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Neuropathy
Submitted by – Dinesh choudhary
INTERNATIONAL SCHOOL OF MEDICINE
GROUP - 24
disease or dysfunction of one or more peripheral nerves,
typically causing numbness or weakness.
Pain - burning, short jabs , tight or band
like pressure, painful
hypersensitivity of non noxious
stimuli
Paresthesia “pain and needle” sensations
Sensory loss “ชช” “no sensation” “like block of
wood”
Weakness - distal symmetrical weakness
- proximal symmetrical weakness – GBS
- unilateral limb weakness
- brachial plexus
- lumbosacral plexus
Neuropathy from History
and physical exam
Mononeuropathy Mononeuropathy multiplexPolyneuropathy
axonal demyelinating
Entrapment
DM
Subclinical
polyneuropathy
Vasculitis
DM(rare)
HNPP
MMN
CIDP(rare)
Neuropathy from History
and physical exam
Mononeuropathy Mononeuropathy multiplexPolyneuropathy
axonal demyelinating
DM
Toxic
Metabolic
Nutritional
deficiency
Paraprotein
emia
CA
idiopathic
Hereditary
subacute chronicacute
GBS(axonal)
Porphyria
acute subacute chronic
GBS
Diphtheria
CIDP
Paraprot
einemia
Hereditary
Neuronopathy
Axonopathy
Demyelination
Polyneuropathy
Poly(radiculopathy)
Neuronopathy
Peripheral neuropathy is caused by damage to your
peripheral nerves. Peripheral nerves are nerves that
are not located in the brain or spinal cord. They are
found throughout your body and help you feel
things. They also control the function of your organs.
The damage is usually to nerves in the hands, feet,
arms, and legs.
Mees’ line in arsenic
Arsenic
Thallium Lead
 Peripheral neuropathy may be classified in a varieties of
ways-
 according to the
1.number of nerves affected
 Mononeuropathy
 Mononeuritis multiplex
 Polyneuropathy
2.the type of nerve cell affected
motor
sensory
autonomic
 Mononeuropathy means a process affecting a single
nerve.
 Mononeuritis multiplex (multiple mononeuropathy
and/or multifocal neuropathy) affects several or
multiple nerves.
 Polyneuropathy describes diffuse, symmetrical
disease, usually commencing peripherally.
The course may be
- acute, chronic, static, progressive,
relapsing or towards recovery.
Polyneuropathies are motor, sensory,
sensorimotor and autonomic.
Neuropathy ..paras
-Metabolic
-Toxic or drug
-Nutritional
deficiency
Polyneuropathy
caused by
• Mixture of UMN & LMN signs
• No sensory deficit
• Progressive course
• No sphincter muscle or ocular muscle
involvement
Neuropathy ..paras
 Diabetic Neuropathy is a nerve disorder which is
found in patients who have diabetes
 Damage to nerves in Peripheral Nervous Systems
Classification of Diabetic neuropathies
Symmetric
1. Distal, primarily sensory
polyneuropathy
a. Mainly large fibers affected
b. Mixed (a)
c. Mainly small fibers affected
(a)
2. Autonomic neuropathy
3. Chronically evolving proximal motor
neuropathy (a,b)
Asymmetric
1. Acute or subacute proximal motor
neuropathy (a,b)
2. Cranial mononeuropathy (b)
3. Truncal neuropathy (a,b)
4. Entrapment neuropathy in the limbs
 Different Types
 Diffuse Peripheral
Neuropathy
 Diffuse Autonomic
Neuropathy
 Localized Peripheral
Neuropathy
 Exact cause is unknown
 Theories behind Neuropathy
 High Glucose Concentration
 Chemical changes in nerves
 Damaged blood vessels
 Genetic Disposition
 Depends on part of body being affected.
 Diffuse Peripheral
 Pain
 Numbness and tingling in the limbs
 Sensitivity to touch
 More susceptible to feet injury and infections
 Loss of Balance and Control
 Loss of sensation
 Diffuse Autonomic
 Bladder infections
 Stomach disorders
 dizziness
 Localized neuropathy
 Pain in front of thigh, lower back, chest stomach and behind
eyes
 Double vision
 Paralysis of one side of the face
 Based upon symptoms
 Pain Assessment
 Screening Test for lost sensation
 Nerve Conduction Study
 Electromyography
 Ultrasound
 Nerve Biopsy (extreme cases)
 Treat symptoms and not neuropathy
 Manage your glucose levels
 Drug Therapy can be used but is not suggested
 Pain Medication
 Early treatment more successful and reversing
damage. Later stages of neuropathy irreversible
 the peripheral nerves have been damaged by too
much alcohol use. The peripheral nerves transmit
signals between the body, the spinal cord, and the
brain.
 Thiamine, folate, niacin, vitamins B6 and B12, and
vitamin E are all needed for proper nerve function.
Drinking too much can alter levels of these nutrients
and affect the spread of alcoholic neuropathy.
Fortunately, abstaining from alcohol can help restore
your nutritional health.
 Alcoholic neuropathy can affect both movement and
sensation. Symptoms range from slight discomfort to major
disability. Although the condition is not life threatening, it
can decrease your quality of life. Some areas of the body
affected by alcoholic neuropathy include:
 numbness
 tingling and burning
 prickly sensations
 muscle spasms and cramps
 muscle weakness and atrophy
 Alcoholic neuropathy is the result of damage to these
nerves. The damage may be the direct result of long
periods where you drank too much alcohol.
Nutritional problems linked to alcohol use, such as
vitamin deficiency, can also cause nerve damage.
 nerve biopsy
 nerve conduction tests
 upper GI and small bowel series
 neurological examination
 electromyography
 esophagogastroduodenoscopy (EGD)
 kidney, thyroid, and liver function tests
 complete blood count (CBC)
 vitamin supplements to improve nerve health (folate,
thiamine, niacin, and vitamins B6, B12, and E)
 prescription pain relievers (tricyclic antidepressants and
anticonvulsants)
 medication for people with problems urinating
 physical therapy to help with muscle atrophy
 orthopedic appliances to stabilize extremities
 safety gear, such as stabilizing footwear, to prevent
injuries
 special stockings for your legs to prevent dizziness
 Disorders of peripheral nerves are the most common
neurological complications of systemic amyloidosis;
an illness where a protein called amyloid is deposited
in tissues and organs. Amyloidosis can affect
peripheral sensory, motor or autonomic nerves and
deposition of amyloid lead to degeneration and
dysfunction in these nerves.
 The typical symptoms of amyloid neuropathy are due
to sensory and autonomic dysfunction. Patients may
experience painful paresthesias (unusual sensations),
numbness and balance difficulties due to sensory
dysfunction and persistent nausea, vomiting,
diarrhea, constipation, incontinence, sweating
abnormalities or sexual dysfunction due to autonomic
nerve involvement.
 Diagnosis of amyloid neuropathies is based on
history, clinical examination and supporting
laboratory investigations. These include
electromyography with nerve conduction studies,
skin biopsies to evaluate cutaneous nerve innervation,
and nerve and muscle biopsies for histopathological
evaluation. In cases of familial amyloidosis, genetic
testing in the blood may be useful.
 Treatment of amyloid neuropathies is directed at both
preventing further deposition of amyloid in
peripheral nerves and treating painful symptoms.
Depending on the type of amyloid protein, patients
may benefit from liver or bone marrow transplant.
Neuropathic pain due to amyloid neuropathy can be
treated with anti-seizure medications,
antidepressants, or analgesics including opiate drugs.
In severe painful conditions patients may be referred
to the Blaustein Chronic Pain Clinic for a
multidisciplinary approach to pain management.
Neuropathy ..paras
 Most common type ---
Acute inflammatory demyelinating polyneuropathy
(AIDP)
 Symptoms and Signs
Muscles weakness – facial and orophyrengial
cardiac arrhythmias, GI stasis, urinary retention, and
pupillary changes. An unusual variant (Fisher variant)
may cause only ophthalmoparesis, ataxia, and areflexia.
Guillain Barre syndrome
Neuropathy ..paras
 Clinical evaluation
 Electrodiagnostic testing
 CSF analysis
 Neurophysiology
Diagnostic Criteria for Guillain-Barre Syndrome
REQUIRED
1. Progressive weakness of 2 or more limbs due to neuropathy
2. Areflexia
3. Disease course <4 weeks
4. Exclusion of other causes [e.g., vasculitis (polyarteritis nodosa, systemic lupus erythematosus,
Churg-Strauss syndrome), toxins (organophosphates, lead), botulism, diphtheria, porphyria, loc
alized spinal cord or cauda equina syndrome]
SUPPORTIVE
1. Relatively symmetric weakness
2. Mild sensory involvement
3. Facial nerve or other cranial nerve involvement
4. Absence of fever
5. Typical CSF profile (acellular, increase in protein level)
6. Electrophysiologic evidence of demyelination
 Intensive supportive care
 IV immune globulin (IVIG) or plasma exchange
 Rihablisation
 Respiratory failure
 Pain
Scattered
distribution of
sensory loss in
Multiple
Mononeuropathy
Can found in:
 Classic PAN
 Churg-Strauss disease
 Wegener’s granulomatosis
 Overlap syndrome
 Vasculitis associated with connective tissue
disease
 Sjóģren syndrome
 Lyme disease
 Leprosy
 Diabetes mellitus
Multiple
mononeuropathy
with vasculitis
Mycobacterium leprae – coolest tissue in the body
Tuberculoid (high-resistance) leprosy – single patch of
hypoesthesia or anesthetic skin in any location
Lepromatous (low resistance) leprosy – numerous bacilli, wide
spread skin thickening, cutaneous anesthesia, anhydrosis
sparing axilla, groin and skin beneath the scalp hair
 Nerve root disorders result in segmental radicular
deficits (eg, pain or paresthesias in a dermatomal
distribution, weakness of muscles innervated by the
root). Diagnosis may require neuroimaging,
electrodiagnostic testing, and systemic testing for
underlying disorders. Treatment depends on the cause
but includes symptomatic relief with NSAIDs, other
analgesics, and corticosteroids.
Radiculopathy
Cervical
Neuropathy ..paras
Neuropathy ..paras
 Causes
Compressive : herniated disc, spondylosis,
tumor
Infiltrative : tumor seeding, infection
Inflammatory : immune-mediated
 Brachial plexus
 Lumbosacral plexus
 Trauma
 Tumor infiltration
 Infection by viral
 Immune-mediated
 Delayed effects of radiotherapy
Traction
birth injury
(Erb’s
palsy)
Acute pain
in back of
shoulderPostmastectomy
and radiation
Brachial plexopathy
 Upper C5,6 or Erb-Duchenne type
 Lower C8, T1 or Dejerine-Klumpke type
 Total
Klumpke’s
palsy (injury
of lower
brachial
plexus
C7,C8,T1)
and often
Horner’s
syndrome
Erb’s
palsy
(injury
of upper
brachial
plexus
C5,C6)
 Multiple spinal roots and peripheral nerves
 Roots : T12-S4
 Nerves : iliohypogastric, ilioinguinal,
genitofemoral, lateral femoral cutaneous,
femoral, obturator, superior gluteal, inferior
gluteal, sciatic, posterior femoral cutaneous,
pudendal nerves
Lumbar plexopathy Sacral plexopathy
Clinical manifestation
 Tumors : CA cervix, prostate, bladder, colorectal,
kidney, breast, testis, ovary, sarcoma, lymphoma
 Compressed by aortic aneurysm
 Radiation plexopathy
 Plexitis : follow herpes zostor
 Diabetic amyotrophy
 Trauma (rare)
 As a manifest of mononeuropathy multiplex
Neuropathy ..paras
Median nerve
Carpal tunnel syndrome
Anterior interosseous syndrome
Pronator syndrome
Ligament of Struthers
 Carpal tunnel syndrome
Nocturnal pain or paresthesia
Thenar atrophy
Neuropathy ..paras
Neuropathy ..paras
Atrophy
Sensory loss
Ulnar nerve
Lesion at condylar groove
Lesion at wrist and hand
Guyon’s canal
 At elbow : Condylar groove or in cubital
tunnel
 Wasting hypothenar eminence and web
space of (1st
dorsal interossei)
 Claw hand
Neuropathy ..paras
Neuropathy ..paras
Neuropathy ..paras
Radial nerve
Saturday night palsy
Posterior interosseous syndrome
Cheiralgia parestheticaCheiralgia paresthetica
 Axillary lesion : weak triceps and radial innervated m.
 Mid-upper arm lesion : ‘Saturday night palsy’ (spiral
groove or intermuscular septum) : wrist drop, normal
triceps, variable motor and sensory deficit
 Posterior interosseous : weak extensor of thumb and
other fingers, no sensory loss
 Superficial radial n. : terminal cutaneous br.
Radial nerve
Wrist drop
Lateral femoral cutaneous nerve of
thigh (L2 and L3)
• Meralgia paresthetica
• Pure sensory
Femoral nerve
Femoral nerve (L2,3,4)
• Mix sensorimotor
• Quadriceps femoris or knee
extensor
• Weakness of hip flexor in
intraabdominal lesion
• Sensory deficit over
anteromedial aspect of thigh
and perhaps leg
• Absent or diminished knee
jerk
Obturator nerves
• L2,3,4
• Hip adductors
• vulnerable during obstetric and gynecological
procedures
Sciatic
Sciatic nerve
•L4-S3
 Composed of 2 main nerves of leg : common peroneal
and tibial nerve
 Paralysis of all muscles below knee plus hamstrings
and for high lesion, external rotators of thigh
 Sensory loss below knee except anteromedial aspect
of leg and foot
Common peroneal nerve
• Foot-drop
• Paralysis of anterior and
lateral compartment of leg
• Sensory loss over dorsum
of foot and toes and
anterolateral aspect of leg
Neuropathy ..paras
Tibial nerve
 Medial division of sciatic nerve
 Lesions at ankle
 Tarsal tunnel syndrome
 Pain and paresthesia in sole
 Paralysis of intrinsic muscles of foot
 Tenderness of Tinel’s sign at flexor retinaculum
 Sural nerve compression syndrome
 Pure sensory
 Numbness on lateral aspect of foot
Neuropathy ..paras
Neuropathy ..paras
Chorda tympani
Clinical features :
 postauricular pain (few days)
 lower motor neuron facial weakness
 impaired taste
 hyperacusis
Neuropathy ..paras
 Bell’s palsy : idiopathic, HSV 1
 Ramsay Hunt syndrome : external ear pain with presence of
herpes zoster vesicles in auditory canal and pinna, VZV
 Trauma : blunt impact to temporal bone
 Middle ear infection : otitis media (infrequent in ATB era),
mastoid pain persist after acute infection resolved
 Neoplasm : rarely compressed by CPA tumor but due to
surgery for tumor removal
Management
Reassurance – not a stroke
Short course of prednisolone 60 mg/day
Prognosis :
complete recovery 75%
satisfactory 15%
poor function 10%
Neuropathy ..paras
Neuropathy ..paras

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Neuropathy ..paras

  • 1. Neuropathy Submitted by – Dinesh choudhary INTERNATIONAL SCHOOL OF MEDICINE GROUP - 24
  • 2. disease or dysfunction of one or more peripheral nerves, typically causing numbness or weakness.
  • 3. Pain - burning, short jabs , tight or band like pressure, painful hypersensitivity of non noxious stimuli Paresthesia “pain and needle” sensations Sensory loss “ชช” “no sensation” “like block of wood” Weakness - distal symmetrical weakness - proximal symmetrical weakness – GBS - unilateral limb weakness - brachial plexus - lumbosacral plexus
  • 4. Neuropathy from History and physical exam Mononeuropathy Mononeuropathy multiplexPolyneuropathy axonal demyelinating Entrapment DM Subclinical polyneuropathy Vasculitis DM(rare) HNPP MMN CIDP(rare)
  • 5. Neuropathy from History and physical exam Mononeuropathy Mononeuropathy multiplexPolyneuropathy axonal demyelinating DM Toxic Metabolic Nutritional deficiency Paraprotein emia CA idiopathic Hereditary subacute chronicacute GBS(axonal) Porphyria acute subacute chronic GBS Diphtheria CIDP Paraprot einemia Hereditary
  • 9. Peripheral neuropathy is caused by damage to your peripheral nerves. Peripheral nerves are nerves that are not located in the brain or spinal cord. They are found throughout your body and help you feel things. They also control the function of your organs. The damage is usually to nerves in the hands, feet, arms, and legs.
  • 10. Mees’ line in arsenic Arsenic Thallium Lead
  • 11.  Peripheral neuropathy may be classified in a varieties of ways-  according to the 1.number of nerves affected  Mononeuropathy  Mononeuritis multiplex  Polyneuropathy 2.the type of nerve cell affected motor sensory autonomic
  • 12.  Mononeuropathy means a process affecting a single nerve.  Mononeuritis multiplex (multiple mononeuropathy and/or multifocal neuropathy) affects several or multiple nerves.  Polyneuropathy describes diffuse, symmetrical disease, usually commencing peripherally.
  • 13. The course may be - acute, chronic, static, progressive, relapsing or towards recovery. Polyneuropathies are motor, sensory, sensorimotor and autonomic.
  • 16. • Mixture of UMN & LMN signs • No sensory deficit • Progressive course • No sphincter muscle or ocular muscle involvement
  • 18.  Diabetic Neuropathy is a nerve disorder which is found in patients who have diabetes  Damage to nerves in Peripheral Nervous Systems
  • 19. Classification of Diabetic neuropathies Symmetric 1. Distal, primarily sensory polyneuropathy a. Mainly large fibers affected b. Mixed (a) c. Mainly small fibers affected (a) 2. Autonomic neuropathy 3. Chronically evolving proximal motor neuropathy (a,b) Asymmetric 1. Acute or subacute proximal motor neuropathy (a,b) 2. Cranial mononeuropathy (b) 3. Truncal neuropathy (a,b) 4. Entrapment neuropathy in the limbs
  • 20.  Different Types  Diffuse Peripheral Neuropathy  Diffuse Autonomic Neuropathy  Localized Peripheral Neuropathy
  • 21.  Exact cause is unknown  Theories behind Neuropathy  High Glucose Concentration  Chemical changes in nerves  Damaged blood vessels  Genetic Disposition
  • 22.  Depends on part of body being affected.  Diffuse Peripheral  Pain  Numbness and tingling in the limbs  Sensitivity to touch  More susceptible to feet injury and infections  Loss of Balance and Control  Loss of sensation  Diffuse Autonomic  Bladder infections  Stomach disorders  dizziness
  • 23.  Localized neuropathy  Pain in front of thigh, lower back, chest stomach and behind eyes  Double vision  Paralysis of one side of the face
  • 24.  Based upon symptoms  Pain Assessment  Screening Test for lost sensation  Nerve Conduction Study  Electromyography  Ultrasound  Nerve Biopsy (extreme cases)
  • 25.  Treat symptoms and not neuropathy  Manage your glucose levels  Drug Therapy can be used but is not suggested  Pain Medication  Early treatment more successful and reversing damage. Later stages of neuropathy irreversible
  • 26.  the peripheral nerves have been damaged by too much alcohol use. The peripheral nerves transmit signals between the body, the spinal cord, and the brain.  Thiamine, folate, niacin, vitamins B6 and B12, and vitamin E are all needed for proper nerve function. Drinking too much can alter levels of these nutrients and affect the spread of alcoholic neuropathy. Fortunately, abstaining from alcohol can help restore your nutritional health.
  • 27.  Alcoholic neuropathy can affect both movement and sensation. Symptoms range from slight discomfort to major disability. Although the condition is not life threatening, it can decrease your quality of life. Some areas of the body affected by alcoholic neuropathy include:  numbness  tingling and burning  prickly sensations  muscle spasms and cramps  muscle weakness and atrophy
  • 28.  Alcoholic neuropathy is the result of damage to these nerves. The damage may be the direct result of long periods where you drank too much alcohol. Nutritional problems linked to alcohol use, such as vitamin deficiency, can also cause nerve damage.
  • 29.  nerve biopsy  nerve conduction tests  upper GI and small bowel series  neurological examination  electromyography  esophagogastroduodenoscopy (EGD)  kidney, thyroid, and liver function tests  complete blood count (CBC)
  • 30.  vitamin supplements to improve nerve health (folate, thiamine, niacin, and vitamins B6, B12, and E)  prescription pain relievers (tricyclic antidepressants and anticonvulsants)  medication for people with problems urinating  physical therapy to help with muscle atrophy  orthopedic appliances to stabilize extremities  safety gear, such as stabilizing footwear, to prevent injuries  special stockings for your legs to prevent dizziness
  • 31.  Disorders of peripheral nerves are the most common neurological complications of systemic amyloidosis; an illness where a protein called amyloid is deposited in tissues and organs. Amyloidosis can affect peripheral sensory, motor or autonomic nerves and deposition of amyloid lead to degeneration and dysfunction in these nerves.
  • 32.  The typical symptoms of amyloid neuropathy are due to sensory and autonomic dysfunction. Patients may experience painful paresthesias (unusual sensations), numbness and balance difficulties due to sensory dysfunction and persistent nausea, vomiting, diarrhea, constipation, incontinence, sweating abnormalities or sexual dysfunction due to autonomic nerve involvement.
  • 33.  Diagnosis of amyloid neuropathies is based on history, clinical examination and supporting laboratory investigations. These include electromyography with nerve conduction studies, skin biopsies to evaluate cutaneous nerve innervation, and nerve and muscle biopsies for histopathological evaluation. In cases of familial amyloidosis, genetic testing in the blood may be useful.
  • 34.  Treatment of amyloid neuropathies is directed at both preventing further deposition of amyloid in peripheral nerves and treating painful symptoms. Depending on the type of amyloid protein, patients may benefit from liver or bone marrow transplant. Neuropathic pain due to amyloid neuropathy can be treated with anti-seizure medications, antidepressants, or analgesics including opiate drugs. In severe painful conditions patients may be referred to the Blaustein Chronic Pain Clinic for a multidisciplinary approach to pain management.
  • 36.  Most common type --- Acute inflammatory demyelinating polyneuropathy (AIDP)  Symptoms and Signs Muscles weakness – facial and orophyrengial cardiac arrhythmias, GI stasis, urinary retention, and pupillary changes. An unusual variant (Fisher variant) may cause only ophthalmoparesis, ataxia, and areflexia.
  • 39.  Clinical evaluation  Electrodiagnostic testing  CSF analysis  Neurophysiology
  • 40. Diagnostic Criteria for Guillain-Barre Syndrome REQUIRED 1. Progressive weakness of 2 or more limbs due to neuropathy 2. Areflexia 3. Disease course <4 weeks 4. Exclusion of other causes [e.g., vasculitis (polyarteritis nodosa, systemic lupus erythematosus, Churg-Strauss syndrome), toxins (organophosphates, lead), botulism, diphtheria, porphyria, loc alized spinal cord or cauda equina syndrome] SUPPORTIVE 1. Relatively symmetric weakness 2. Mild sensory involvement 3. Facial nerve or other cranial nerve involvement 4. Absence of fever 5. Typical CSF profile (acellular, increase in protein level) 6. Electrophysiologic evidence of demyelination
  • 41.  Intensive supportive care  IV immune globulin (IVIG) or plasma exchange  Rihablisation  Respiratory failure  Pain
  • 42. Scattered distribution of sensory loss in Multiple Mononeuropathy
  • 43. Can found in:  Classic PAN  Churg-Strauss disease  Wegener’s granulomatosis  Overlap syndrome  Vasculitis associated with connective tissue disease  Sjóģren syndrome  Lyme disease  Leprosy  Diabetes mellitus
  • 45. Mycobacterium leprae – coolest tissue in the body Tuberculoid (high-resistance) leprosy – single patch of hypoesthesia or anesthetic skin in any location Lepromatous (low resistance) leprosy – numerous bacilli, wide spread skin thickening, cutaneous anesthesia, anhydrosis sparing axilla, groin and skin beneath the scalp hair
  • 46.  Nerve root disorders result in segmental radicular deficits (eg, pain or paresthesias in a dermatomal distribution, weakness of muscles innervated by the root). Diagnosis may require neuroimaging, electrodiagnostic testing, and systemic testing for underlying disorders. Treatment depends on the cause but includes symptomatic relief with NSAIDs, other analgesics, and corticosteroids.
  • 50.  Causes Compressive : herniated disc, spondylosis, tumor Infiltrative : tumor seeding, infection Inflammatory : immune-mediated
  • 51.  Brachial plexus  Lumbosacral plexus
  • 52.  Trauma  Tumor infiltration  Infection by viral  Immune-mediated  Delayed effects of radiotherapy
  • 53. Traction birth injury (Erb’s palsy) Acute pain in back of shoulderPostmastectomy and radiation Brachial plexopathy
  • 54.  Upper C5,6 or Erb-Duchenne type  Lower C8, T1 or Dejerine-Klumpke type  Total
  • 55. Klumpke’s palsy (injury of lower brachial plexus C7,C8,T1) and often Horner’s syndrome Erb’s palsy (injury of upper brachial plexus C5,C6)
  • 56.  Multiple spinal roots and peripheral nerves  Roots : T12-S4  Nerves : iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, femoral, obturator, superior gluteal, inferior gluteal, sciatic, posterior femoral cutaneous, pudendal nerves
  • 57. Lumbar plexopathy Sacral plexopathy Clinical manifestation
  • 58.  Tumors : CA cervix, prostate, bladder, colorectal, kidney, breast, testis, ovary, sarcoma, lymphoma  Compressed by aortic aneurysm  Radiation plexopathy  Plexitis : follow herpes zostor  Diabetic amyotrophy  Trauma (rare)  As a manifest of mononeuropathy multiplex
  • 60. Median nerve Carpal tunnel syndrome Anterior interosseous syndrome Pronator syndrome Ligament of Struthers
  • 61.  Carpal tunnel syndrome Nocturnal pain or paresthesia Thenar atrophy
  • 65. Ulnar nerve Lesion at condylar groove Lesion at wrist and hand Guyon’s canal
  • 66.  At elbow : Condylar groove or in cubital tunnel  Wasting hypothenar eminence and web space of (1st dorsal interossei)  Claw hand
  • 70. Radial nerve Saturday night palsy Posterior interosseous syndrome Cheiralgia parestheticaCheiralgia paresthetica
  • 71.  Axillary lesion : weak triceps and radial innervated m.  Mid-upper arm lesion : ‘Saturday night palsy’ (spiral groove or intermuscular septum) : wrist drop, normal triceps, variable motor and sensory deficit  Posterior interosseous : weak extensor of thumb and other fingers, no sensory loss  Superficial radial n. : terminal cutaneous br.
  • 74. Lateral femoral cutaneous nerve of thigh (L2 and L3) • Meralgia paresthetica • Pure sensory
  • 76. Femoral nerve (L2,3,4) • Mix sensorimotor • Quadriceps femoris or knee extensor • Weakness of hip flexor in intraabdominal lesion • Sensory deficit over anteromedial aspect of thigh and perhaps leg • Absent or diminished knee jerk
  • 77. Obturator nerves • L2,3,4 • Hip adductors • vulnerable during obstetric and gynecological procedures
  • 79.  Composed of 2 main nerves of leg : common peroneal and tibial nerve  Paralysis of all muscles below knee plus hamstrings and for high lesion, external rotators of thigh  Sensory loss below knee except anteromedial aspect of leg and foot
  • 80. Common peroneal nerve • Foot-drop • Paralysis of anterior and lateral compartment of leg • Sensory loss over dorsum of foot and toes and anterolateral aspect of leg
  • 83.  Medial division of sciatic nerve  Lesions at ankle  Tarsal tunnel syndrome  Pain and paresthesia in sole  Paralysis of intrinsic muscles of foot  Tenderness of Tinel’s sign at flexor retinaculum  Sural nerve compression syndrome  Pure sensory  Numbness on lateral aspect of foot
  • 87. Clinical features :  postauricular pain (few days)  lower motor neuron facial weakness  impaired taste  hyperacusis
  • 89.  Bell’s palsy : idiopathic, HSV 1  Ramsay Hunt syndrome : external ear pain with presence of herpes zoster vesicles in auditory canal and pinna, VZV  Trauma : blunt impact to temporal bone  Middle ear infection : otitis media (infrequent in ATB era), mastoid pain persist after acute infection resolved  Neoplasm : rarely compressed by CPA tumor but due to surgery for tumor removal
  • 90. Management Reassurance – not a stroke Short course of prednisolone 60 mg/day Prognosis : complete recovery 75% satisfactory 15% poor function 10%