I. The peripheral nervous system carries signals between the central nervous system and the rest of the body. It has three main components - cranial, spinal, and autonomic. There are three main types of nerve fibers - A, B, and C - which differ in diameter, myelination, and function. II. Peripheral neuropathies can be acquired through systemic diseases, trauma, infections, or inherited genetically. Common acquired neuropathies include diabetic neuropathy, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and alcoholic neuropathy. Inherited forms include Charcot-Marie-Tooth disease and hereditary liability to pressure palsies.

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

4. 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 μm in diameter. Myelinated.
Function: Motor and sensory (vibration, proprioception).
Conduction velocity: 10–70 metres/second.
TYPE B 3 μm diameter.
Thinly myelinated.
Function: Mainly preganglionic autonomic, some pain and temperature.
Conduction velocity: 7–5 metres/second.
TYPE C < 1 μm diameter. Unmyelinated.
Function: Sensory – pain and temperature.
Conduction velocity: < 2 metres/second.

5. 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.

7. 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.

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

9. 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

10. 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

11. 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

12. 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.

13. 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

15. 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

17. 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.

18. 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

19. 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.

20. 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)

21. 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.

22. 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.

23. CLINICAL FEATURE
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.

25. 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.

26. 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.

27. 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.

29. 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

31. 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

33. THYROID/PITUITAR
Y 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.

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

37. 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.

39. 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 2nd or 3rd 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.

42. 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.

43. 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.

45. 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.

46. 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

48. 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.

49. 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.

50. 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.

51. 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.

52. 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.

53. 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.

55. 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.

56. 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.

57. 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.

58. 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.

59. 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.

60. 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.

61. 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.

62. 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.

63. 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.

64. 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