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    Neuropathy

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    Neuropathy

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    Neuropathy

    Uploaded by

    jana

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    © All Rights Reserved
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    NEUROPATHY

    DEFINITION
    Neuropathy is defined as a disease or
    injury of the peripheral sensory, motor, or
    autonomic nerves.
    Can be : - pure motor
    - pure sensory
    - mixed sensorimotor
    - autonomic
    Category
    Usually categorized separately :
    Neuronopathy : selective injury to the cell body of the
    axon
    Radiculopathy : selective injury to the nerve roots
    distal to their origin
    Plexopathy : injury to the brachial or lumbosacral
    plexus
    CLASSIFICATION
    1. BASED ON THE ONSET OF NEUROPATHY:

    ACUTE NEUROPATHY
    eg. : ACUTE IDIOPATHIC POLYNEUROPATHY
    CHRONIC NEUROPTHY
    eg. : BERI BERI
    DIABETES MELLITUS
    LEPROSY
    2. BASED ON SEVERITY

    1.MILD NEUROPATHY : SENSORY ONLY


    2.MODERATE NEUROPATHY : SENSORY,
    MOTOR, AND DECREASE OF TENDON
    REFLEXES
    3.SEVERE NEUROPATHY : SENSORY,
    MOTOR, DECREASE OF TENDON REFLEXES,
    MUSCLE ATROPHY
    3. BASED ON THE NUMBER OF
    NERVES INVOLVED
    1. MONONEUROPATHY SIMPLEX :
    ONLY ONE PHERIPHERAL NERVE INVOLVED.

    2. MONONEUROPATHY MULTIPLEX (MULTIFOCAL


    NEURPATHY) :
    MULTIPE, SCATTERED NERVES IN AN IRREGULAR
    DISTRIBUTION

    3. POLYNEUROPATHY :
    SEVERAL NERVES INVOLVED, SYMMETRICAL, SAME
    ONSET AND DISTAL PREDOMINANT.
    4. BASED ON LESION SITE

    1 DISTAL AXONOPATHY :
    AXONAL LESION
    2. MYELINOPATHY :
    DISORDER OF MYELIN SHEATH.
    3. NEUROPATHY :
    DISORDER OF CELL BODY AT ANTERIOR HORN
    CELLS, SPINAL CORD OR DORSAL ROOT
    GANGLION.
    ETIOLOGY
    1. IDIOPATHIC INFLAMMATORY NEUROPATHIES
    - ACUTE IDIOPATHIC POLYNEUROPATHY
    (GUILLAIN BARRE SYNDROME)
    - CHRONIC INFLAMMATORY DEMYELINATING
    POLYNEUROPATHY

    2. METABOLIC AND NUTRITIONAL NEUROPATHIES


    - DIABETES, HYPOTHYROIDI, ACROMEGALY
    - UREMIA
    - LIVER DISEASES
    - VIT B1, OR VIT B12 DEFICIENCY
    ETIOLOGY
    3. INFECTIVE AND GRANULOMATOUS
    NEUROPATHIES:
    AIDS, LEPROSY. DIPHTHERY, SARCOIDOSIS

    4. VASCULITIS NEUROPATHIES:
    - POLYARTERITIS NODOSA
    - RHEUMATOID ARTHRITIS
    - SYSTEMIC LUPUS ERYTHEMATOSUS
    ETIOLOGY

    5. NEOPLASTIC AND PARAPROTEINEMIC


    NEUROPATHIES:
    - COMPRESSION AND IRITATION BY TUMOR
    - PARANEOPLASTIC SYNDROME
    - PARAPROTEINEMIAS
    - AMYLOIDOSIS
    ETIOLOGY
    6. DRUGS INDUCED AND TOXIC NEUROPATHIES
    -DAPSONE, ISONIAZIDE, PHENYTOIN, PIRIDOXYNE,
    VINCRISTIN, HIDRALAZINE.
    - ALCOHOL
    - TOXINS : ORGANOPHOSPHAT
    ARSENIC
    LEAD
    THALIUM
    GOLD
    ETIOLOGY (cont.d)
    7. HEREDITARY NEUROPATHIES
    - IDIOPATHIC
    HEREDITARY MOTOR AND SENSORY NEUROPATHIES
    HEREDITARY SENSORY NEUROPATHIES
    FAMILIAL AMYLOIDOSIS
    - METABOLIC
    PORPHYRIA
    METACHROMATIC LEUCODYSTROPHY
    ABETALIPOPROTEINEMIA
    ETIOLOGY
    8. ENTRAPMENT NEUROPATHIES
    - UPPER LIMBS
    MEDIAN NERVE (CARPAL TUNNEL SYNDROME)
    ULNAR NERVE
    RADIAL NERVE
    - LOWER LIMBS
    PERONEAL NERVE
    FEMORAL NERVE
    OBTURATOR NERVE
    PATHOGENESIS
    Can be divided into 4 major categories :
    1. Neuronal degeneration : results from damage to the motor or
    sensory nerve cell bodies, with subsequent degeneration
    2. Wallerian degeneration : results from damage to the axon at a
    specific point below the cell body, with degeneration distal to the
    injury.
    3. Axonal degeneration : results from diffuse axonal damage. The
    distal portion undergoes the earliest and most severe change
    followed by gradual proximal ascent with continued injury (dying
    back phenomenon)
    4. Segmental demyelination : results from injury to the myelin sheath
    without injury to the axon
    PATHOPHYSIOLOGY

    1. NEUROPRAXIS :
    - the mildest form
    - conduction disruption only
    - intact nerve continuity
    - recovery in minutes or weeks
    PATHOPHYSIOLOGY
    2. AXONOTMESIS:
    - AXONAL DAMAGE FOLLOWED BY
    DEGENERATION
    - ENDONEURAL SHEATH REMAINS
    INTACT
    - POSSIBLE REGENERATION
    PATHOPHYSIOLOGY
    3. NEUROTMESIS:

    - PARTIAL OR TOTAL NERVE DAMAGE


    - SURGICAL INTERVENTION IS NEEDED
    - 50% RECOVER
    CLINICAL SYMPTOMS
    1. SENSORY SYMPTOMS :
    Involvement of sensory axons produces
    impairment of sensation with dysesthesias or
    paresthesias.
    CLINICAL SYMPTOMS
    2. MOTOR SYMPTOMS :
    Involvement of motor axons produces muscle
    wasting and weakness followed by atrophy and
    fasciculations
    - LMN TYPE MUSCLE WEAKNESS
    - FOOT DROP
    - WRIST DROP
    CLINICAL SYMPTOMS
    3. CHANGE OF TENDON REFLEXES The
    tendon reflexes supplied by the
    affected nerve are depressed or absent.

    decreased or absent of tendon reflexes


    CLINICAL SYMPTOMS
    4. AUTONOMIC :
    Involvement of axons supplying autonomic
    function produces loss of sweating, alteration
    in bladder fuction, constipation, and impotence
    in male
    DIAGNOSIS
    1. CLINICAL SYMPTOMS AND SIGNS
    2. LABORATORY STUDIES
    3. CHEST X-RAY
    4. LP
    5. ECG
    6. BIOPSY : sural nerve or radial cutaneus nerve
    7. ELECTROPHYSIOLOGY: EMG
    NCV
    DIABETIC NEUROPATHY
     Neuropati diabetik :
    adanya gejala dan atau tanda disfungsi saraf perifer pd orang dgn
    diabetes setelah dieksklusikan penyebab lain.

     Prevalence : 10 - 20 % (symptomatic)
     Diabetic Neuropathy :
    ▫ 50% of diabetic patients
    ▫ type 1 than type 2
    ▫ the most common : chronic sensorimotor
    ▫ 50% asymptomatic
    ▫ 10-20% needs specific treatment
    PATHOGENESIS
    The etiology is uncertain.

    4 hypothesis (not necessarily exclusive) :


    1. Hyperglycemia-polyol-myoinositol hypothesis.
    2. Microvascular hypothesis
    3. Structural changes at the node of Ranvier.
    4. Vasculitic neuropathy.
    DIABETIC NEUROPATHIC SYNDROMES
    DISTAL SYMMETRIC NEUROPATHY :
    - large fiber sensory neuropathy
     numbness, paresthesias, dysesthesias,
    hyperesthesias, ataxia.
    - sensorimotor neuropathy
     any of the above plus distal weakness
    DIABETIC NEUROPATHIC SYNDROMES
    Small Fiber Neuropathy :
    - “pure” small fiber neuropathy
     numbness, paresthesias, painful dysesthesias,
    hyperesthesias.
    - Diabetic neuropathy cachexia
     subacute, severe neuropathic pain, rapid
    weight loss
    - Autonomic neuropathy
     erectile dysfunction, orthostasis, cardiac
    dysrhythmia, diarrhea, constipation
    DIABETIC NEUROPATHIC SYNDROMES
    Ischemic Mononeuropathy.
    - cranial (eg. CNs III, VI,VII)
     diplopia, pupil-sparing third nerve palsy,
    hemifacial weakness
    - Radicular (thoracic, lumbosacral)
     pain, followed by numbness or weakness in a
    radicular distribution
    - Peripheral (eg. Femoral)
     pain, followed by numbness, weakness or
    both in territory of a single nerve
    DIABETIC NEUROPATHIC SYNDROMES
    Regional Neuropathic Syndromes.
    - Diabetic amyotrophy
     subacute weakness and atrophy of
    proximal leg muscles
    - Diabetic thoracoabdominal neuropathy.
     subacute weakness, numbness, and
    atrophy in thorax and abdomen
    DIAGNOSIS
    THERAPY
    Intensive diabetic therapy
    Maintain ideal body weight
    Adjuvant analgetics :
    TCA antidepressants
    carbamazepine
    gabapentin
    intravenous lidocaine, etc
    Adjuvant Analgetics
    CARPAL TUNNEL SYNDROME
    80% in WOMEN, A COMMON TEMPORARY
    PHENOMENON DURING PREGNANCY
    PRESSURE TO THE NERVE WHEN PASSING
    BENEATH THE FLEXOR RETINACULUM 
    OBSTRUCTION OF VENOUS CIRCULATION
    AND EDEMA  ISCHEMIA  INCREASING
    PRESSURE ON THE NERVE  ISCHEMIC
    ATROPHY OF NERVE FIBERS
    Etiology
    1. Hereditary : HMSN type III
    2. Traumatic : dislocation, fracture, hematoma, wrist sprain
    3. Infection : tenosynovitis, tbc, sarcoidosis
    4. Metabolic : amyloidosis, gout
    5. Endocrine : acromegaly, DM, hypothyroidism, pregnancy
    6. Neoplastic : ganglion cysts, lipoma , myeloma
    7. Collagen vascular diseases : RA, polymyalgia rheumatica,
    SLE
    8. Degenerative disease : OA
    9. Iatrogenic : radial artery puncture, shunt for dialysis,
    anticoagulant therapy
    Clinical Symptoms
    The earliest symptoms : numbness and paresthesias in
    the sensory distribution of the median nerve in the
    hand (thumb, index, middle and lateral half of the
    ring finger)
    Later on : pain, worst at night
    Late : inability to screw bottle caps or grip properly
    SIMPLE CLINICAL TESTS FOR CTS
    PHALEN’S SIGN (PHALEN’S MANEUVRE):
    is present when tingling (paresthesia) is experienced in the
    distribution of the median nerve when the wrist is held in
    forced flexion (90o for 30-60 seconds)

    TINEL’S SIGN (HOFFMANN-TINEL’S SIGN) :


    is present when tingling (paresthesia)is experienced when
    tapping lightly with a finger or a tendon hammer over a
    compressed or regenerating peripheral nerve. The tingling
    is present in the distribution of the damaged nerve.
    Therapy
    Identified causes should be treated
    Corticosteroid injection around the median nerve
    in the carpal tunnel.
    Surgical division of the transverse ligament (flexor
    retinaculum)
    Endoscopic carpal tunnel release
    Tarsal Tunnel Syndrome
     impingement &
    inflammation of the
    posterior tibial nerve
    within the tarsal tunnel
    History
    Tarsal tunnel syndrome
    Symptoms
     pain, numbness, or
    parasthesia along
    medial or plantar aspect
    of foot
     may mimic plantar

    fasciitis
    Onset
     Acute or chronic
    History
    Tarsal tunnel syndrome
     ankle
    injury (acute)
     Repetitive stress

    associated with pes


    planus foot
     Previous history of

    tarsal fx
    History
    Tarsal tunnel syndrome
    Possible related factors
     Training surface
     Distance
     Shoes
    Neurological Tests
    Tarsal Tunnel Syndrome
    Tinel’s sign
    Decreased sensation
    over nerve distribution
    Management
    Tarsal Tunnel Syndrome
    Ice
    NSAIDs
    Orthotics
    Surgical release (in
    severe cases)
    PERONEAL NEUROPATHY
    N. Peroneus communis dibentuk oleh gabungan 4
    divisi posterior
    bagian atas pleksus sakral yaitu dari L4—5 dan S1-
    2. Pada paha, saraf ini merupakan komponen
    N.sciatic sampai bagian atas daerah popliteal,
    dimana N.Peroneus communis mulai berjalan
    sendiri.
    etiologi
    Meskipun suatu mono neuropati N.peroneal
    communis ataupun percabangannya sering
    terlihat, tetapi kondisi ini sangat jarang disebabkan
    oleh suatu entrapment.
    Penyebab yang sangat sering adalah akibat tekanan
    dari luar seperti penekanan pada saraf selama
    jongkok atau duduk bersilang kaki, trauma,
    diabetes dan lepra.
    Peroneal nerve palsy paling sering diakibatkan
    oleh duduk bersilang kaki yang mana
    menyebabkan saraf peroneal terjepit antara caput
    fibula dan condylus femur externa serta patella
    pada tungkai yang berlawanan.
    Mekanisme lain yang diketahui sebagai penyebab
    peroneal nerve palsy adalah trauma langsung,
    dislokasi lutut, fraktur tibia dan fibula
    GEJALA KLINIS
    Gejala klinis peroneus neuropati dapat dibedakan menurut level
    lesinya antara lain:
    1. Lesi pada kaput fibula
    Sebagian besar kelumpuhan saraf peroneus terjadii pada daerah
    kaput fibula, dimana saraf tersebut terletak superfisial dan rentan
    terhadap cedera
    Cabang profunda lebih sering terkena dari pada saraf yang lain
    Jika ke 2 cabang terkena (superfisial dan profuna) menimbulkan
    parese/paralise jari kaki, dorso fleksi kaki dan jari kaki, serta
    bagian lateral distal dari tungkai bawah
    Jika hanya cabang profunda yang terkena, menimbulkan deep
    peroneal nerve syndrome
    2. Anterior tibial (deep peroneal) nerve syndrome
    Saraf ini bisa terkena cedera pada kaput fibula atau lebih distal
    Kelainan ini menimbulkan parese/paralise jari kaki dan
    dorsofleksi kaki
    Gangguan sensoris terbatas pada kulit di sela jari-jari antara
    jari kaki 1 dan 2
    Saraf ini dapat juga tertekan pada pergelangan kaki, sehingga
    menyebabkan anterior tarsal tunnel syndrome yang
    menimbulkan gejala parese dan atropi pada M.extensor
    digitorum brevis. Sedangkan gangguan sensoris bisa terdapat
    atau tidak pada kulit di sela jari-jari antara kaki 1 dan 2
    3. Superficial peroneal nerve syndrome
    Lesi bisa pada kaput fibula atau lebih distal
    Menimbulkan parese dan atropi pada M.Peronei
    dan gangguan eversi kaki
    Gangguan sensoris pada kulit bagian lateral distal
    tungkai bawah dan dorsum kaki, sedangkan kulit
    di sela jari-jari antara jari kaki 1 dan 2 masih baik
    Differential diagnosis:
    Radikulopati L5
    High aciatic mononeuropathy yang mengenai
    serabut peroneus kommunis
    Terapi:
    Konservatif, menghindari faktor kompresi
    Operasi
    Physical therapy

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