IPHREHAB: APPROACH FOR NEUROGENIC DISORDER TREATMENT

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APPROACH FOR NEUROGENIC DISORDER TREATMENT

Approach for neurogenic disorder treatment 

With the above in mind, I felt the need to produce an approach that is in some ways uniquely useful to the clinician. 

The approach is therefore characterized by the following:

1. links between mechanics and physiology of the nervous system

2. integration of neurodynamics with musculoskeletal functions

3. a new movement diagram that enables the clinician integrate musculoskeletal and neural mechanisms

4. a new system for determining the kind and extensiveness of examination and treatment based on

neurodynamics and neuropathodynamics

5. the concept of neurodynamic sequencing and various options in assessment and treatment

6. new diagnostic categories of specific dysfunctions based on neuropathodynamics

7. treatment progressions derived from the above.

Nevertheless, it is common for therapists to diagnose more frequently the problems they have recently learned about, which raises the possibility of false diagnosis due to raw enthusiasm. At all times, the reader will realize that clinical neurodynamics is only one aspect of management of the person in pain and all other relevant information should be included in clinical decision making. For instance, the existence of a neural problem does not necessarily mean that a treatment with a neurodynamic technique is warranted. This could be because other treatments may attack the causative mechanisms more effectively or neurodynamic application may be contraindicated. Clearly, the biopsychosocial approach to neural problems will place this

book in its rightful place as just a modality of treatment that will be effective in some patients and not in

others.

Clinical neurodynamics is for clinicians dealingwith musculoskeletal disorders with peripheral neurogenic pain mechanisms, including those of the nerve root and peripheral nerve. There is no assumption that all problems are as such, or that the treatments presented in this book act only on peripheral mechanisms. The clinician will naturally and responsibly establish that it is appropriate to treat patients with clinical neurodynamics before doing so.

IPHREHAB: NEUROGENIC DISORDER TREATMENT

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NEUROGENIC DISORDER TREATMENT

Neurogenic disorders are common and their incidence is probably underestimated (Bennett 1997).

With many recent developments in their management, it is merciful that they can now be treated with non-invasive physical methods.

The notion of adverse neural mechanics has been present for many

years and probably longer than we know. 

Wittingly or unwittingly, the first known description of a neurodynamic

test was on the Edwin Smith Papyrus by Imhotep in 2800 BC, in which a leg straightening manoeuvre was performed in the diagnosis of low back pain in workers injured whilst building the Egyptian pyramids (Beasley 1982; Dyck 1984).

However, between then and now, much has happened and it is fascinating to note that, in addition to the neurodynamic tests for the lower quarter, the three major tests for the upper limb nerves (median, radial and ulnar) had been documented and illustrated

pictorially by the 1920s and 1950s (Bragard 1929; Von Lanz & Wachsmuth 1959). Their antitension counterpart postures were also illustrated

next to these neurodynamic tests.

In the context of therapy, neural mobilization has undergone massive development, particularly in the last thirty-five years since Gregory Grieve, Geoffrey Maitland, Robert Elvey and David Butler published

their work. Such an awareness of mechanical function of the nervous system has developed to the point where, for therapists dealing with pain and the musculoskeletal system, proficiency in neurodynamics has become a standard requirement. 


Nevertheless, an author whose work passed relatively unnoticed was Grieve (1970). The reason this paper is important is that in it Grieve commented on, for the first time that I am aware of in the physiotherapy literature, the notion of sensitivity of neural tissues being a key factor in whether they produce symptoms. He remarked on the possibility that inflamed neural tissues may well be more likely to produce abnormal neurodynamic tests as opposed to those on which pressure was exerted by pathologies such as disc bulges. He also alluded to the possibility that nervous system processing could be a means by which neurodynamic tests might change with spinal manual therapy. These aspects have undergone somewhat of a renaissance and they turn out to be key facets of current thinking in clinical neurodynamics.

IPHREHAB:SPINAL CORD INJURY CURE AND TREATMENT VIA OLFACTORY ENSHEATHING CELLS

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SPINAL CORD INJURY CURE AND TREATMENT VIA OLFACTORY ENSHEATHING CELLS


Olfactory En-sheathing Cells & Spinal Cord Injury Cure:
Damage to the spinal cord
Damaging the spinal cord prevents nerve messages travelling to and from the brain. These messages control most functions of the human body, including touch and sensation, muscle movement, bladder control and sexual function. With the loss of these messages, the body is paralysed below the level of injury.


Can nerves in the spinal cord re grow after injury?
Repairing damage to the spinal cord is very complex, as there are many spinal neurons killed by not only the initial injury, but in the hours, days and weeks following the accident. More neurons are also killed as the body begins to kill neurons close to the injury site (secondary damage). 


As the nervous system develops in the foetus, some nerves cells are programmed to die after they have finished their usefulness. In a spinal cord injury, this self destructive mechanism is triggered again, and some of the neurons around the injury site begin to self destruct or commit suicide in a process called apoptosis.


During the body's response to an injury to the spinal cord, the body forms an impenetrable scar tissue at the site of the injury which acts as a barrier to any neurons that might be trying to grow. Any neurons which have escaped damage may lose their insulating myelin sheath, and so can’t function and pass messages to and from the brain via the spinal cord.


To repair a spinal cord injury, scientists not only have to solve all the problems above, but would then need to find a treatment which makes the neurons grow in exactly the right part of the spinal cord, and form synapses with exactly the right neurons.


Regenerating spinal cord neurons:
In order to encourage the damaged neurons to grow again, a way needs to be found to stimulate the neurons by introducing growth factors.


One of the most recent discoveries is the olfactory ensheathing cell (OEC), also known as the olfactory ensheathing glial cell (OEGC), which is taken from the lining of the nose.


When the olfactory cells are added to a solution containing a scar reducing compound, and the combined solution is added to a damaged spinal cord in rats, the spinal cord was shown to regenerate resulting in a recovery of sensation and movement. The olfactory ensheathing cells provide an environment that promotes axon growth.
Geoff Raisman and his group in London have found ways of injecting these olfactory ensheathing cells into the spinal cord of humans.


The results have been very encouraging and human trials will begin in collaboration with The Royal National Orthopaedic Hospital, Stanmore. When these olfactory ensheathing cells come in contact with the normally barrier-like astrocytes of the glial scar. ‘It’s almost like they knock on the door and the astrocytes open up’ said Geoff Raisman.


Further research and trials are ongoing which include an enzyme to break down the inhibitory proteoglycans in the glial scar tissue to allow neurons to grow, the use of Schwann cells (from the peripheral nervous system) to encourage nerves to grow, and Olfactory ensheathing cells to ensure the axons could grow out of the graft and back into the spinal cord.

IPHREHAB: Spinal Cord Injury : Quadriplegic and Paraplegic Injuries

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Spinal Cord Injury : Quadriplegic and Paraplegic Injuries

Paraplegic and quadriplegic (tetraplegic) are terms used to describe the medical condition, for a person who has been paralysed due to a spinal cord injury. This classification depends on the level and severity of a persons paralysis, and how it affects their limbs.

This  provides patient information about acute spinal cord injuries, as well as treatment, symptoms, information on long term rehabilitation issues and peer support, to help improve the quality of life of those affected by a spinal cord injury.

What is a Spinal Cord Injury ?

A spinal cord injury (SCI) is typically defined as damage or trauma to the spinal cord that in turn results in a loss or impaired function resulting in reduced mobility or feeling.

Typical common causes of damage to the spinal cord, are trauma (car/motorcycle accident, gunshot, falls, sports injuries, etc), or disease (Transverse Myelitis, Polio, Spina Bifida, Friedreich's Ataxia, etc.). The resulting damage to the spinal cord is known as a lesion, and the paralysis is known as quadriplegia or quadraplegia / tetraplegia if the injury is in the cervical (neck) region, or asparaplegia if the injury is in the thoracic, lumbar or sacral region.

The spinal cord injury level is usually refered to alpha numerically, relating to the affected segment in the spinal cord, ie, C4, T5, L5 etc.

It is possible for someone to suffer a broken neck,or a broken back without becoming paralysed. This occurs when there is a fracture or dislocation of the vertebrae, but the spinal cord has not been damaged.

What is a Complete and Incomplete Spinal Cord Injury

There are typically two types of lesions associated with a spinal cord injury, these are known as a complete spinal cord injury and an incomplete spinal cord injury. A complete type of injury means the person is completely paralysed below their lesion. Whereas an incomplete injury, means only part of the spinal cord is damaged. A person with an incomplete injury may have sensation below their lesion but no movement, or visa versa. There are many types in incomplete spinal cord injuries, and no two are the same.

Such injuries are known as Brown Sequard Syndrome, Central Cord Syndrome, Anterior Cord Syndrome and Posterior Cord Syndrome.

What is Spinal Cord Injury Rehabilitation

Someone with a spinal cord injury will have a long road of rehabilitation ahead of them, usually at a spinal cord injury rehabilitation centre or spinal injury unit, and it is important that they keep their sense of humor on their bad days to help them maintain a positive attitude.

Generally, paraplegics will be in hospital for around 5 months, where as quadriplegics can be in hospital for around 6 - 8 months, whilst they undergo rehabilitation. Both paraplegics and quadriplegics should have some kind of rehabilitation and physiotherapy before they are discharged from hospital, to help maximise their potential, or help them get used to life in a wheelchair, and to help teach techniques which make everyday life easier.

Disabled sports, and wheelchair based sports can be an excellent way to build stamina, and help in rehabilitation by giving confidence and better social skills. The ultimate reward for many disabled sportsmen and women, is to win at the paralympic games, which will be coming to London in 2012.

Spinal Cord Injury Cure and Treatment

A cure for long term paralysis is still some years in the future, but clinical trials are taking place with Olfactory Ensheathing Glial (OEG) cells and Embryonic Stem Cell based Therapy.

and conservative treatment via physiotherapy and rehabilitation approaches.

Paraplegic and Quadriplegic Discussion Forum

If you have any spinal cord injury related questions, please visit our discussion forums and join in on the many topics there. We will do our best to help you, or at the very least, put you in contact with someone who can if we can't. The discussion forum is intended to be a free flow of information between spinally injured people, carers, and their friends, and everyone is welcome.

Even if you don't have any questions, take a look at the forum anyway, as you may be able offer help and advice to others who have questions.

Quadriplegic, Tetraplegic, Paraplegic and it's Definition

Quadraplegic is derived from two separate words from two different languages, Latin and Greek. The word “Quadra”, meaning “four” which is derived from latin, relates to the number of limbs. “Plegic”, is derived from the Greek word “Plegia”, meaning paralysis.

Put the two together, and you have “Quadraplegia”.

“Tetra” is derived from the Greek word for “Four”. “Para” is derived from the Greek word for "two" Hence: Tetraplegic and Paraplegic.

In Europe, the term for 4 limb paralysis has always been tetraplegia. The Europeans would never dream of combining a Latin and Greek root in one word.

In 1991, when the American Spinal Cord Injury Classification system was being revised, the definition of names was discussed. The British are more aware of Greek versus Latin names. Since Plegia is a greek word and quadri is Latin, the term quadriplegia mixes language sources. Upon review of the literature, it was recommended that the term tetraplegia be used by the American Spinal Cord Association so that there are not two different words in English referring to the same thing.

IPHREHAB : PAIN MODULATION AND MECHANISM

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PAIN MODULATION

• Variability of pain caused by similar injuries.
• Psychological variability.
• Even suggestions of pain relief helpful.
• Existing brain circuits modulate pain transmission pathways.

• One of these circuits has links with hypothalamus, midbrain, medulla oblongata.
• This pathway selectively controls spinal pain transmission neurons through descending pathways.
• Attention, suggestion and opiods work and modulate pain through this pathway.
• Endogenous opiod peptides such as enkephalins and endorphins work through this pathway. 

• Prolonged pain and fear are the most  reliable activating factors for endogenous opiod pathway.
• Released during surgical procedures and even by placebo.

Pain modulating circuits can suppress and enhance pain.

• Both pain-inhibiting  and pain-facilitating neurons in the medulla project to and control spinal pain transmission. Hence pain can be generated without any peripheral nocuous stimuli.
• Increased activity of these circuits is seen during migraine.
• Pain can also be induced by suggestions-psychological factors contribute to pain.

NEUROPATHIC PAIN:

1. Lesions in central and peripheral pathways results in loss or impairment of pain sensation.
2. Paradoxically the damage may also produce pain- diabetic neuropathy, herpes zoster.
3. Also damage to spinothalamic tract or thalamus can also produce pain.
4. Severe and notoriously intractable to standart treatment.
5. Unusually burning, tingling or electric shock like quality.
6. Examination-Sensory deficit in the area of pain.
7. Hyperpathia/allodynia.
8. Topical preprations (5% lidocaine) helpful.

Mechanisms

• Sensitized primary afferent neurons.
• Damaged primary afferent neurons.
• Sensitized nociceptors.-generate impulses in absence of stimulus.
• Increased concentration of sodium channels.
• Sensitivity to norepinephrine.

Sympathetically Maintained Pain

• Causalgia in peripheral nerve injury.
• Pain often begins after a delay of hours to days or even weeks.
• Pain accompanied by swelling of extremity, periarticular osteoporosis and arthritic changes in distal joints.
• Pain relief by sympathetic blockages.

Similar events- reflex sympathetic dystrophy- without nerve damage including fractures, soft tissue injuries, MI, stroke.

Treatment :

• History, Evaluate, examine.
• Remove cause.
• Analgesics NSAIDS, Opiods

IPHREHAB : ANKLE SPRAIN CAUSE AND TREATMENT

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ANKLE SPRAIN:

An ankle sprain is a common injury and usually results when the ankle is twisted, or inverted. The term sprain signifies injury to the soft tissues, usually the ligaments, of the ankle. On the lateral side of the ankle, there are three ligaments that make up the lateral ligament complex. These include the anterior talofibular ligament (ATF), the calcaneo–fibular ligament (CF) and the posterior talofibular ligament (PTF). The very common inversion injury to the ankle usually injures the anterior talofibular ligament and the calcaneo–fibular ligament. The ATF ligament keeps the ankle from sliding forward and the CF ligament keeps the ankle from rolling over on its side.

Causes of Ankle Sprain

ANKLE SPRAIN

A ligament is made up of multiple strands of tissue–similar to a nylon rope. A sprain results in tearing of the ligaments. The tear can be a complete tear of all the strands of the ligament or a partial tear, where a portion of the strands of the ligament are torn. The ligament is weakened by the injury which depends on the degree of the tear. The lateral ligaments are by far the most commonly injured ligaments in a typical inversion injury of the ankle. An inversion injury simply means that the ankle tilts over to the inside (towards the other foot), and the pressure of all your body weight is forced onto the outside edge of the foot. This causes the ligaments on the outside of the ankle to stretch and possibly tear.

Symptoms of Ankle Sprain

Initially the ankle is swollen, becomes painful, and may turn eccyhmotic (bruised). The bruising, and the initial swelling, is due to ruptured blood vessels from the tearing of the soft tissues. Most of the initial swelling is actually bleeding into the surrounding tissues. This initial swelling due to bleeding then increases due to edema fluid leaking into the tissues as well over the next 24 hours.

Diagnosis of Ankle Sprain

The diagnosis of an ankle sprain is usually made by examination of the ankle and x–rays to make sure that there is no fracture of the ankle. If there is a complete rupture of the ligaments suspected, your doctor may order stress x–rays as well. These x–rays are taken while someone twists or stresses the ligaments.

Treatment of Ankle Sprain

Elevation will help control the swelling.

Gentle compression and ice will control swelling.

Mild pain relievers will help with the pain.

Crutches will prevent weight bearing.

Healing of the ligaments usually takes about six weeks. The swelling may be present for several months. A physical therapist may be suggested to help you regain full function of your injured ankle.

Treatment may vary depending on how bad your ankle sprain is.

 In each case, the first line of treatment is to calm the inflammation and halt the swelling. 

The RICE (Rest, Ice, Compression, Elevation) principle can help address each of these needs.

Rest: 

A brace or splint will keep the ankle in a safe position, helping you avoid more strain to the sore area. In severe cases, you may require a pair of crutches to limit weight through the foot.

Ice:

Cold therapy, in the form of an ice pack, can aid in slowing the inflammatory process and in limiting pain.

Compression:

An elastic wrap can compress the sore area, keeping the swelling to a minimum.

Elevation:

Keeping the ankle elevated above the level of your heart will help drain the extra fluid (edema) back into the blood system and reduce swelling.

Range of motion exercises:

As healing gets underway, it is important to begin a series of movement exercises for the range of motion (ROM). At first, you’ll work on simply bending and straightening the ankle. These exercises will keep the ankle from becoming stiff.

Strength progression: 

Next, you’ll begin strengthening the muscles around the ankle. Isometrics may be chosen in the early stages of rehabilitation. These are strengthening exercises in which the muscles are working but the joint stays still. Isometrics allow you to exercise with the ankle at different angles, helping you stay away from painful positions of the ankle. These exercises provide the benefit of reducing overall pain and swelling.

Balance exercises:

Balance exercises are especially important following an ankle ligament injury. Remember, healthy ligaments send information to the brain about the position of a joint. Once a ligament has been injured, these nerves are unable to receive and send the needed information to the brain. Balance exercises help retrain the new nerves and help you regain your proprioceptive sense around the joint.

IPHREHAB : STRETCH MARK ON BREAST AND TREATMENT

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Stretch Marks on Breast

Why do you get stretch marks on breasts? 

Stretch marks can appear on any part of the body and can be quite emotionally disturbing for almost any individual. The fact that today’s world seems to place such a high significance in the way a person looks makes things even more emotionally traumatic. Stretch marks, while being of no real medical seriousness, can greatly affect an individual’s quality of life because of the amount of confidence it can dent.

It can completely dictate the kind of clothes that one wears, thereby greatly influencing ones aesthetic appeal. Stretch marks on the breasts, just like the stretch marks on any part of the body, are a result of the constant expansion and contraction of the skin to adjust to the fluctuations in a person’s weight, as a result of weight gain or dieting. While it is possible to reduce the prominence of the stretch marks, complete removal can prove completely impossible.

While a number of big cosmetic brands may market some of their lotions and creams as the perfect solution, even the cosmetic industry have not yet found a way to completely remove the stretch marks and the lotions will simply reduce the prominence of these marks. Another very common reason for the occurrence of stretch marks is going through a pregnancy, as this is also characterized by rapid weight gain and loss.

While there isn’t really much one can do about stretch marks that have already developed, following a healthy and balanced diet will help moisturize the skin, causing the stretch marks to fade away to some degree.

 The logic behind this is to make sure that your skin remains firm and as elastic as possible. One of the most effective home remedies to achieve this is to mix the ingredients of ¼ cup of Aloe Vera gel, ½ cup of olive oil, the liquid content of 6 vitamin E capsules and the liquid content of 4 vitamin A capsules. Once blended together, store the mixture in a fridge and topically apply the mixture over all the locations of your body where the stretch marks normally occur. The application of Aloe Vera gel over the affected areas also helps significantly lighten the prominence of stretch marks. Increase your intake of seeds and nuts that contain zinc as it is a vital ingredient in the removal of stretch marks.  The application of cocoa butter twice a day over the affected area will also help considerably as will the application of pure lavender oil.

IPHREHAB : TISSUE EXPANSION IN THE TREATMENT OF BURN SCARS

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TISSUE EXPANSION IN THE TREATMENT OF BURN SCARS

SUMMARY. Major post-burn scars are a serious morphological and functional problem and old techniques like skin grafts and distant flaps are not very effective to improve the final result. Expansion of the local skin allows us to obtain very large local flaps and the replacement of the scar tissue with a good skin for colour and texture. We have used the tissue expansion technique in the treatment of burn scars in the head and neck, trunk, upper and lower extremities. In the head and neck, tissue expansion is useful to obtain good results but the complication rate is higher than in the treatment of other pathologies with the same technique. Good results are obtained in the back where very large amounts of scarred tissue can be removed. In the thorax the morphological results are less satisfactory because of the hypertrophic scars resulting after the operation. In the thigh a good cosmetic improvement has very often been achieved; in the leg, on the contrary, we have observed the highest rate of complications: the use of tissue expansion in this area must be very careful and limited to selected cases.

In the last few years tissue expansion has improved thanks to technical refinements in plastic surgery.

In the past, the treatment of bum scars was carried out by the use of skin grafts or the transposition of local flaps. With skin grafts recurrence of contracture, chronic breakdowns and unsatisfactory cosmetic outcomes were observed; local flaps may be insufficient to resurface large defects after debridement or excision of a post-bum scar.

Expansion of the local skin makes it possible to obtain very large local flaps and to replace a great amount of scar tissue with a good skin for colour and texture (Argenta, 1985; Chang, 1986; Cohen 1988; Manders, 1984; Nordstrom, 1985; Radovan, 1979).

We have used the tissue expansion technique in the surgical treatment of burn scars in the head and neck, trunk, and the upper and lower extremities. We report a few cases to illustrate our surgical procedures.

Case report 1 (Fig. 1)

A 48-year-old man had sustained a burn of the back 23 years previously. In recent years he observed a recurrent ulceration in the centre of the scar. A biopsy did not show malignant cells but the recurrence of chronic breakdown was an indication for surgical excision of the scar tissue. In the first operation two tissue expanders were placed; one (1200 cc) was inserted in the paravertebral area and the other (1700 cc) in the right gluteal region. Two months later partial removal of the scar including the ulcerated area and reconstruction with the expander flap were performed. A re-expansion was performed one year later and 3 tissue expanders were placed at gluteal and lateral the level of the paravertebral thoracic regions.

Three months later removal of the expander, excision of the scar and reconstruction were performed. The ultimate result is satisfactory; further refinements can he achieved with a final expansion.

Case report 2 (Fig. 2)

A 32-year-old woman had sustained a bum of the face, neck and upper extremities at the age of six months. Scar and contractures of the cheek and oral region were inacceptable for the patient.

A preliminary expansion was performed by inserting an expander in the left side of the neck; a second expansion was carried out one year later on the opposite side of the neck: during expansion a breakdown was observed of the expanding tissue with partial exposure of the prosthesis. This complication did not impair the reconstructive procedure which yielded a satisfactory cosmetic result.

Discussion

In our series tissue expansion has yielded satisfactory results if compared with old techniques such as skin grafts or local flaps. However, the tissue expansion complication rate is higher in the treatment of large post-burn scars than in the treatment of other pathologies such as haemangiomas, giant naevi, post-mastectomy defects, bone exposure, etc.

The extensive scarring probably weakens the surrounding skin and impairs microvascularity.

We have observed that the complication rate is different in the various body areas.

In the head and neck the treatment of post-burn alopecia is satisfactory; the coverage of extensive facial or neck defects is often less satisfactory than in the treatment of other pathologies with the same technique: impairment of the expanding tissue, inflammation and exposure of the implant may be observed. In the thorax the morphological results may be compromised by the high rate of hypertrophic scars after the operation.

Excellent results have been obtained in the back, where very large amounts of scarred tissue can be removed in a single operation; re-expansion is also reliable and very useful to perform removal of scars.

In the thigh, good cosmetic improvement has very often been achieved; in the leg, on the contrary, we have observed the highest rate of complications. The use of tissue expansion in this area must be very careful and limited to selected cases: probably the stiffness of the tissue impairs the venous and lymphatic function and causes complications during tissue expansion: the fibrosis surrounding scar tissue may reduce venous and lymphatic flow from the expanding area and compromise tissue subjected to continuous mechanical stretching.

On the basis of our experience, tissue expansion is undoubtedly a method of choice in the treatment of post-burn scars; expansion must by very careful where stiffness of the tissue or terminal vascularization is present (leg, finger). At the level of the knee, elbow and neck, a very large amount of expanded skin is always necessary to carry out adequate reconstruction.

IPHREHAB : MENTAL RETARDATION AND MANAGEMENT TEAM

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MENTAL RETARDATION AND MANAGEMENT TEAM


Management Team
• Management of a case of mental retardation is  undertaken by a team consisting of psychiatrist or physical medicine expert, psychologist and a special educationalist.
•  The other members of team included are speech therapist, physicooccupational therapist, social worker and a vocational counsellor.
After a thorough assessment, the case is referred to either special school whenever possible, home based training or vocational training.


•  In overall management, there is very significant role of counsellor to help the parents in understanding and accepting the child's problem.
•  This requires a life long adjustment. In order to assist the parents in dealing effectively with the situation, counselling for behaviour modification is essential, as a part of the whole rehabilitation management plan.
•  The focus of counselling depends upon the individual needs and requirement of the mentally retarded and his family.


•   The parent counselling is done as given below;
(1)    To provide information regarding the condition of the mentally retarded child. The counsellor should explain child's condition in simple words to the parents and give enough trial.
Further information regarding management of his associated medical problem and other disabilities must be made available to the parents. The false hopes should be avoided.


(2)    Development of correct attitudes towards their handicapped child. Usually parents have wrong beliefs, ideas and thoughts regarding causes and treatment of their disabled child. They blame each other for being responsible for the birth of such child due to lack of awareness. Parents tend to believe that the child would become normal in due course of time. Hence counsellor should give correct information on the nature, causes and treatment of mentally retarded child.


Educational and Treatment Settings
• Only about 8 percent of mentally retarded students attend regular schools. The majority of mentally retarded students attend schools for children with special needs; a minority are home schooled.
There are real advantages to be had by mainstreaming mentally retarded children into regular schools where they can interact with non-disabled peers
• Some mildly mentally retarded children can attend a regular school with learning support. While attending regular classes most of the day, they may also attend a learning support classroom.
• Special education and learning support classrooms are designed to help children learn both academic and independent living skills.
• Special education is closely tied to social training and vocational training in that special education classes are designed to encourage self-determination.
• Traditional learning environments are not always beneficial for students who have more severe forms of mental retardation.
•  In order to ensure that students who have more severe forms of mental retardation are properly accommodated, they may be placed in a special school.
•  Such alternative schools are staffed by special education and learning support professionals. 


Useful Methods for Teaching Mentally Retarded Students
•  Mentally retarded individuals do better in environments where visual aides such as charts, pictures, and graphs are used as much as possible. Such visual components are useful for helping students to understand what is expected of them.
• The typical academic curriculum also incorporates social skills training and practical learning. Social skills help students navigate through social situations, maintain meaningful relationships, and thrive in the work environment.
 • Individuals with mental retardation benefit from the same teaching strategies used to teach individuals with learning disabilities, attention deficit/hyperactivity disorder, and autism.
• It is helpful to break tasks down into small steps and introduce the task one step at a time to avoid overwhelming the individual.
•  Once the student has mastered one step, the next is introduced.
•  Mentally retarded individuals do better in environments where visual aides such as charts, pictures, and graphs are used as much as possible. Such visual components are useful for helping students to understand what is expected of them.
•  Individuals with mental retardation require immediate feedback in order to make a connection between their answers, behaviors, or questions and the teacher's responses.
•  A delay in providing feedback may interrupt the connection between cause and effect in the student's mind, and the point will be lost.
•   Most people are kinesthetic learners who learn by doing, by completing a hands-on tasks and appreciating the results.
•  This is especially true for mentally retarded students who cannot comprehend abstract lectures very easily at all.


For example, a teacher who wants to teach the concept of gravity has several options: She can tell students that things are pulled towards the earth by a force known as gravity; she can show students how gravity works by dropping something; or she can instruct the students to drop something while teaching the concept.

IPHREHAB : Lumbar Traction AND TREATMENT

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Lumbar Traction

• To be effective, lumbar traction must overcome lower extremity weight (¼-½ of body weight)
• Friction is a strong counter force against lumbar traction
• Split table is used to reduce friction

General Technique for Applying Lumbar Tx

• Traction harness use

– Clip buckle versus velcro

– Vinyl versus cotton

– Adjustable lengths, pads

– Placement of lumbar belts 

• skin versus clothes – dissipate traction force)

– Use of thoracic belts on lower, lateral ribs

• Not in axilla

– The thoracic belt is placed on after the pelvic belt

Mechanical Traction Application

• Motorized lumbar traction
• Assess body weight
• Remove material that may interfere with halter
• Adjust halter accordingly

1. Traction halter = Pelvis
2. Stabilization harness = 8th-10th Ribs

• Unlock split table and align target spinal segment over the opening in the table
• Secure and connect halter
• Align angle of pull to correspond with specific pathology
• Explain treatment to patient and give safety switch

Effects on Lordosis (prone)

• Patients with sever pain and muscle spasms may tolerate prone traction better

• Pillows and harness to control lordosis

• Rope angle

– Always low

– Pillows can decrease or increase lordosis

• Pelvic harness

– May be placed to effect lordosis, as with supine

– Harness is never placed posteriorly in prone

– Rarely anterior

– As a rule, it is placed laterally to maintain other positional effects

• Treatment in prone 

– Allows performance of other modalities without position changes 

– Allows for easy palpation of the interspinous spaces to determine the level and degree of spinal motion 

General Technique for Applying Lumbar Tx

• Patient position

– Prone versus supine (comfort, goals)

– Prone 

• Disc

• Pillows under abdomen to flatten lordosis, under thighs or chest to increase extension

– Supine

• Mobilization

• pillows under knees to decrease lordosis

– Initial soft tissue stretch on soft tissue should come from positioning 

Effects of Lordosis (supine)

• Leg Position

– Up on a stool, decreases lordosis

– Flat, normal lordosis is maintained

– 90/90 position should flatten back, less than that decreases in increments

• Rope Angle

– Flat low pull maintains

– With increased (elevated) rope angle, lordosis decreases

• Pelvic Harness

– Greatest effect on lordosis

– Posterior pull decreases lordosis

– Lateral pull maintains lordosis

– Anterior pull increases lordosis

– Positions between these will result in incremental changes 

Patient Positioning

Supine

Increases flexion

• Supine + Flexion

Further increasing flexion

46-60 = L5-S1

60-75 = L4-L5

75-90 = L3-L4

90 = Posterior inter vertebral space

• Extension

Opens facet joints and increases distraction in upper lumbar

Initiation of Treatment

• Set controls to zero and turn on unit
• Adjust ratio
• Tension

1. Approximately 25% of body weight
2. Radicular pain caused by disk herniation: 30 to 60% of body weight

• Duration

1. Corresponding to pathology

• Instruct patient to remain relaxed

Termination of Treatment

• Tension
• Gradually reduce over 3 or 4 cycles
• Gain slack and turn unit OFF
• Many units have an auto OFF sequence
• Remove halter from unit and patient
• Patient remains in position for 5 minutes after the treatment

Patient Positioning

Prone

• Used when excessive flexion or lying supine causes pain
• Beneficial

1. Allows other modalities to be used during traction
2. Effects the lower disk protrusions

• Optimal Position
• Experience
• Trial and error

Traction Technique

• Angle of pull
• C spine supine better.  25* flexion
• L spine Flex hip and knees, symmetrical or prone or unilateral technique

IPHREHAB : CERVICAL TRACTION TREATMENT

IPHREHAB


Cervical Treatment Set-up

• Neck – placed in 25-30° flexion
• Straightens normal lordosis of C-spine
• Must have at least 15° flexion to separate facet joint surfaces
• Body must be in straight alignment
• Be aware that C-spine traction can cause residual lumbar n. root pain if improperly set up.
• Duration – 10-20 minutes most common

CERVICAL TREATMENT WITH TRACTION MACHINE

• Remove any jewelry, glasses, or clothing that may interfere
• Lay supine, place pillows, etc. under knees
• Secure halter to cervical region placing pressure on occipital process & chin (minor amount)
• Align unit for 25-30° of neck flexion 
• Remove any slack in pulley cable
• On:Off sequence 3:1 or 4:1 ratio

General Technique for Applying Cervical Tx

• Saunders

– Saunders or similar traction devices utilize a sliding track, with placement of the head on a pad on the carriage to decrease the tension load necessary to produce a traction force by eliminating most of the friction

– Stabilization is provided by a head strap and posterior pads that are tightened against the occiput and the mastoid processes 

Cervical Treatment 

Following treatment, gradually reduce tension & gain slack

Have patient remain in position for a few minutes after treatment 

Effectiveness of Cervical Traction

Cervical traction has been linked to 5 mechanical factors

Position of the neck

Force of applied traction

Duration of traction

Angle of pull

Position of patient

IPHREHAB: Spontaneous Subarachnoid Hemorrhage

IPHREHAB

Spontaneous Subarachnoid Hemorrhage

This is the fourth most frequent cerebrovascular disorder following atherothrombosis, embolism, and primary intracerebral hemorrhage. Saccular aneurysms are also called berry” aneurysms; actually they take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure.

Aneurysms are multiple in 20 percent of patients

In childhood , rupture of saccular aneurysms is rare, and they are seldom found at routine postmortem examination; beyond childhood, they gradually increase in frequency to reach their peak incidence between 35 and 65 years of age.

Approximately 90 to 95 percent of saccular aneurysms lie on the anterior part of the circle of Willis.

Clinical picture

• Prior to rupture, saccular aneurysms are usually asymptomatic. Exceptionally, if sufficiently large to compress pain-sensitive structures, they may cause localized cranial pain.
• The presence of a partial oculomotor palsy with dilated pupil may be indicative of an aneurysm of the posterior communicating-- internal carotid junction.
• With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space(where the circle of Willis lies).
• Rupture of the aneurysm usually occurs while the patient is active rather than during sleep , and in some instances sexual intercourse, straining at stool, lifting heavy objects, or other sustaining exertion precipitates the ictus. In patients who survive the initial rupture, the most feared complication is rerupture, an event that may occur at any time from minutes up to 2 or 3 weeks later.
• In less severe cases, consciousness, if lost , may be regained within a few minutes or hours, but a residual of drowsiness, confusion, and amnesia accompanied by  severe headache and stiff neck persists for several days.
• Since the hemorrhage is confined to the subarachnoid space, there are few or no focal neurologic signs.
• AVM is another most common cause for SAH
• Convulsive seizures, usually brief and generalized.

• Vasospasm  Delayed hemiplegia or other focal deficit usually appears 3 to 12 days after rupture and rarely before or after this period. These delayed accidents and the focal narrowing of a large artery or arteries, seen on angiography, are refered to as vasospasm.
• Hydrocephalus  If a large amount of blood ruptures into the ventricular system or floods the basal subarachnoid space, The patient then may become confused or unconscious as a result of acute hydrocephalus. A subacute hydrocephalus due to blockage of the CSF pathways by blood may appear after 2 to 4 weeks.

Laboratory Findings  

A CT scan will detect blood locally or diffusely in the subarachnoid spaces or within the brain or ventricular system in more than 90 percent of cases and in practically all cases in which the hemorrhage has been severe enough to cause momentary or persistent loss of consciousness.

In all other cases a lumbar puncture should be undertaken when the clinical features suggest a subarachnoid hemorrhage. Usually the CSF is grossly bloody within 30 min of the hemorrhage, with RBC counts up to 1 million per cubic millimeter or even higher.

Carotid and vertebral angiography is the only certain means of demonstrating an aneurysm and does so in some 85 percent of patients in whom the correct diagnosis of spontaneous subarachnoid hemorrhage is made on clinical grounds.

MRI and MRA detect most aneurysms of the basal vessels but are as yet of insufficient sensitivity to replace conventional angiography. Even when MRA or “ CT angiography  “ demonstrates the aneurysm, the surgeon usually requires the kind of anatomic definition that can only be obtained by conventional angiography. 

Establish the diagnosis

If there is a typical history, marked neck stiffness and no focal neurological deficit, lumbar puncture is still the best way to make the diagnosis, revealing uniformly blood-stained CSF. 

If the history is typical with marked neck stiffness, but the patient remains in coma or shows a marked focal neurological deficit, a CT scan is a safer way to establish the diagnosis (revealing blood in the subarachnoid space),since lumbar puncture may lead to worse condition in this group of patients (whose coma or focal neurological deficit may indicate the presence of an associated intracerebral blood clot).

Treatment 

• This is influenced by the neurologic and general medical state of the patient as well as by the location and morphology of the aneurysm.
• The general medical management in the acute stage includes the following , in all or part: 
• bed rest
• fluid administration to maintain above-normal circulating volume and central venous – pressure
• use of elastic stockings and stool softeners
• administration of beta-blockers
• calcium channel blockers

Treatment 

• intravenous nitroprusside
• or other medication to reduce greatly elevated blood  pressure and then maintain systolic blood pressure at 150 mmHg or less;
• and pain-relieving medication for headache ( this alone will often reduce the hypertension ).
• The prevention of systemic venous thrombosis is critical, usually accomplished by the use of cyclically inflated whole-leg compression boots.

Treatment 

• The use of anticonvulsants is controversial; many neurosurgeons administer them early, with a view of preventing a seizure-induced risk of rebleeding.
• Calcium channel blockers are being used extensively to reduce the incidence of stroke from vasospasm. Nimodipine 50 mg, administered intravenus, is currently favored.
• Notable advances in the techniques for the obliteration of aneurysms, particularly the operating microscope, and the management of circulatory volume have significantly improved the outcome of patients with ruptured aneurysms.
• Both the risk of rerupture of the aneurysm and some of the secondary problems that arise because of the massive amount of blood in the subarachnoid space can be obviated by early obliteration of the aneurysm.
• lumbar puncture is carried out for diagnostic purposes if the CT scan is inconclusive; thereafter this procedure is performed only for the relief of intractable headache, to detect recurrence of bleeding, or to measure the intracranial pressure prior to surgery. 
• Advice from specialist neurosurgical units should be sought. Patients who have withstood their first bleed well are submitted to carotid and vertebral angiography within a few days to establish whether or not an operable aneurysm is present. Patients who do not recover from their first bleed well, patients with inoperable aneurysms should be nursed in bed for a few weeks and then mobilized over a further few weeks, being encouraged to return to full normal activities at about 3-4 months.
• Prevent re-bleeding

Rehabilition

Since the incidence of significant damage to the brain is high  in patients surviving subarachnoid haemorrhage, many will not be able to return to normal activities.

They will need support from relatives,  nurses, physiotherapists, speech therapists, occupational therapists, social workers and specialist units in rehabilitation.

Course and prognosis

 Patients with the typical clinical picture of spontaneous subarachnoid hemorrhage in whom an aneurysm or arteriorvenous malformation cannot be demonstrated angiographically have a distinctly better prognosis than those in whom the  lesion is visualized.

 Vasospasm and rebleeding were the leasing causes of morbidity and mortality in addition to the initial bleed. In respect to rebleeding , Aoyagi and Hayakawa found that this occurred within 2 weeks in 20 percent of patients, with a peak incidence in the 24 h after the initial bleed.

IPHREHAB : INTRACEREBRAL HEMORRHAGE & TREATMENT

IPHREHAB


INTRACEREBRAL HEMORRHAGE & TREATMENT
The management of patients with large intracerebral hemorrhages and coma includes the maintenance of adequate ventilation, use of controlled hyperventilation to a Pco2 of 25 to 30 mmHg, monitoring of intracranial pressure (ICP) in some cases and its control by the use of tissue-dehydrating agents such as mannitol (osmolality kept at 295 to 305 mosmol/L and Na at 145 to 150 meq), and  limiting intravenous infusions to normal saline.


Rapid reduction in blood pressure, in the hope of reducing further bleeding , is not recommended, since it risks compromising cerebral perfusion in cases of raised intracranial pressure. On the other hand, sustained mean blood pressure  of greater than 110mmHg may exaggerate cerebral edema and risk extension of the clot. It is at approximately this level of acute hypertension that the use of beta-blocking drugs(esmolol, labetalol) or angiotensin-converting enzyme inhibitory drugs is recommended.


In contrast to cerebral hemorrhage, the surgical evacuation of cerebellar hematomas is a generally accepted treatment and is a more urgent matter because of the proximity of the mass to brainstem and the risk of abrupt progression to coma and respiratory failure.




Course and Prognosis
The immediate prognosis for large and medium-size cerebral clots is grave; some 30 to 35 percent of patients die in 1 to 30 days.
Either the hemorrhage extends into the ventricular system or intracranial pressure is elevated to levels that preclude normal perfusion of the brain.
Sometimes the hemorrhage itself seeps into vital centers such as the hypothalamus or midbrain.


A volume of 30 ml or less, calculated from the CT scan, predicted a generally favorable outcome.
In patients with clots of 60 ml or larger and an initial Glasgow Coma Scale score of 8 or less, the mortality was 90 percent. As remarked earlier, it is the location of the clinical effects.

IPHREHAB : Embolic infarction

IPHREHAB


Embolic infarction
This is one of the most common cause of stroke. In most cases of cerebral embolism, the embolic material consists of a fragment that has broken away from a thrombus within the heart. Embolism due to fat, tumor cells, fibrocartilage, amniotic fluid, or air is a rare occurrence and seldom enters into the differential diagnosis of stroke.

Clinical Picture

Of all strokes, those due to cerebral embolism develop most rapidly. The embolus strikes at any time of the day or night. Getting up to go to the bathroom is a time of danger. The neurologic picture will depend on the artery involved and the site of obstruction.

It  is important to repeat that an embolus may produce a severe neurologic deficit that is only temporary; symptoms disappear as the embolus fragments. In other words , embolism is a common cause of a single evanescent stroke that may reasonably be called a prolonged TIA. Also as already pointed out, several emboli can give rise to two or three transient  attacks of differing pattern or , rarely , of almost identical pattern.

Causes of cerebral embolism:

Cardiac origin

Noncardiac origin

Undetermined origin

Laboratory Findings

Not infrequently the first sign of myocardial infarction is the occurrence of embolism; therefore it is advisable that an ECG and echocardiogram be obtained in all patients with stroke of uncertain origin. Prolonged study of heart rhythm with Holter monitoring should be undertaken.

In some 30 percent of cases, cerebral embolism produces a hemorrhagic infarction. CT scanning or MRI may be helpful in showing the more intense hemorrhagic infarcts, particularly if the scan is repeated on the second or third day.

Course and prognosis

Most patients survive the initial insult, and in many the neurologic deficit may recede relatively rapidly, as  indicated above. The eventual prognosis is determined by the occurrence of further emboli and the gravity of the underlying illness- cardiac failure myocardial infarction, bacterial endocarditis  and so on.

Treatment and prevention

Three phases of therapy : General medical management in the acute phase, Measures directed to restoring the circulation Physical therapy and rehabilitation These are much the same as described above the prevention of atherothrombotic infarction.

IPHREHAB : DIFFERENTIAL DIAGNOSIS AND TREATMENT CEREBRAL THROMBOSIS AND TIAs

IPHREHAB

DIFFERENTIAL DIAGNOSIS CEREBRAL THROMBOSIS AND TIA


Differential Diagnosis
Vascular disorders are mistaken for ischaemic stroke include intracerebral hemorrhage, subdural or epidural hematoma , and subarachnoid hemorrhage from rupture of an aneurysm or vascular malformation. These condition can often be distinguished by a history of trauma or of excruciating headache at onset, a more marked depression of consciousness, or by the presence of neck stiffness on examination. They can be excluded  by CT scan or MRI.


Differential Diagnosis: Other structural brain lesion such as tumor or abscess can also produce focal cerebral symptoms of acute onset. Brain abscess is suggested by concurrent fever, and both abscess and tumor can usually be diagnosed by CT scan or MRI. Metabolic disturbances, particularly hypoglycemia and hyperosmolar nonketotic hyperglycemia, may present in stroke like fashion. The serum glucose level should therefore be determined in all patients with apparent stroke.

Treatment of Cerebral Thrombosis and Transient Ischemic Attacks

The current treatment of it may be divided into four parts:

Management in the acute phase

Measures to restore the circulation and arrest the pathologic process

    1. Thrombolytic agents ( t-PA only for completed stroke,w/in 3~6hrs ) 2.Anticoagulant drugs ( Heparin, LMWH & warfarin)

    3. Antiplatelet drugs ( Aspirin  or  Clopidogrel, Dipyridamole or   Ticlopidine )

    4.Difibrase

    5. Neuroprotective agents: barbiturates, opioid  antagonist naloxone,Manitol

Treatment

Treatment of cerebral edema and raised intracranial pressure

Acute surgical revascularization 

Surgery for symptomatic carotid stenosis, Carotid endarterectomy, intralumenal stents, extracranial-intracranial bypass

Physical therapy and rehabilitation.

Measures to prevent further strokes and progression of vascular disease.

• Since the primary objective in the treatment  of  atherothrombotic disease is prevention , efforts to control the risk factors must continue. 
• Aspirin
• Hypotensive agents
• Oversedation should be avoided
• Systemic hypotension, severe anemia should be treated promptly
• Particular care should be taken to maintain the systemic blood pressure, oxygenation  and intracranial  blood flow during surgical procedures, especially in elderly patient.

Course and Prognosis

When the patient is seen early in the cerebral thrombosis, it is difficult to give an accurate prognosis.

As for the eventual or long-term prognosis of the neurologic deficit , there are many possibilities.

It must be mentioned that having had one thrombotic stroke, the patient is at risk in the ensuing months and years of having a stroke at the same or another site, especially if there is hypertension or diabetes mellitus.

IPHREHAB : HYPOTONIA MANIFESTATION

IPHREHAB :

HYPOTONIA MANIFESTATION


Signs and objective manifestations
Hypotonic patients may display a variety of objective manifestations that indicate decreased muscle tone.
Motor skills delay is often observed, along with hypermobile or hyperflexible joints, drooling and speech difficulties, poor reflexes, decreased strength, decreased activity tolerance, rounded shoulder posture, with leaning onto supports, and poor attention and motivation.
The extent and occurrence of specific objective manifestations depends upon the age of the patient, the severity of the hypotonia, the specific muscles affected, and sometimes the underlying cause. For instance, some hypotonics may experience constipation, while others have no bowel problems.

§Since hypotonia is most often diagnosed during infancy, it is also known as "floppy infant syndrome" or "infantile hypotonia." Infants who suffer from hypotonia are often described as feeling and appearing as though they are "rag dolls" or a "sack of jello," easily slipping through one's hands.

§They are unable to maintain flexed ligaments, and are able to extend them beyond normal lengths. Often, the movement of the head is uncontrollable.

§Hypotonic infants often have difficulty feeding, as their mouth muscles cannot maintain a proper suck-swallow pattern, or a good breastfeeding latch.

Developmental delay

Most low-tone infants have delayed developmental milestones, but the length of delay can vary widely. Motor skills are particularly susceptible to the low-tone disability.

Gross motor skills, and fine motor skills, both are affected. 

Hypotonic infants are late in lifting their heads while lying on their stomachs, rolling over, lifting themselves into a sitting position, remaining seated without falling over, balancing, crawling, and walking. Fine motor skills delays occur in grasping a toy or finger, transferring a small object from hand to hand, pointing out objects, following movement with the eyes, and self feeding.  

§Speech difficulties can result from hypotonia. Low-tone children learn to speak later than their peers, even if they appear to understand a large vocabulary, or can obey simple commands.

§ Difficulties with muscles in the mouth and jaw can inhibit proper pronunciation, and discourage experimentation with word combination and sentence-forming.

Diagnosis

Diagnosing a patient includes obtaining family medical history and a physical examination, and may include such additional tests as computerized tomography (CT) scans, magnetic resonance imaging (MRI) scans, electroencephalogram (EEG), blood tests, genetic testing (such as chromosome karyotyping and tests for specific gene abnormalities), spinal taps, electromyography muscle tests, or muscle and nerve biopsy.

Mild or benign hypotonia is often diagnosed by physical and occupational therapists through a series of exercises designed to assess developmental progress, or observation of physical interactions.

§Since a hypotonic child has difficulty deciphering his spatial location, he may have some recognizable coping mechanisms, such as locking the knees while attempting to walk.

§ A common sign of low-tone infants is a tendency to observe the physical activity of those around them for a long time before attempting to imitate, due to frustration over early failures.

§ Developmental delay can indicate hypotonia

Prognosis and treatment

There is currently no known treatment or cure for most (or perhaps all) causes of hypotonia, and objective manifestations can be life long. 

In some cases, muscle tone improves over time, or the patient may learn or devise coping mechanisms that enable him to overcome the most disabling aspects of the disorder. However, hypotonia caused by cerebellar dysfunction or motor neuron diseases can be progressive and life-threatening. 

Along with normal pediatric care, specialists who may be involved in the care of a child with hypotonia include developmental pediatricians (specialize in child development), neurologists, neonatologists (specialize in the care of newborns), geneticists, occupational therapists, physical therapists, speech therapists, orthopedists, pathologists (conduct and interpret biochemical tests and tissue analysis), and specialized nursing care. 

If the underlying cause is known, treatment is tailored to the specific disease, followed by symptomatic and supportive therapy for the hypotonia. 

In very severe cases, treatment may be primarily supportive, such as mechanical assistance with basic life functions like breathing and feeding, physical therapy to prevent muscle atrophy and maintain joint mobility, and measures to try and prevent opportunistic infections such as pneumonia. 

Treatments to improve neurological status might involve such things as medication for a seizure disorder, medicines or supplements to stabilize a metabolic disorder, or surgery to help relieve the pressure from hydrocephalus (increased fluid in the brain). 

Breast Feeding

Low-tone infants often have difficulty feeding, especially coordinating the suck-swallow reflex required for proper breastfeeding.

Take longer to breastfeed because of the poor timing of sucking bursts and the need for long rests. 

They will also require greater feeding frequency

A baby with low muscle tone may suck better when the head and bottom are level, indicating pillow support in the lap.

If nursing is too frustrating and stressful for mother and child, breast milk can be expressed by use of a breast pump and fed through a bottle.