Peripheral Nerve Diseases.

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Diseases of Peripheral

Nerves

Dr.Subramaniyan K,MD
Introduction

Peripheral nerves are composed of sensory, motor and autonomic


elements.
Diseases can affect the cell body of a neuron or its peripheral
processes, namely the axons or the encasing myelin sheaths.
Most peripheral nerves are mixed and contain sensory and motor as
well as autonomic fibers.
What is Peripheral Neuropathy?

It is defined as alteration in function and structure of the Motor,


Sensory or Autonomic components of a peripheral nerve.
It can be anywhere along the pathway from the nerve roots to their
termination in the tissues of the trunk and extremities.
Symptoms and signs of nerve impairments are sensory changes or
loss and motor weakness in the distribution of the involved nerve
fiber.
Pathophysiology

A. Wallerian degeneration
B. Axonal degeneration
C. Primary neuronal degeneration
D. Segmental demyelination
Common causes of Injuries to Nerves

1. Metabolic
2. Nutritional
3. Industrial or environmental toxins
4. Traumatic or compressions
5. Drug induced
6. Connective tissue processes or vasculitis
7. Infections
8. Entrapment syndromes
Common conditions associated with carpal tunnel syndrome

1. Diabetes mellitus
2. Arthritis
3. Obesity
4. Thyroid disease
5. Pregnancy
6. Trauma
Diabetic neuropathy

Involvement of the peripheral and autonomic nervous systems is


probably the most common complication of diabetes
Clinical diabetic neuropathy is categorized into distinct syndromes
according to the neurologic distribution, although many overlap
syndromes occur
Approximately 5o% of individuals will eventually develop neuropathy
Pathogenesis of Diabetic neuropathy
Classification of Diabetic neuropathy

Distal symmetric polyneuropathy


Autonomic neuropathy
Asymmetric involvement of multiple peripheral nerves -
mononeuropathy multiplex
Traumatic or Compressions
Drug induced
AIDP
Acute Inflammatory Demyelinating Polyneuropathy

Acute inflammatory demyelinating polyneuropathy (AIDP) is an autoimmune


process characterized by progressive areflexic weakness and mild sensory
changes.
Sensory symptoms often precede motor weakness.
Acute inflammatory demyelinating polyneuropathy is believed to be caused by
an immunologic attack that is directed against myelin components. This
results in a demyelinating polyneuropathy.
AIDP is the most common form of Guillain-Barre syndrome (GBS).
Guillain-Barre syndrome

GBS refers to a group of heterogeneous but related disorders of peripheral


nerves with an acute onset, which is considered to be due to an autoimmune
process and is usually postinfectious.
The two most common forms of GBS are AIDP and acute motor axonal
neuropathy (AMAN), with the latter comprising 10% of GBS cases.
Clinical manifestations

Progressive course (days to 4 weeks)


Relatively symmetric symptoms and signs
Fairly mild sensory symptoms and signs
Cranial nerve involvement, especially bilateral facial palsy
Autonomic dysfunction
The typical patient with Guillain-Barré syndrome (GBS), which in
most cases will manifest as acute inflammatory demyelinating
polyradiculoneuropathy (AIDP).
Presents 2-4 weeks following a relatively benign respiratory or
gastrointestinal illness with complaints of finger dysesthesias and
proximal muscle weakness of the lower extremities.
The weakness may progress over hours to days to involve the arms,
truncal muscles, cranial nerves, and muscles of respiration. Variants
of GBS may present as pure motor dysfunction or acute
dysautonomia.
The classic clinical picture of weakness is ascending and
symmetrical in nature. The lower limbs are usually involved before
the upper limbs. Proximal muscles may be involved earlier than the
more distal ones. Trunk, bulbar, and respiratory muscles can be
affected as well.
Cranial nerve involvement:
Facial droop (may mimic Bell palsy)
Diplopias
Dysarthria
Dysphagia
Ophthalmoplegia
Pupillary disturbances
Respiratory manifestations

Upon presentation, 40% of patients have respiratory or oropharyngeal


weakness. Typical complaints include the following:
Dyspnea on exertion
Shortness of breath
Difficulty swallowing
Slurred speech
Ventilatory failure with required respiratory support occurs in up to one third of patients at
some time during the course of their disease.
Treatment

Patients who are diagnosed with GBS should be admitted to a


hospital for close monitoring until it has been determined that the
course of the disease has reached a plateau or undergone reversal.
Although the weakness may initially be mild and nondisabling,
symptoms can progress rapidly over just a few days.
Continued progression may result in a neuromuscular emergency
with profound paralysis, respiratory insufficiency.
Approximately one third of patients require admission to an ICU,
primarily because of respiratory failure.
After medical stabilization, patients can be treated on a general
medical/neurologic floor, but continued vigilance remains important
in preventing respiratory, cardiovascular, and other medical
complications.
Patients with persistent functional impairments may need to be
transferred to an inpatient rehabilitation unit.
Immunomodulatory treatment has been used to hasten recovery.
Intravenous immunoglobulin (IVIG) and plasma exchange have
proved equally effective.
Corticosteroids (oral and intravenous) have not been found to have
a clinical benefit in GBS. Consequently, this class of drugs is not
currently employed in treatment of the syndrome.
Thank you

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