Clinical Aproch To Peripheral Neuropathy & Flaccid Quadruparesis Final

CLINICAL APPROCH TO
PERIPHERAL NEUROPATHY
&
FLACCID QUADRUPARESIS
DR USHA KHADTARE
GGMC & JJH
Dr Usha Khadtare 20/06/2024 1

SITE ETIOLOGY
Muscle disorders: Polymyositis, Toxic Myopathy, ICU Myopathy, Inflammatory myopathy Periodic paralysis
Hypokalaemia Infections, MND, Alchohol
Neuromuscular junction Myasthenia Gravis , Eaton-Lambert syndrome , ,Tetanus, Neuromuscular Blocking

disorders: Agents, Plant and Snake Toxins
Neuropathies: Guillain-Barre syndrome Traumatic neuritis , Postdiphtheric neuropathy , Porphyria

Vasculitis Myelin: AIDP, Diphtheria ,vit B12 deficiancy
Polyradiculomyelopathy: CMV, Carcinomatous Meningitis
Anterior horn cell Poliomyelitis Non polio enteroviruses

disorders:
Dorsal Root Ganglia: Herpes, CMV, Rabies
Spinal Drcord
Usha Khadtare
disease: Transverse Myelitis Spinal Cord compression,20/06/2024
Space Occuping7 Lesions, Anterior Spinal
Artery Syndrome
PERIPHERAL NEUROPATHY

Types of nerve injury

History
Acute Guillain-Barré syndrome (GBS),
acute porphyria, vasculitis, neuralgic amyotrophy and some forms of toxic neuropathies
have acute presentations.
A relapsing course is found in chronic inflammatory demyelinating polyradiculoneuropathy
(CIDP), acute porphyria, Refsum disease, hereditary neuropathy with liability to pressure
palsies (HNPP), familial brachial plexus neuropathy, and repeated episodes of toxin
exposure.
trauma or ischemic infarction
vasculitis, autoimmune disorders, or cryoglobulinemia
Relapsin A relapsing course is found in chronic inflammatory demyelinating polyradiculoneuropathy

g/ (CIDP), acute porphyria, Refsum disease, hereditary neuropathy with liability to pressure palsies
recurren (HNPP), familial brachial plexus neuropathy, and repeated episodes of toxin exposure.
t
chronic , inquiries about similar symptoms and bony deformities (such as pes cavus) family history in
immediate relatives often point to a familial polyneuropathy.(
Dr Usha Khadtare
30%)
20/06/2024 33
The presence of constitutional symptoms such as weight loss, malaise, and anorexia suggests an
underlying systemic disorder as a cause of the polyneuropathy.
History
 The history should also include toxin and medication exposures ; Lyme disease or HIV; trauma;
 family history of neurologic diseases or skeletal deformities;
 and recent travel(compressive neuropathies or exposure to toxins or infections.)
 immunization status (influenza, meningococcus, shingles, and rabies )
 A history of childhood clumsiness, high arches, or difficulty with shoe fitting may suggest a hereditary
neuropathy.
 weight loss associated with infections or malignancies,
 swallowing dysfunction, dysautonomia suggesting CNS involvement, skin and joint changes suggesting rheumatoid
arthritis or other autoimmune disease,
 anemia consistent with conditions such as chronic kidney disease or vitamin B12 deficiency, and symptoms of an
underlying endocrinopathy or an autoimmune process.
 Mimickers of peripheral neuropathy should also be considered. These include upper motor neuron diseases,
myelopathies, syringomyelia, dorsal column disorders such as tabes dorsalis, and psychogenic symptoms.
Examination
neurologic examination, testing of the cranial nerves, fundoscopy, assessment for muscle fasciculations (including
tongue), and evaluation of muscle bulk and tone.
An underlying systemic illness should be considered if there are new changes in breathing or cardiac function,
rashes or skin lesions, or lymphadenopathy.
Nerve compression or injury from trauma or medical procedures ( the sciatic nerve, fibular nerve, and femoral
cutaneous nerve).-carpal tunnel syndrome, cubital tunnel syndrome, and radiculopathy from spinal degeneration.
Combining vibratory sensation testing with a 128-Hz tuning fork plus sensory testing with a 10-g Semmes-Weinstein
monofilament increases the sensitivity and specificity for the diagnosis of peripheral neuropathy compared with
either test alone in patients with diabetes.
Asymmetry and nonanatomic distribution warrant consideration of psychogenic etiologies or less common
diagnoses, including vasculitis, myxedema, rheumatoid arthritis, sarcoidosis, or neoplastic infiltration Signs of long-
standing neuropathy such as calf atrophy, hammer toes, and pes cavus should
Dr Usha Khadtare 20/06/2024
prompt concern
37
for hereditary
neuropathies
INVESTIGATION
 First-line screening test for neuropathy Blood count, ESR Blood sugar Liver and renal function tests Serum
vitamin B12 Paraprotein levels Thyroid function tests Vasculitis profile
 Biothesiometry
 NCV
late responses (F response and H reflex)
Conduction block refers to a decline in the compound muscle action potential exceeding 20% on proximal
stimulation compared to that on distal stimulation.
The slowing of nerve conduction velocity, prolongation of terminal latency, temporal dispersion and
conduction block are consistent with demyelinating neuropathy.
 (EMG).

Investigation
 Cerebrospinal fluid (CSF) is useful in CIDP, AIDP and chronic immune-mediated axonal neuropathies where the levels of
CSF protein are elevated. Borrelia, sarcoidosis or human immunodeficiency virus (HIV).
 Anti-Hu antibody -paraneoplastic neuropathy and undisclosed malignancy usually of the lung and ovary.
 Antiganglioside antibodies -multifocal motor neuropathy with conduction block (MMN-CB).

 Anti-GQ1b IgG antibodies are a marker of Miller Fisher syndrome.
 hereditary demyelinating neuropathy, -PMP22 duplication test followed by DNA sequencing of PMP22, MPZ, EGR2 and
periaxin

NERVE BIOPSY
 Sensory nerve biopsy is an established diagnostic procedure, but should be

performed in the center where facilities for electron microscopy, teased fiber
technique and immunohistochemistry are available
 Nerve biopsy can be helpful in the diagnosis of CIDP in which the presence of
inflammatory cells or macrophage-mediated demyelination on electron
microscopy is diagnostic.
 Patients with axonal neuropathy simulating the axonal form of Charcot Marie
Tooth can occasionally turn out to have amyloid, especially if there is the
involvement of small fibers. Diagnosis can be made by transthyretin mutations
without resorting to biopsy, but biopsy is helpful in the absence of a genetic
marker.

NERVE BIOPSIES
 Nerve biopsies are now rarely indicated for evaluation of neuropathies. The
primary indication for nerve biopsy is suspicion for amyloid neuropathy or
vasculitis. In most instances, the abnormalities present on biopsies do not help
distinguish one form of peripheral neuropathy from another (beyond what is
already apparent by clinical examination and the NCS). Nerve biopsies should
only be done if the NCS are abnormal. The sural nerve is most commonly
biopsied because it is a pure sensory nerve and biopsy will not result in loss of
motor function. In suspected vasculitis, a combination biopsy of a superficial
peroneal nerve (pure sensory) and the underlying peroneus brevis muscle
obtained from a single small incision increases the diagnostic yield. Tissue can be
analyzed by frozen section and paraffin section to assess the supporting
structures for evidence of inflammation, vasculitis, or amyloid deposition.
Semithin plastic sections, teased fiber preparations, and electron microscopy are
used to assess the morphology of the nerve fibers and to distinguish axonopathies
from myelinopathies.
TREATMENT
 Symptomatic & Supportive & Etiological
 Nonpharmacologic -foot hygiene, wearing appropriate footwear, weight loss, and physical therapy and gait
 Gabapentinoids (gabapentin [Neurontin], pregabalin [Lyrica]) and antidepressants (amitriptyline, nortriptyline [Pamelor],
venlafaxine, duloxetine [Cymbalta], bupropion [Wellbutrin])
 Treatment of etiological factor
 Medications
 Pain killer- nonsteroidal anti-inflammatory drugs, opioids, tramadol , or oxycodone
• Anti-seizure medications: Medications such as gabapentin, Neurontin, and pregabalin Side effects can involve dizziness and
drowsiness.
• Topical treatments: Capsaicin cream As counter irritant, Lidocaine patches.
• Antidepressants: tricyclic antidepressants, as amitriptyline, and nortriptyline , The serotonin and norepinephrine reuptake
inhibitor duloxetine and the extended-release antidepressants venlafaxine and desvenlafaxine

Referance
 Harrison
 Photos from Google

 THANK YOU

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CLINICAL APPROCH TO

Dr Usha Khadtare 20/06/2024 1

Neuromuscular junction Myasthenia Gravis , Eaton-Lambert syndrome , ,Tetanus, Neuromuscular Blocking

Neuropathies: Guillain-Barre syndrome Traumatic neuritis , Postdiphtheric neuropathy , Porphyria

Polyradiculomyelopathy: CMV, Carcinomatous Meningitis

Anterior horn cell Poliomyelitis Non polio enteroviruses

Dorsal Root Ganglia: Herpes, CMV, Rabies

Dr Usha Khadtare 20/06/2024 18

Dr Usha Khadtare 20/06/2024 23

Relapsin A relapsing course is found in chronic inflammatory demyelinating polyradiculoneuropathy

Dr Usha Khadtare 20/06/2024 41

 Antiganglioside antibodies -multifocal motor neuropathy with conduction block (MMN-CB).

Dr Usha Khadtare 20/06/2024 42

 Sensory nerve biopsy is an established diagnostic procedure, but should be

Dr Usha Khadtare 20/06/2024 43

Dr Usha Khadtare 20/06/2024 47

Dr Usha Khadtare 20/06/2024 48

Dr Usha Khadtare 20/06/2024 49

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