transient period of flaccidity,
by the loss or considerable reduction of extensor tone in the legs, despite the reappearance of hyperreflexia, adductor spasm, and clonus. On the strength of these findings it seems that lesions must involve the dorsal half of the lateral funiculus to produce spastic hypertonus in man. Presumably lesions here interrupt the inhibitory dorsal reticulospinal tract to cause spasticity. In patients already spastic, extensive anterior cordotomy, but not partial anterior cordotomy, abolishes extensor tone. This, like the results of animal experiments, suggests that the medial reticulospinal tract originating in the excitatory areas of the brainstem
reticular formation5' is more important than the vestibulospinal
tract in maintaining spastic extensor tone. The human medial reticulospinal tract runs in the sulcomarginal territory, in association with the median longitudinal bundles, and is likely to have been spared by Bucy's limited incisions.
In summary, two major balancing descending systems exist controlling tone in humans: on the one hand, the inhibitory dorsal reticulospinal tract; and, on the other, the facilitatory medial reticulospinal and vestibulospinal tracts.
Propriospinal and segmental influences
The striking feature of the hypertonicity and hyperreflexia that develops following complete transection of the spinal cord is the variable period of spinal shock that precedes the tone changes. During this period, which
may last several weeks, muscles are toneless and areflexic below the level of transection, as might be expected following the simultaneous loss of inhibitory and excitatory supraspinal influences on segmental and propriospinal reflexes. The delayed appearance of tone and reflexes has
lead to the suggestion that plasticity within the spinal cord, namely receptor hypersensitivity and sprouting of axon terminals, is responsible for hypertonicity in complete spinal cord lesions. This hypertonicity, may differ from the velocity dependent spasticity seen in partial cord lesions, and result from virtually continuous flexor spasms. Loss or reduction of knee and ankle jerks, paraplegia in flexion, and mass reflexes (exaggerated flexor spasms which also involve bowel and bladder contraction) are common in this situation.
Peripheral effects
Recent studies have challenged the classic view that exaggerated
stretch reflexes are the major cause of established spasticity. In the swing phase of gait, the tibialis anterior shows abnormally high levels of activity, despite the lack of any EMG activity in its antagonist, the triceps surae muscle. This suggests that mechanical changes in the extensor apparatus of the ankle, rather than muscle activity in the triceps surae itself, lead to increased resistance to dorsiflexion movements. Direct measurement of the resistance of the relaxed ankle to slow displacement in hemiparetic subjects has confirmed the importance of mechanical factors.2 Factors that might contribute to the increased mechanical resistance to movement are alterations in tendon compliance2 and physiological, morphometric, and histochemical changes in muscle fibres.
Given the velocity dependence of the stretch reflex, these mechanical factors may be particularly important during functional movements of the leg, which occur at low angular velocities. How the influence of central and mechanical factors on tone and function change with time is, as yet, unclear.
There is limited evidence to suggest that stretch reflex gain reduces over the months to years following the initial lesion. Conversely, if we are to assume that contractures represent the extreme end of the mechanical factors resisting limb movement, then there is reason to believe
that their development is delayed. The issue of the natural history of central and mechanical factors is an important one, as early treatment of hypertonia may avert mechanical changes. This has been the finding in
an animal model of spasticity, and has prompted an investigation of the disease modifying effects of botulinum toxin in spastic cerebral palsy.
Conclusion
Normal tone consists of a balance between inhibitory effects on stretch reflexes mediated by the dorsal reticulospinal tract and facilitatory effects on extensor tone, mediated by the medial reticulospinal tract, and, to a lesser extent in humans, by the vestibulospinal tract. In cortical and capsular lesions some of the drive on the inhibitory centre in the caudal brainstem is lost resulting in a spastic hemiplegia, in which antigravity posture predominates, but flexor spasms are unusual. In practice
partial spinal lesions usually involve the lateral corticospinal and dorsal reticulospinal tract, as most commonly seen in multiple sclerosis where demyelinating lesions have a predeliction for the lateral funiculi. Damage to the corticospinal tract leads to paresis, while loss of inhibitory influences from the dorsal reticulospinal tract, leaves the effects of the medial reticulospinal and Vestibulospinal tracts unopposed. In this situation there is often severe spasticity with tone being greatest in the
antigravity muscles, so that paraplegia in extension may be seen. Extensor and flexor spasms are common, although the former tend to predominate. This is the clinical picture of multiple sclerosis relatively early in its course.
The present hypothesis may also explain the marked spasticity in the legs in the presence of spasms, but little or no weakness in many patients with hereditary spastic paraparesis. Here, there is involvement of the dorsal
reticulospinal tract in the thoracolumbar cord with a degree of sparing of the corticospinal tracts. Support for this comes from pathological reports and from the relative normality of electromyographic responses in leg
muscles to electrical stimulation of the motor cortex in patients with this condition.
In severe or complete cord lesions there is loss of all supraspinal influence on the cord. Hypertonicity is not as marked as in some cases of incomplete cord lesions, as the descending excitatory systems are no longer acting unopposed. Flexion spasms are very prominent, however,
as flexor reflexes are released from the inhibitory influences of the dorsal reticulospinal, vestibulospinal and medial reticulospinal tracts. Paraplegia in flexion may then supervene. This is often the clinical picture of advanced multiple sclerosis, when lesions have also interrupted
function in the descending tracts of the anterior funniculus.
Of course the pattern of spasticity is not fixed and solely determined by the degree of damage to different descending pathways. Stimulation of flexor reflex afferents-for example, by pressure sores, can transform
paraplegia in extension into paraplegia in flexion. Conversely, standing reduces flexor tone and favours extensor tone, a phenomenon that is readily used to advantage in physiotherapy. An additional factor in complete transection is the delayed reorganisation within the isolated cord, which may underline the change in balance from flexor to extensor spasms sometimes seen a year or more after division of the cord.
Acquired pathology rarely respects neuroanatomical boundaries and it may be that further investigation in humans requires the technique of lesion superimposition that has proven so useful in other contexts.
References:-
1.
doi: 10.1136/jnnp.57.7.773
J Neurol Neurosurg Psychiatry 1994 57: 773-777
P Brown
Editorial
2.
Tuesday, December 21, 2010
Migraine
Headache is one of the most common cause of loss of work days. Migraine is a very common disease heard among the mass. Its also called as vascular haeadache because of suspected pathology. The typical migraine headache is unilateral pain (affecting one half of the head) and pulsating in nature, lasting from 4 to 72 hours; symptoms include nausea, vomiting, photophobia (increased sensitivity to light), phonophobia (increased sensitivity to sound), and is aggravated by routine activity. Approximately one-third of people who suffer from migraine headaches perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur.
But its very difficult for a qualified doctor to brand a headache as Migraine. As there is no direct test to proove a headache as Migraine, other than clinical symptom (which cant be taken for 100% sure scientific proof in the world of documentation), and there is possibility of more grave cause of headache and so greater cause of worry and anxiety to the patient and responsibility to the doctor; it becomes a diagnosis of exclusion.
So, yesterday when I got a young doctor as a patient with complaint of single episode of throbbing headache associated with nausea, vomiting and altered sensation on right arm (all features of raised intracranial tension present), lasting for more than 4 hours, I had no option but to evaluate it thoroughly because the presentation was more looking like aneurysmal bleed or possibility of sinus thrombosis was impossible to be ruled out clinically. Though all her reports came within normal limits, we could not have bypassed it.
The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system. Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system. Migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy, although in some women migraines may become more frequent during pregnancy. Alltogether its more common in women.
There are many types. Usually prophylactic medication is started after controlling the acute episode of headache. Usually the pain subsides over a period of few years as the patient age crosses 40 years. Anxiety and hormonal status is supposed to have profound role. Its a bnign disease with almost no mortality but a big nuiance.
But its very difficult for a qualified doctor to brand a headache as Migraine. As there is no direct test to proove a headache as Migraine, other than clinical symptom (which cant be taken for 100% sure scientific proof in the world of documentation), and there is possibility of more grave cause of headache and so greater cause of worry and anxiety to the patient and responsibility to the doctor; it becomes a diagnosis of exclusion.
So, yesterday when I got a young doctor as a patient with complaint of single episode of throbbing headache associated with nausea, vomiting and altered sensation on right arm (all features of raised intracranial tension present), lasting for more than 4 hours, I had no option but to evaluate it thoroughly because the presentation was more looking like aneurysmal bleed or possibility of sinus thrombosis was impossible to be ruled out clinically. Though all her reports came within normal limits, we could not have bypassed it.
The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system. Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system. Migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy, although in some women migraines may become more frequent during pregnancy. Alltogether its more common in women.
There are many types. Usually prophylactic medication is started after controlling the acute episode of headache. Usually the pain subsides over a period of few years as the patient age crosses 40 years. Anxiety and hormonal status is supposed to have profound role. Its a bnign disease with almost no mortality but a big nuiance.
Story of finding room met at Banaras Hindu University
Today my friends reminded me of the days of Banaras Hindu University.
It was 1991 mid august, dont remember exact date. I had finished the admission process and was suggested that I should select the Hostel room. I was little surprised. In Bihar while studying at Langat Singh College, it took almost 6 months after admission to get the final list of students for the hostel. By the time the "brave" people had already occupied their prefered rooms. That time I had opted to stay out of the hostel of the campus in some lodge. Here they were saying me immediate occupation! When I showed my ignorance and surprise by repeating the question that the hostel will be alloted now itself, I got an "emphatic" yes in reply.
I had to walk almost 2 kilometers to come to the Broacha Hostel. On the way I asked 3 people about the distance and direction of the hostel and when I felt its still too far, then I asked where will be classes held? And when they said me that it was near the same place where I have finished the admission formalities just now, I was really depressed.
I walked to the Hostel office. There was a crowd there. A mixture of freshers (MURGA) and seniors (helping them as well as ragging them). I paid the hostel fees and finished the registration. Warden's' there were surprised when I wrote only the village name below my father's name. Dont you need to write some lane or some thing? Is it only your house in your village? I told them confidently that the postman brings the letters regularly with this address only. Then I was told ok, go and find your room met! Sir, how will I do that? Go out and see your classmets. Find out who can be your room met! I was in total confusion.
I came out of the office and was standing and trying to figure out where from to start. It was post Mandal and Kamandal era. People were sharply divided on caste lines. Though I was not very particular but I felt it will be better if I get some one of my caste. But how to find? At least from Bihar! How can I ask caste and state from some one?
I was just thinking of all these things. Suddenly some one started shouting "Is there any one from Patna?" Some one told something and they talked some thing and the person came back. Again shouted "Is there anyone from Patna?" I was keeping quite. I cant claim myself from Patna. In the mean time this gentleman chaged the city. "Is there any one from Muzaffarpur?" To this I was looking at him curiously. He shouted for almost 3 to 4 times. Then I moved towards him. I raised my hand. He asked you are from Patna? No, I am from Muzaffarpur. You are from Muzaffarpur? No, Not exactly, I am originaly from Samastipur, I have done my I. Sc from Langat Singh College. One younger looking person was overhearing all this. This gentleman asked him, "OK Murari"? Murari whispered Muzaffarpur is OK. In the mean time this gentlman did ask my father's name which I said.
We both went to the warden in side the hostel office and requested that we have found the room met. He told me now to go and find the room. We both walked together to the first floor towards "A" block. He already had some idea about the hostel. His elder brother's friends were here. Good. He told me that we will go to the "A" block first floor. On the way as we were walking on the first floor towards "A" block, we did not talk anything else. I was particular that we will opt for a room which should have a floor over it so that it will not get warm in summer. To me there was no other criteria about room selection! So, we decided on Room number 45 over which was the warden's house. We came back and told our option. We were told that the room is booked already! We were given the option of room number 46. We were told to go and verify the room whether we liked the room. That once booked, it will not be changed. We both ran and saw the room. I did not have any problem any way. We booked the room number 46. Looked at each other once more, shook hands and parted ways . . .
No one asked caste from each other. I did not have courage. He was probably sure after knowing my father's name and Langat Singh College. On joining the Hostel we came to know that we are from the same caste.
While coming back from Varanasi I went to my friend Rohit's house in Muzaffarpur. I was told that he had gone for admission at BHU! I was happily surprised! I told his mother that I am coming back after admission there! Later my friend complained why I did not inform him after I got the letter of admission from BHU? He had opted for a room met with which he was not that happy.
As we started living in the hostel Rohit used to stay in our room most of the time . . .We were three in the room made for two.
It was 1991 mid august, dont remember exact date. I had finished the admission process and was suggested that I should select the Hostel room. I was little surprised. In Bihar while studying at Langat Singh College, it took almost 6 months after admission to get the final list of students for the hostel. By the time the "brave" people had already occupied their prefered rooms. That time I had opted to stay out of the hostel of the campus in some lodge. Here they were saying me immediate occupation! When I showed my ignorance and surprise by repeating the question that the hostel will be alloted now itself, I got an "emphatic" yes in reply.
I had to walk almost 2 kilometers to come to the Broacha Hostel. On the way I asked 3 people about the distance and direction of the hostel and when I felt its still too far, then I asked where will be classes held? And when they said me that it was near the same place where I have finished the admission formalities just now, I was really depressed.
I walked to the Hostel office. There was a crowd there. A mixture of freshers (MURGA) and seniors (helping them as well as ragging them). I paid the hostel fees and finished the registration. Warden's' there were surprised when I wrote only the village name below my father's name. Dont you need to write some lane or some thing? Is it only your house in your village? I told them confidently that the postman brings the letters regularly with this address only. Then I was told ok, go and find your room met! Sir, how will I do that? Go out and see your classmets. Find out who can be your room met! I was in total confusion.
I came out of the office and was standing and trying to figure out where from to start. It was post Mandal and Kamandal era. People were sharply divided on caste lines. Though I was not very particular but I felt it will be better if I get some one of my caste. But how to find? At least from Bihar! How can I ask caste and state from some one?
I was just thinking of all these things. Suddenly some one started shouting "Is there any one from Patna?" Some one told something and they talked some thing and the person came back. Again shouted "Is there anyone from Patna?" I was keeping quite. I cant claim myself from Patna. In the mean time this gentleman chaged the city. "Is there any one from Muzaffarpur?" To this I was looking at him curiously. He shouted for almost 3 to 4 times. Then I moved towards him. I raised my hand. He asked you are from Patna? No, I am from Muzaffarpur. You are from Muzaffarpur? No, Not exactly, I am originaly from Samastipur, I have done my I. Sc from Langat Singh College. One younger looking person was overhearing all this. This gentleman asked him, "OK Murari"? Murari whispered Muzaffarpur is OK. In the mean time this gentlman did ask my father's name which I said.
We both went to the warden in side the hostel office and requested that we have found the room met. He told me now to go and find the room. We both walked together to the first floor towards "A" block. He already had some idea about the hostel. His elder brother's friends were here. Good. He told me that we will go to the "A" block first floor. On the way as we were walking on the first floor towards "A" block, we did not talk anything else. I was particular that we will opt for a room which should have a floor over it so that it will not get warm in summer. To me there was no other criteria about room selection! So, we decided on Room number 45 over which was the warden's house. We came back and told our option. We were told that the room is booked already! We were given the option of room number 46. We were told to go and verify the room whether we liked the room. That once booked, it will not be changed. We both ran and saw the room. I did not have any problem any way. We booked the room number 46. Looked at each other once more, shook hands and parted ways . . .
No one asked caste from each other. I did not have courage. He was probably sure after knowing my father's name and Langat Singh College. On joining the Hostel we came to know that we are from the same caste.
While coming back from Varanasi I went to my friend Rohit's house in Muzaffarpur. I was told that he had gone for admission at BHU! I was happily surprised! I told his mother that I am coming back after admission there! Later my friend complained why I did not inform him after I got the letter of admission from BHU? He had opted for a room met with which he was not that happy.
As we started living in the hostel Rohit used to stay in our room most of the time . . .We were three in the room made for two.
Cold Chennai!
Whats happenning to Chennai? Continuous cloud for almost one month! All water reservoir full - more than the strength! Temperature not above 25 degree celsius! I am feeling need to get warm cloths! No need of fan! Need blanket even in day time! Global warming has showed its maximum effect here only!
Land should be compensated
Now a days, despite of the "famous" land ceiling act of the government of India in place, companies acquire land. Because of this both the government and the companies are at odds with the masses . . . partly because of cheap politics also . . . But what makes the most important issue is, government and private companies are hell bent to "snatch" the lands at their cost! Can a famer argue that they will buy the medicine only at this price! Or he wants this brand of oil or cloth only at this price! Will government help them? Surely not. Most of my friends will brand me an impractical maverick or at least a joker. Then why some one should snatch the land of the farmers without their willingness? What is the logic behind continuing the land ceiling act any more?
I feel, if companies or government want land, they should buy that from the farmer on marcket price . . . as per the will and wish of the government. Land should be compensated, and must be compesared heavily as land is the only property . . . only real property in this world.
Sunday, December 19, 2010
Is this dusk for corruption and high handedness in India?
Corruption is the result of continued occupation of the helm of the society/ country by the people who are not concerned about the people. Without going in to the history of it like who started it first or when did it start first; I would like to say that corruption in India after independence has ruined the country but equaly its the attitude of high handedness. You go to the office and ask for some thing . . . the question session will culminate on "who are you"? They are not asking your identity card, they are asking how high handed are you? If you are just a common man, you go to hell! You are not going to be heard untill unless you are having a solid support behind you.
Both corruption and high handedness go hand in hand at least in India. Similar people are indulged in both - they are people in power, authority, greedy and igonarant. RTI has helped up to some extent but as I term it, its like belling the cat! IAS people who are responsible for any work in this country, are the most ignorant and insensitive lot towards the common mass (as some times its said thatn doctors are not sensitive towards patients' difficulties!).
Recently few inactions by governments are the indications that time is turning. If the masterly inactivity of the central government is to be taken to the best optimistic note, people like Manmohan Singh, Sonia Gandhi, Pranav Mukherjee, Chidambaram and Ahluwalia are as clean as pure (GANGA JAL) water. No one can expect them to be involved in any type of wrong doing . . . And they are not protecting any one too . . . Start from arrest of the MCI chief Dr. Desai to the 2G and 3G spectrum scams . . . their attitude has been of masterly inactivity.
On the top of all this statements of Sonial Gandhi and Rahul Gandhi at the congress plenary and their 5 fold plan against corruption shows that at least they are not going to keep quite on corruprion . . . Looking at A. Raja's episode, it apears that he had hijacked the government . . . misguided and arm - twisted them . . . But looking at the Gandhis' yesterday's statements and actions of CBI in last few days, it has been sign of a new dawn in the administrative erena of India.
If it goes like this, I am sure corrupt, ignorant, non- concerned people will not be any more in the mainstream of the adminstration . . . is my optimistic hope. I am also hopefull because Central government is not alone. Bihar government under the leadership of Nitish Kumar is also taking similar rather more bold action. I am hopefull that it will be followed by the other states.
But, as we were worried about the outcome of the 2010 Bihar assembly elections, we will have to think of whether such people (like the 5 calling the shots in the central government named above) will be able to survive in the sea of corrupt system/ society . . . Will they not need full security from the side of sensible intellectuals . . .
Both corruption and high handedness go hand in hand at least in India. Similar people are indulged in both - they are people in power, authority, greedy and igonarant. RTI has helped up to some extent but as I term it, its like belling the cat! IAS people who are responsible for any work in this country, are the most ignorant and insensitive lot towards the common mass (as some times its said thatn doctors are not sensitive towards patients' difficulties!).
Recently few inactions by governments are the indications that time is turning. If the masterly inactivity of the central government is to be taken to the best optimistic note, people like Manmohan Singh, Sonia Gandhi, Pranav Mukherjee, Chidambaram and Ahluwalia are as clean as pure (GANGA JAL) water. No one can expect them to be involved in any type of wrong doing . . . And they are not protecting any one too . . . Start from arrest of the MCI chief Dr. Desai to the 2G and 3G spectrum scams . . . their attitude has been of masterly inactivity.
On the top of all this statements of Sonial Gandhi and Rahul Gandhi at the congress plenary and their 5 fold plan against corruption shows that at least they are not going to keep quite on corruprion . . . Looking at A. Raja's episode, it apears that he had hijacked the government . . . misguided and arm - twisted them . . . But looking at the Gandhis' yesterday's statements and actions of CBI in last few days, it has been sign of a new dawn in the administrative erena of India.
If it goes like this, I am sure corrupt, ignorant, non- concerned people will not be any more in the mainstream of the adminstration . . . is my optimistic hope. I am also hopefull because Central government is not alone. Bihar government under the leadership of Nitish Kumar is also taking similar rather more bold action. I am hopefull that it will be followed by the other states.
But, as we were worried about the outcome of the 2010 Bihar assembly elections, we will have to think of whether such people (like the 5 calling the shots in the central government named above) will be able to survive in the sea of corrupt system/ society . . . Will they not need full security from the side of sensible intellectuals . . .
Sunday, December 12, 2010
When to consult a neurosurgeon must Part - 2 Headache
If headache is only in the morning - you get up with a headache which is severe to wake you up and you feel like vomiting (pregnancy ruled out) and relieved by vomiting, you must contact a neurosurgeon immediately. Other things which may be associated with such condition is deterioration in vision and giddiness.
Headache which is found all through the days might also be because of problems inside the brain and head but can be managed leisurely, but headache described above is clear cut idication of a neurosurgical problems only and needs urgent help.
Headache which is found all through the days might also be because of problems inside the brain and head but can be managed leisurely, but headache described above is clear cut idication of a neurosurgical problems only and needs urgent help.
When to consult a neurosurgeon must Part - 1
If vision is deteriorating and your ophthalmologist is happy with your spects, instead of changing the ophthalmologist, go to a neurosurgeon.Visual problems may be due to diseases in side the head (not always brain) and not due to eyes.
If you feel some one around you has difficulty in seeing but he feels he is alright, take him to a neurosurgeon, visual problems due to brain may not be noticed by the patient!
If you feel some one around you has difficulty in seeing but he feels he is alright, take him to a neurosurgeon, visual problems due to brain may not be noticed by the patient!
Tuesday, December 7, 2010
Ethics, media and present furore!
Ethics in any profession is a moral binding. It like discipline. Its like to know as a child that we should walk on the left side on the road. But go to USA you will have to walk on right side! These variations you know as you grow . . . as you... learn the tricks of survival!
Even on Indian roads no one will put you behind bars for just walking on right side. But while walking on right (wrong) side if you are dashed, no will have sympathy for you! Law cant protect you!People are ignorant most of the time, but suddenly/ anytime they become conscious, specialy when there is danger sign, For that we should know the discipline . . . and try to follow it all the time . . . if you want to remain away from the problems.
In medicine the present teaching is - consider every patient as potential litigation! Thats why medicine practice is a nuiance.I hope I have clarified. If still you have any questioon please tell me.
I think brandng any one like Barkha Datta .. . I will forgiveher. I know what has happened to heris just splash of the corrupt system. I know she is not a beneficiary. She has just transmitted . . .
And mind it, at times you have no option ... You know I have carried the love letter of my old girl friend to her new boy friend! And I have written operation notes to preotect my boss! And I know a junior doctor who came out of the post graduation course because he refused to write something wich was not true!
And I have got scolding also for not writing the truth while trying to protect some other doctor!World is so confusing yaar!
But knowing does not mean a binding!
Its just a knowledge!
Apply it like a "MASTER', not like a "CLERK" (servant).
Even on Indian roads no one will put you behind bars for just walking on right side. But while walking on right (wrong) side if you are dashed, no will have sympathy for you! Law cant protect you!People are ignorant most of the time, but suddenly/ anytime they become conscious, specialy when there is danger sign, For that we should know the discipline . . . and try to follow it all the time . . . if you want to remain away from the problems.
In medicine the present teaching is - consider every patient as potential litigation! Thats why medicine practice is a nuiance.I hope I have clarified. If still you have any questioon please tell me.
I think brandng any one like Barkha Datta .. . I will forgiveher. I know what has happened to heris just splash of the corrupt system. I know she is not a beneficiary. She has just transmitted . . .
And mind it, at times you have no option ... You know I have carried the love letter of my old girl friend to her new boy friend! And I have written operation notes to preotect my boss! And I know a junior doctor who came out of the post graduation course because he refused to write something wich was not true!
And I have got scolding also for not writing the truth while trying to protect some other doctor!World is so confusing yaar!
But knowing does not mean a binding!
Its just a knowledge!
Apply it like a "MASTER', not like a "CLERK" (servant).
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