PERIPHERAL NEUROPATHY

PERIPHERAL NEUROPATHY. TYPES, ASSESMENT AND MANAGEMENT OF ALL TYPES

1. - Dr. Aishwarya Rai, PT MPT 1 st Year, Neurology. Jyoti Rao Phule Subharti College of Physiotherapy.

2. The function of the peripheral nervous system is to carry impulses to and from the central nervous system. These impulses regulate motor, sensory and autonomic activities. The peripheral nervous system is comprised of structures that lie outside the pial membrane of the brain stem and spinal cord and can be divided into cranial, spinal and autonomic components . Axons within the peripheral nerve vary structurally. This is related to function. Three distinct fibre types can be distinguished: TYPE A 2–20 μ m in diameter. Myelinated . Function: Motor and sensory (vibration, proprioception ). Conduction velocity: 10–70 metres /second. TYPE B 3 μ m diameter. Thinly myelinated . Function: Mainly preganglionic autonomic, some pain and temperature. Conduction velocity: 7–5 metres /second. TYPE C < 1 μ m diameter. Unmyelinated . Function: Sensory – pain and temperature. Conduction velocity: < 2 metres /second.

3. DISTAL AXONOPATHY Degeneration of distal most part of axons which slowly advances towards the cell body. Due to toxic or metabolic derangement of neurons. MYELINOPATHY Loss of myelin sheath which causes complete block of conduction of action potentials through the axon of nerve cells. Eg : GBS, leukodystrophy . NEUROPATHY Destruction of neurons of PNS. Eg : MND, effect of vincristine , infection of herpes zoster.

4. Polyneuropathy describes damage to the peripheral nervous system. Polyneuropathy /Peripheral Neuritis is the dysfunction of the peripheral nervous system by nerve damage. It can be the result of the underlying disease and also the diseases affecting the nerves.

5. POLYNEUROPATHY Conditions where there is primary degeneration of nerve parenchyma. POLYNEURITIS Inflammation of the peripheral nerves.

6. ANALGESIA absent sensitivity to a painful stimulus HYPERALGESIA increased sensitivity to a painful stimulus HYPOALGESIA reduced sensitivity to painful stimulus HYPERAESTHESIA increased sensitivity to any stimulus HYPOAESTHESIA reduced sensitivity to any stimulus HYPERPATHIA increased sensitivity with increasing threshold to repetitive stimulation ALLODYNIA pain provoked by a non-painful stimulus PARAESTHESIA a ‘pins and needles’ sensation

7. MAJOR SYMPTOMS Numbness of feet with tingling sensation Weakness In coordination Pain Burning sensation Invisible 'glove like‘ sensation Abnormal heart rate Reduced sweating Decreased libido

8. Disease of a single peripheral or cranial nerve is termed mononeuropathy . It can be caused by compression to the nerve, carpel tunnel syndrome or some infection and nerve inflammation causing tingling feet. mononeuropathy

9. mononeuritis complex When many single nerves are damaged one by one, this is described as mononeuritis multiplex. It can occur when multiple nerves are damaged in the body due to diabetes mellitus (diabetic neuropathy), Churg -Strauss syndrome, HIV, amyloidosis and rheumatoid arthritis. It is present with dull pain in legs and back mostly at night.

10. Polyneuropathy affects nerve cells anywhere in the body irrespective of the nerve path. It can cause changes in axon, neurons cell bodies and myelin sheath surrounding axons. Polyneuropathy produces symptoms such as numb feet, burning, erectile dysfunction and imbalance in bladder function. polyneuropathy

11. The fourth pattern in the peripheral type of neuropathy is the autonomic neuropathy causing alterations in the autonomic nervous system. It affects the non-involuntary nerves reaching urinary bladder, digestive system, sexual organs and the heart. Chronic diabetic patients are prone to this neuropathy. Autonomic neuropathy can also be present in combination with other neuropathies. It produces symptoms such as incontinence of urine, pain in abdomen with vomiting, diarrhea or constipation, tachycardia, hypotension and impotency. autonomic neuropathy

12. I. Acquired peripheral neuropathies are grouped into three broad categories: Those caused by systemic disease, Those caused by trauma from external agents Those caused by infections or autoimmune disorders affecting nerve tissue. II. Inherited forms of peripheral neuropathy. Inherited forms of peripheral neuropathy are caused by inborn mistakes in the genetic code or by new genetic mutations. Some genetic errors lead to mild neuropathies with symptoms that begin in early adulthood and result in little, if any, significant impairment. More severe hereditary neuropathies often appear in infancy or childhood. POLYNEUROPATHIES

13. TRAUMA It is the most common cause of injury to a nerve. Injury or sudden trauma, such as from automobile accidents, falls, and sports related activities, can cause nerves to be partially or completely severed, crushed, compressed, or stretched, sometimes so forcefully that they are partially or completely detached from the spinal cord. Less dramatic traumas also can cause serious nerve damage. Broken or dislocated bones can exert damaging pressure on neighboring nerves, and slipped discs between vertebrae can compress nerve fibers where they emerge from the spinal cord. Acquired peripheral neuropathies – ETIOLOGY

14. Acquired peripheral neuropathies – ETIOLOGY Systemic diseases are disorders that affect the entire body and often cause peripheral neuropathy. These disorders may include metabolic and endocrine disorders. Nerve tissues are highly vulnerable to damage from diseases that impair the body's ability to: • Transform nutrients into energy, • Process waste products, or • Manufacture the substances that make up living tissue. Eg . Diabetes mellitus, characterized by chronically high blood glucose levels, is a leading cause of peripheral neuropathy.

15. ETIOLOGY Hormonal imbalances Vitamin deficiencies and alcoholism Vascular damage and blood diseases Connective tissue disorders and chronic Inflammation Cancers and benign tumors Repetitive stress frequently leads to entrapment Neuropathies Toxins (Hg, Ar , Th , Pb ) Anticancer drugs, Anticonvulsants, Antiviral agents, and Antibiotics Infections and autoimmune disorders Viruses ( herpes varicella zoster, Epstein-Barr virus, cytomegalovirus, and herpes simplex, HIV). Bacteria ( Lyme disease, diphtheria, and leprosy)

16. GUILLAIN BARRE SYNDROME It is acutely or sub-acutely generalized ascending type of polyneuropathy . is the most common cause of acute progressive flaccid paralysis. Guillain-Barre syndrome typically, manifests as rapidly progressing limb weakness, accompanied by paresthesias and often cranial nerve dysfunction. The age of onset is 40 years. AETIOLOGY- The condition may follow viral infection, e.g. varicella -zoster, mumps and cytomegalovirus. It is also associated with Mycoplasma , Campylobacter, infections, immunizations with both live and dead vaccines (rabies, typhoid, tetanus, influenza),blood transfusions, drugs( antidepessants ) antitoxins, trauma, surgical stress and, rarely, malignant disease and immunodeficiency.

17. PATHOPHYSIOLOGY Both antibody and cell-mediated reactions to peripheral nerve myelin are involved. Some patients produce antibodies to myelin glycoproteins or gangliosides , others develop a T cell mediated assault on myelin basic protein. Segmental demyelination results with secondary axonal damage if the process is severe. Perivascular infiltration with lymphocytes occurs within peripheral nerves and nerve roots. Lymphocytes and macrophages release cytotoxic substances (cytokines) which damage Schwann cell/myelin. When axon damage and nerve cell death occur, regeneration cannot take place.

18. CLINICAL FEATURES The cardinal features of GBS are weakness, paresthesias , and diminished or absent DTRs. The initial neurological symptoms vary from patient to patient. Distal, usually symmetrical, paresthesias involving the toes, finger, or both herald the onset of the disorder in at least 50% of patients. As the disease progress, these paresthesias typically spread proximally but seldom extended beyond ankles and wrists. Facial paresthesias , which are usually perioral , are less common. Gradually weakness in lower extremities especially in proximal muscles, so that patients may feel difficulty in climbing stairs and rising from chairs. Weakness soon spreads to the upper extremities. However, some times the illness progresses, leading to complete paralysis of arms and legs. About one quarter of the time, the paralysis continues up the chest causing respiratory dysfunction. Cranial nerve (VII, Facial diaplegia ), occasionally, fasciculations are noted. Sometimes deep pain also occur, which is more prominent in shoulder girdle, back and posterior thighs and is notoriously more severe in night. Substantial sensory abnormalities are found infrequently and contrast with the high incidence of sensory symptoms. Typically, vibration and proprioception , the sensory modalities mediated over large myelinated fibers, are the most severely affected.

19. CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY (CIDP) Generally less dangerous, usually damages sensory and motor nerves, leaving autonomic nerves intact. This slowly progressive steroid-dependent polyneuropathy can occur at any age (mean age of onset in the 5th decade). CIDP is an apparent immune-mediated disorder of PNS. The term chronic inflammatory demyelinating polyradiculopathy was coined to emphasize that the disorder is a chronic process that results in demyelination as well as inflammatory cell response in peripheral nerves and spinal nerve roots; typically, there is a mononuclear cell infiltration involving the endoneurium and epineurium of peripheral nerve fibers. The predominant physiological feature is Segmental demylination , although usually there is some degree of axon loss as well. These pathological changes have been found to involve roots, plexuses, proximal nerve trunks, as well as some autonomic nerves.

20. CHRONIC IDIOPATHIC SENSORY NEUROPATHY (CISN) This is basically a sensory form of CIDP with limb ataxia, numbness and pain, loss of proprioception , normal muscle strength but generalized areflexia .

21. ALCOHOLIC POLYNEUROPATHY Alchoholic Neuropathy is a disorder involving decreased nerve functioning caused by damage that results from excessive drinking of alcohol. The onset is often insidious and presents with distal symmetric dominant sensory-dominant polyneuropathy confined to the legs. Painful sensations with or without burning represents the initial and major symptom. Other manifestations are dysesthesias , paresthesias or sensory ataxia. Autonomic features may be present (commonly abnormal sweating or diarrhea, less frequently postural hypotension, vomiting, micturition difficulties, impotence and retrograde ejaculation). Electrophysiological studies show axonal neuropathy predominantly affecting the sensory nerves. Progression is gradual continuing over months or years. Abstinence reveals gradual improvement in the polyneuropathy . Rapidly progressive polyneuropathy resembling GBS but without raised protein or slowed NCVs can occur in alcoholics.

22. IDIOPATHIC PERIPHERAL FACIAL PALSY (BELL PALSY) The incidence of Bell palsy is 2-3%. Retroauricular pain usually precedes the paralysis by 1 or 2 days. Almost 50% show maximal paralysis in 2 days. Recovery takes weeks - 2 month. Ramsay-Hunt syndrome (zoster around the ear, acute peripheral facial palsy, and symptoms involving the VIII cranial nerve) is caused by a reactivation of VZV( Varicella Zoster Virus). The same virus causes acute peripheral facial palsy without skin lesions (zoster sine herpete ). About 15% of patients will have permanent sequelae . The facial palsy associated with Ramsay-Hunt syndrome is more severe and has a lower recovery rate than that of Bell palsy. The diagnosis of Ramsay-Hunt syndrome is relatively easy in the presence of typical skin rash.. A combination of acyclovir (4000 mg daily for 5 days) and prednisone (60 mg/day for 4 days) provide a 100% cure rate if started within 3 days after the onset.

23. DIABETIC NEUROPATHIES Diabetic neuropathies are a family of nerve disorders caused by diabetes. People with diabetes can, over time, have damage to nerves throughout the body. Neuropathies lead to numbness and sometimes pain and weakness in the hands, arms, feet, and legs. Problems may also occur in every organ system, including the digestive tract, heart, and sex organs. People with diabetes can develop nerve problems at any time, but the longer a person has diabetes, the greater the risk. An estimated 50% of those with diabetes have some form of neuropathy, but not all with neuropathy have symptoms. The highest rates of neuropathy are among people who have had the disease for atleast 25 years

24. THYROID/PITUITARY NEUROPATHIES Mucinous deposits in soft tissue resulting in nerve compression and carpal tunnel-like symptoms have been implicated in neuropathy associated with hyperthyroidism. Neuropathy associated with excess growth hormone or acromegaly has been associated with subperineurial -tissue proliferation and diminished myelinated and unmyelinated fibers.

25. AIDS-ASSOCIATED NEUROPATHY Polyneuropathy affects as many as one-third of individuals with acquired immunodeficiency syndrome (AIDS), most commonly manifested as distal, symmetrical polyneuropathy .

26. HEREDITARY SENSORIMOTOR NEUROPATHY (HSMN)/ (CHARCOT-MARIE-TOOTH DISEASE) This is the most common cause of distal leg muscle wasting and weakness (" peroneal muscular atrophy" syndrome), usually accompanied by pes cavus . The age of onset is variable and asymptomatic, yet affected elderly relatives may be identified. In HSMN males are commonly affected, whereas females are more often asymptomatic. Positive sensory symptoms ( paresthesias ) are unusual and should rather suspect acquired neuropathy. Associated features (spastic paraparesis , optic atrophy, retinitis pigmentosa , deafness and mental retardation) can occur.

27. HEREDITARY NEUROPATHY WITH LIABILITY TO PRESSURE PALSIES (HNPP) This condition also known as tomaculous (sausage-like) neuropathy is autosomal dominant with the onset of symptoms is in the 2 nd or 3 rd decade of life and translates in a tendency to develop painless focal and recurrent demyelinating sensory and motor peripheral mononeuropathies due to unusual vulnerability to pressure or traction. Exposed nerves such as ulnar nerve, radial nerve and superficial peroneal nerve are especially vulnerable. Painless brachial plexus lesions may result from traction or prolonged abnormal postures. Recovery occurs over days, weeks or months, but permanent disability may develop after recurrent episodes. Typically, patients experience tingling of the fingertips when using scissors.

28. HEREDITARY SENSORY AND AUTONOMIC NEUROPATHY Five clinical different entities have been described under hereditary sensory and autonomic neuropathies - all characterized by progressive loss of function that predominantly affects the peripheral sensory nerves. Their incidence has been estimated to be about 1 in 25,000. Hereditary Sensory Radicular Neuropathy: It is transmitted as autosomal dominant trait and is characterized by a sensory deficit in the distal portion of the lower extremities, chronic perforating ulcerations of the feet and progressive destruction of underlying bones. Congenital Sensory Neuropathy: It is characterized by onset of symptoms in early infancy or childhood. Upper & lower extremities are affected with chronic ulcerations and multiple injuries to fingers and feet. Pain sensation is affected predominantly and deep tendon reflexes are reduced. Autoamputation of the distal phalanges is common and so is neuropathic joint degeneration.

29. Familial dysautonomia , Riley-Day syndrome: It is an autosomal recessive disorder seen predominantly in Jews of eastern European descent. Patients present with sensory and autonomic disturbances. Newborns have absent or weak suck reflex, hypotonia and hypothermia. Retarded physical development, poor temperature and motor in coordination are seen in early childhood. Other features include reduced or absent tears, depressed deep tendon reflexes, absent corneal reflex, postural hypotension and relative indifference to pain. Scoliosis is frequent. Intelligence remains normal. Many patients die in infancy and childhood. Congenital Insensitivity to Pain and Anhidrosis : It is an autosomal recessive condition and affectes infants present with episodes of hyperthermia unrelated to environmental temperature, anhidrosis and insensitivity to pain. Palmar skin is thickened and charcot joints are commonly present. Hereditary Sensory and Autonomic Neuropathy: It also manifests with congenital insensitivity to pain & anhidrosis . There is a selective absence of small myelinated fibers differentiating it from type 4.

30. Diagnosing peripheral neuropathy is often difficult because the symptoms are highly variable. A thorough neurological examination is usually required and involves; Taking an extensive patient history (including the patient's symptoms, work environment, social habits, exposure to any toxins, history of alcoholism, risk of HIV or other infectious disease, and family history of neurological disease). Performing tests that may identify the cause of the neuropathic disorder, Conducting tests to determine the extent and type of nerve damage.

31. CSF protein is elevated in most patients but often not until the second or third week of illness. Cells are usually absent but in 20% up to 50 cells/mm3 may be found. Some antibodies have been identified as being associated with some sub-types including: AMAN: anti-GD1a and GM1 Acute sensory neuropathy: anti-GD1b Nerve conduction studies When carried out early in the illness, these may be normal. Findings of multifocal demyelination soon develops with slowing of motor conduction, conduction block and prolonged distal motor latencies. Ancillary investigations Performed to identify any precipitating infection: e.g. viral and bacterial studies. Electrolytes are checked for inappropriate secretion of antidiuretic hormone and immune complex glomerulonephritis . CT Scan Nerve Biopsy Skin Biopsy MRI EMG

32. HISTORY: Including family and medical history or any exposure to any other drugs should be assessed. FAMILY HISTORY : Majority have a family history of the condition, or having neuropathy in family history. Presentation of pes cavus or abnormal gait represents of having some inherited disorder like CMT. Family tree tracking both sides of the family for 3 generations to rule out who was affected and what mode of inheritance is present whether anybody had trouble with walking, balance, tripping, falling, or with their hands or sensations should be find out. An autosomal dominant type will have people affected in all generation and male-to-male transmission can be seen thus males are severely affected. Whereas autosomal recessive pedigrees may have only one person or sibling affected with no family history • At times with no family history does not preclude the diagnosis, as new mutations are relatively caused. MEDICAL HISTORY : Includes difficulty in balancing and problems in finding well-fitting shoes owing to high foot arches and as history of surgery been done of tendon transfer like tight heel cords, hammer toe straightening and arthrodesis of ankle.

33. OBSERVATION: Analysis of movement, observation of the condition and shape of muscle contours should be noted. Functional difficulty like clumsiness in gripping a cup or difficulty in manipulating small items such as bottle tops because of wasting of the intrinsic hand muscles. Even muscle imbalances will lead to shortening of unopposed muscle groups resulting in contractures and deformities. CRANIAL NERVE EXAMINATION: Generally cranial nerves are normal at times abnormalities in papillary constriction and in optic nerve. SENSORY EXAMINATION: like pinprick, light touch, proprioception , vibration, graphesthesia and temperature should be assessed in terms of extent and pattern of involvement. Both small and large sensory nerve fibres show decreased or absent sensation. Reduction in pinprick and vibration sensation is seen and more pronounced at the toes than in more proximal muscles with Sensory ataxia (i.e., imbalance and incoordination ) due to loss of proprioception may also be seen.

34. MUSCLE STRENGTH: Should be assessed with MMT where decreased strength is noted in the distal muscles of the arms and legs like intrinsic hand and foot muscles and tibialis anterior as distal muscles degenerate (axonal loss) first while maintaining strength in proximal muscles and in the gastrocnemius muscle. They are also associated with atrophy and weakened foot eversion . Hand weakness is also seen in terms of poor finger control, poor handwriting, and difficulty using zippers and buttons, and clumsiness in manipulating small objects. A hand held myometer has been shown sensitive and reliable in assessing neuropathies. Weakness in hand muscles can be assessed by using a grip dynamometer which is used in distal neuropathies. REFLEX TESTING: Should be tested as deep tendon reflexes are diffusely absent ( areflexia ) or reduced ( hyporeflexia ) and can occur in any condition involving nerve damage. GIRTH MEASUREMENT: Is done in order to detect the degree of wasting or atrophy of the muscles.

35. DEFORMITIES: Like pes caves are common and are associated with areflexia ; give the likelihood of having CMT. It results from muscle imbalance as anterior tibialis and the intrinsic foot muscles are affected with sparing of the gastrocnemius muscle thus the stronger pull of gastrocnemies overcomes the weaker pull of anterior tibialis , leading to structural foot deformities. In upper limb, claw hand deformities can be seen. GAIT: Assessment of the gait reveals difficulty in walking, twisting of ankles, slapping of the feet, or loss of a heel-to-toe pattern, and the patient may walk with a high- steppage gait (lifting legs up excessively to clear the toes) which is due to tight heel cord, and weakness in tibialis anterior leading to inadequate strength to pull the foot up during ambulation. Fractures are common. At times may require bilateral aids, such as ankle-foot orthoses , to ambulate. If quadriceps muscle weakens, hyper extension occurs at the knees to produce a rigid structure when weight bearing whereas when proximal muscles in lower limbs like hip abductors weakness is seen it results in positive Trendelenburg sign positive. AUTONOMIC DYSFUNCTION: Sweating due to poor vasomotor control leading to cold feet with blotching or pallor of the skin of the feet is noticed.

36. NEUROPATHIC PAIN (BURNING, TINGLING, SHOOTING): May also occur as a result of the neuropathy, while bone and joint pain may result from pressure on the feet. Muscle cramps and restless legs is also been noticed. Neuropathic pain can be treated with gabapentin , pregabalin , duloxetine , and amitriptyline . Topical lidocaine patches may help localized pain. Narcotic analgesics need to be carefully considered. Joint, bone, and muscle pains require different approaches and should be treated appropriately. RESPIRATORY SYSTEM: Is examined in terms of rate of respiration, chest expansion and vital capacity as in acute phase of polyneuropathy especially in GBS, respiration is compromised and at times the patient may need ventilator for respiratory assistance. FATIGUE TESTING: Fatigue can seen in any activities such as getting tired while writing letters or walking distances. Fatigue severity scale has been demonstrated to be reliable measure in neuropathies. The patient is asked to maintain a diary documentation activities and length of time performing each one and the symptoms of fatigue. Later it is to be analyzed to try and develop a structure to the patients activities that prevent further fatigue and also to check whether this is not leading to disuse by cutting out all activity that cause any degree of fatigue.

37. FUNCTIONAL ASSESSMENT: Is also measured to any change in performance level. For e.g. ability to rise from a chair and standing on heels in case of diabetic neuropathy. ELECTROPHYSIOLOGICAL TESTS: Is done to differentiate between a demyelinating and an axonal process. It serves as a prognostic factor in determining whether there are any axonal changes as seen in GBS where once axonopathy is permanent, there are no changes left for repairing the axon. GENE TESTING AND COUNSELLING: Genes for inherited neuropathies can be identified by deoxyribonucleic acid (DNA) testing. Once a patient is shown to have the gene, counseling can be offered and the implications for other family members are discussed. Prenatal testing can be identify a fetus at risk of developing an inherited neuropathy and give the parents the option of termination.

38. ACUTE NEUROPATHIES: Physical management in acute neuropathies includes prevention of contractures, control of pain and respiratory care. STRETCHING TO PREVENT CONTRACTURES Neuropathy may result in severe disability making the patient totally bed-ridden. When the muscles are not stretched adequately but are left in a shortened position, structural changes, involving loss of sarcomeres , occur and compromises potential recovery. The therapist should ensure that all structures including the nervouAs system are moved through their full range. Adverse neural tension signs can occur if neural tissues are not stretched. Continuous passive motion machine has been suggested as a mean to maintain range of movement. Even passive ROM is given 2-3 times in a day. Tightening of posterior crural muscle group develops rapidly. Able patients should be taught self -stretches in a weight-bearing position. For bedridden patients, foot drop splints should be provided and gentle stretches performed. Thus muscles which crosses two or more joints must be stretched to its full length.

39. POSITIONING: Frequent position changes are recommended in bed ridden patients to prevent selective muscle shortening and pressure sores. Truncal weakness can cause the patient to lie with scapulae retracted, unless a wedge is positioned under the thoracic region as well as the head and shoulders. The pelvis should be supported in a position of posterior tilt with the hip flexors stretched, to prevent shortening. Every two hourly turning helps in preventing pressure sores. If the sore is developed, ultra-violet radiation is given to enhance the healing process. The patient's position is maintained with the help of sand bags, pillows etc. If splint is given, then frequent checking is maintained to avoid the skin breakdown around the application area. MAINTENANCE OF CIRCULATION: Passive exercises help in maintaining the circulation. PAIN: Pain is an early symptom in acute neuropathy such as GBS due to spontaneous discharge in demyelinated sensory neuropathies.

40. RESPIRATORY CARE: In acute cases, the patient may be ventilated and the role of physiotherapist is to help prevent atelectasis when breathing is compromised. Since the respiratory system is involved, the aim would be to maintain clear airway by removing the lung secretions through the following technique: 1. Intermittent positive pressure breathing. 2. Postural drainage. 3. Suction catheter. 4. Vibration and rib shaking. Once the patient is weaned from the ventilator, he is taught effective coughing and good breathing exercises. When there is facial muscle weakness, care must be taken to ensure there is lip seal around the mouth piece when measuring vital capacity. Where the autonomic system is affected, disturbed blood pressure is seen when attempting suction or making early sitting.

41. CHRONIC NEUROPATHIES: Physiotherapy plays a major role in chronic neuropathies which help in maintaining ambulation and prevention of contractures. It helps in facilitating functional recovery in bedridden patients of neuropathies thereby preventing complications and improving the quality of life of patients with chronic neuropathies. STRENGTH TRAINING: The aim is to maintain the strength of weak muscles which can be achieved by the following techniques: 1. Free active exercises. 2. Proprioceptive Neuromuscular Facilitation (PNF). 3. Progressive resisted exercises. 4. Suspension therapy exercises. 5. Equilibrium and righting reactions. Concentrating on the hip and knee helps in compensating and producing a more stable gait pattern. The additional AFO would also increase stability by allowing the development of plantar flexion movement.

42. STRETCHING Regular stretching of 15 to 30 seconds trice a day can prevent or reduce joint deformities that may result from uneven pulling of muscle on bones. Serial night casting for 4 weeks induced a small increase in ankle dorsiflexion range in children and young adults with CMT. RE-EDUCATION OF SENSORY AWARENESS: The sensory system can be stimulated by the cutaneous stimulation which can be given by the different material, textures, shapes and weights. Equilibrium and righting reactions help in re-educating the proprioception of sensory system. Vision can also be used as an alternative system in reeducating the sensory awareness. POSTURAL KINESIOTHERAPY: May be helpful in reducing the need to control joints from three joints (hip, knee, and ankle) to one joint (hip), and proprioceptive kinesitherapy may help to improve coordination.

43. BALANCE TRAINING: Balance training plays major role as weakness and deformities at foot reduces balance thereby increasing walking in stability. Thus it should be emphasize by including the following exercises: 1. Standing with feet apart in comfortable posture. 2. Standing with feet apart and keeping the arms in different positions for support. 3. Standing with close feet. 4. One leg standing. 5. Repeat all the exercises with eyes closed. 6. Balance boards exercises. 7. Quadruped side sitting. 8. Hip extension in quadruped. 9. Bilateral arm and leg raise in quadruped. 10. Weight shifts in forward, backward and sideways direction in quadruped. 11. Tandem walking. Walking sideways and backward. 12. Walking and stopping alternately. 13. Ask the patient to walk in circles. 14. Walk on toes. 15. Walk on heels. 16. Intrinsic strengthening.

44. MOBILITY AIDS: INSOLES: When foot drop exists, light polypropylene splint should be advised. AFO WHEELCHAIR: In some of cases, the neuropathy progresses to render the patient dependent on a wheelchair. For e.g. in the early stages of rehabilitation, a patient with GBS, a reclining wheelchair is valuable to coping up possible fluctuations in blood pressure and to allow gradual accommodation in the upright position. MANUAL DEXTERITY TRAINING: Hand function is also compromised through weakness or paralysis of intrinsic muscles of the thumb and fingers causing difficulty in pincher gripping and finger movement. Normal daily activities such as dressing, bathing, holding cutlery, or writing becomes difficult. Tripod pinch strength and thumb opposition are major determinants of manual dexterity in CMT and should therefore be the focus of intervention strategies that aim to preserve or enhance manual dexterity in CMT. Simple thumb opposition splint may allow a patient to produce legible writing for a longer time, or to grip a cup or knife. At times when there is thenar eminence weakness and wasting is being seen, a night splint cast in a functional position will help prevent severe contracture. Use of putty and rubber bands of different strengths can be used to improve strength of hand and forearm muscles.

45. NEUROPATHIC PAIN MANAGEMENT : Thermotherapy - can reduce muscle spasm thereby relaxing the muscle. Cryotherapy - can be used in case if there is any swelling at some distal joints. Massage - can reduce muscle tension by gentle touch thereby increasing local blood circulation and relaxing muscles and soft tissues. Transcutaneous Electrical Nerve Stimulation (TENS) : is proved to be useful in neuropathic pain. Low rate TENS or Acupuncture Like TENS acts on small diameter C fibers and acts on mechanisms of endogenous opiates thereby blocking pain gate mechanisms. Ultrasound: has also been used in peripheral neuropathy as it reduce muscle spasm and pain thereby acting on both large diameter A fibers and small diameter C-fibers. Cognitive Strategies: are used in treating together the body, mind and soul. Cognitive Behavioural Therapy (CBT) Behavioural interventions: Distraction - listening to music or using imagery techniques can be helpful during brief episodes of pain or painful procedures. Music therapy has been used successfully to reduce disruptive behaviour or aggression attitudes.

46. AEROBIC EXERCISES: Patients with chronic neuropathies show reduced peak oxygen consumption and decreased functional aerobic capacity, and studies shows aerobic exercise improve functional ability and aerobic capacity. Aerobic walking has been used in neuromuscular disorders and was effective in ameliorating peak power output and peak oxygen intake, walking ability, and metabolic changes. HYDROTHERAPY: Is advised as it increases the muscle power, improve coordination and balance of the patient. Care is taken in case of flaccid joint. Pain which is also a feature of polyneuropathy can be relieved by hydrotherapy as water has pain relieving property.

47. NeuroRehabilitation : A Multidisciplinary Approach NeuroGen Brain and Spine Institute Dr. V. C. Jacob (PT) Dr. Hema Biju (OT) Dr. Alok Sharma NEUROLOGY AND NEUROSURGERY ILLUSTRATED Kenneth W. Lindsay PhD FRCS Ian Bone FRCP FACP Geraint Fuller MD FRCP Robin Callander PHYSIOTHERAPY IN NEUROLOGICAL CONDITIONS WITH ASSESSMENT AND TREATMENT PROTOCOLS Gowrishankar Potturi MPT PhD