Lecture 7 - Motor and Sensory Disorder PDF

Motor and Sensory Disorders dr. A. A. Ayu Agung Pramaswari, Sp.N Neurology Department, Faculty of Medicine, Udayana University SENSORY SYSTEM Receptor Organs Somatosensory Tracts Root Entry Zone & Peripheral nerve Posteri...

Motor and Sensory Disorders dr. A. A. Ayu Agung Pramaswari, Sp.N Neurology Department, Faculty of Medicine, Udayana University SENSORY SYSTEM Receptor Organs Somatosensory Tracts Root Entry Zone & Peripheral nerve Posterior Horn Dorsal Root Ganglion Posterior root Peripheral Components of the Somatosensory System Encapsulated end organ → fine touch, discrimination, vibration, pressure Mechanoreceptor (touch & pressure) Tactile corpuscles of Meissner : touch and light pressure Laminated Vater-Pacini Corpuscles: deeper pressure Skin Free Nerve Ending→ Pain, temperature Thermoreceptor (warm and cold) Bulbe of Krause: cold Corpuscles of Ruffini: warm Receptor Nociceptor (pain) Organs Muscle Spindles: respon to stretch Deeper Golgi tendon organs: respon to stretch but a higher treshold Region (muscle, tendon, Other receptor: fasciae, joints) Laminated Vater-Pacini corpuscle, Golgi-Mazzoni corpuscle → pressure, pain  ▪ Afferent fibers from circumscribed area of body run together in peripheral nerve: Peripheral ▪ Superficial & deep sensation nerve (somatic afferent & efferent fibers) ▪ Internal organs, sweat glands, vascular smooth muscle (visceral afferent & efferent fibers) ▪ Proximal to its junction with ventral Dorsal Root root Ganglion ▪ Pseudounipolar ▪ Contain afferent fiber, before making Posterior synaptic contact with second sensory Root neuron SOMATOSENSORY SEGMENTAL INNERVATION (Dermatome) Total: 31 pair spinal nerve. Each dermatome correspond to single spinal cord segment  ▪ Medial portion root: Propioception (origin: muscle spindle, most thick) ▪ Central portion root: touch, vibration, pressure, Dorsal Root Entry discrimination (origin: receptor organ) Somatosensory Zone & Posterior Lateral portion root: pain & temperature (small ▪ Tracts Horn & thin myelin)  Spinocerebellar Tracts Propioceptive: influence muscle tone & Coordinated action Posterior Spinocerebellar Tract ▪ C8-T2 levels: 2nd neuron in Clarke coloumn→ Ascends ipsilaterally in posterior lateral funiculus→ inferior cerebellar peduncle→cerebellar vermis ▪ Upper Cervical levels: travel in the cuneate fasciculus → 2nd neurons in accessory cuneate nucleus of the medulla→ cerebellum. Anterior Spinocerebellar Tract ▪ Ascend ipsilaterally and contralaterally→cerebellu m (2nd neuron in Rexed lamina VII) ▪ Transverse floor of 4th ventricle→midbrain→poste rior direction to cerebellar vermis (superior cerebellar peduncle & superior medullary velum  Posterior Columns Position sense, vibration, pressure, discrimination touch ▪ Posterior funiculus: ▪ Medial gracile fasciculus (Goll): lower limb ▪ Lateral cuneate fasciculus (Burdach)→cervical level: upper limb ▪ Posterior funiculus →gracile & cuneate nucleus in lower medulla→bulbothalamic tract→cross midline, form medial lemniscus→VPL of thalamus→thalamocortical tract→internal capsule (posterior crus)→corona radiata→primary somatosensory cortex in postcentral gyrus Lesion: ▪ Loss Sense of position & movement ▪ Astereognosis(can’t recognize &name objects by their shape and weight) ▪ Agraphesthesia(can’t recognize number/letter drawn in hand palm) ▪ Loss of two-point discrimination ▪ Loss of vibration sense ▪ Positive Romberg sign Anterior Spinothalamic Tracts Pressure & Touch Perception ▪ Impulse from cutaneus receptors→ 1st neuron: DRG →posterior columns 2-15 segment upward, 1-2 segment downward (collateral)→ gray matter of posterior horn→2nd neuron→rise to anterior spinothalamic tract, cross anterior spinal commissure→ascend contralateral anterolateral funiculus→ventral posterolateral nucleus of thalamus (3rd neuron)→postcentral gyrus (thalamocortical tract) Lesion: ▪ Lumbar/thoracic lv: minimal / no impairment of touch ▪ Cervical lv: mild hypesthesia contralateral lower limb Lateral Spinothalamic Tracts Pain, Temperature ▪ Impulse → 1st neuron: DRG →posterior columns→ substantia gelatinosa→2nd neuron : funicular neurons→lateral spinothalamic tract→cross midline in anterior spinal commissure→ ascending contralateral lateral funiculus→thalamus (Ventral Posterateral /VPL)→ thalamocortical tract ▪ Lower limb: laterally; trunk & upper limb: medially Lesion: ▪ Ventral portion spinal cord: pain and temperature sensation ↓ opposite side 1-2 segment below level of lesion. Sense of touch preserved Primary Somatosensory Cortex ▪ Primary somatosensory cortex in postcentral gyrus (parietal lobe) → Brodmann area 3a,3b,2,1 Unilateral lesion: ▪ Subtotal impairment of perception noxious, thermal, tactile stimuli on opposite side body ▪ Total impairment contralateral discrimination and position sense (astereognosis) Somatosensory Deficits Due To Lesion Along Somatosensory Pathways a & b : Cortical or subcortical Clinical sign: -Paresthesia (tingling, etc) and numbness in contralateral limb, distal > proximal -Iritative lesion: sensory focal seizure, motor discharge (jacksonian seizure) c : Below thalamus Clinical sign: -All qualities sensation oppsite side body d : Somatosensory pathway except pain & temperature Clinical sign: -Hypesthesia opposite side body and face, pain and temperature sensation unimpaired e : Trigeminal lemniscus & lateral spinothalamic tract (brainstem) Clinical sign: -Pain & temperature sensation on opposite side body & face, other somatosensory modality unimpared f : Medial lemniscus and anterior spinothalamic tract Clinical sign: -All somatosensory modalities of contralateral half body are impaired (excp. pain & temperature) g : Spinal nucleus & tract of trigeminal nerve & lateral spinothalamic tract Clinical sign: -Impair pain and temperature sensation on ipsilateral half of face and contralateral half of body h : Posterior column lesions Clinical sign: -Loss position and vibration sense, discrimination, etc -Ipsilateral ataxia i : Posterior horn of spinal cord Clinical sign: -Lost ipsilateral pain & temperature, other modality intact (dissociated sensory deficit) k : Posterior root Clinical sign: -Radicular pain & paresthesia -Impairment / loss all sensory modalities in affected area -Atonia, areflexia, ataxia (upper / lower limb) MOTOR SYSTEM FUNCTIONAL AREA OF CEREBRAL CORTEX (MOTOR SYSTEM) Central portion of motor system for voluntary movement: Primary motor cortex area : area 4 Premotor cortex area : area 6 Prefrontal eye field : area 8 Precentral gyrus Postcentral gyrus 4 4 Central sulcus  Pyramidal Tract 1. Corticospinal Tract Anterior corticospinal tract Lateral Corticospinal tract 2. Corticonuclear Tract Corticospinal Tract 1. Motor cortex 2. Cerebral White Matter (corona radiata) 3. Posterior limb of Internal Capsule 4. Central portion of cerebral peduncle (crus cerebri) 5. Pons ▪ 80-85% cross → contralateral lateral 6. Anterior portion of medulla funiculus→ lateral corticospinal tract 7. Decussation of the pyramids ▪ 15-20% do not cross → ipsilateral anterior funiculus → anterior corticospinal tract ▪ cross through anterior commissure of the spinal cord ▪ Remain uncrossed at cervical and thoracic level→bilateral cortical innervation Corticonuclear (Corticobulbar) Tract Some fiber from pyramidal tract branch off through midbrain (crossed & uncrossed) more dorsal course toward the motor cranial nerve nuclei. ▪ Area 4 : Nn. V, VII, IX, X, XI, XII ▪ Area 8 : Nn. III, IV, VI (Corticomesencephalic tract)  Other Motor Tract (Extrapyramidal tract) Corticopontocerebellar tract → from cortex to cerebellum → modulated planned movements From cortex to basal ganglia, the substantia nigra, brainstem reticular formation, other nuclei (midbrain tectum) → via interneurons to efferent tracts at anterior horn→ Tectospinal, Rubrospinal, reticulospinal, vestibulospinal, and others tract →enable the cerebellum, basal ganglia, and brainstem motor nuclei to influence motor function in the spinal cord Lateral and Medial Motor Tracts in the Spinal Cord Mainly project to distal musculature (esp. upper limbs) + short propriospinal connections → voluntary movements of the forearms and hand (precise, fine motor control) Long propriospinal connections → voluntary movements of the trunk and lower limbs (stance and gait)  LESION OF CENTRAL MOTOR PATHWAYS Pathogenesis of central Syndrome of central spastic paresis spastic paresis ▪ Acute phase → Deep tendon reflexes hypoactive + flaccid ▪ ↓ muscular strength & impaired weakness of muscle fine motor control ▪ Reflex return a few days-weeks later & become hyperactive ▪ Spastic increased tone (muscle spindles respond more sensitively to stretch than ▪ Abnormality brisk stretch normal, esp. upper limb flexors & lower limb extensor). reflex, with clonus ▪ Hypersensitivity due to loss of descending central inhibitory ▪ Hypoactivity / absence of control of the fusimotor cells (motor neuron) that innervate exteroceptive reflexes the muscle spindles. (abdominal, plantar, ▪ Intrafusal muscle fiber permanently activated cremasteric reflex) (prestretched) and respond more readily than normal to ▪ Pathological reflex (Babinski futher stretching of the muscle. and varian) ▪ Disturbance of the regulatory circuit for muscle length ▪ Preserved muscle bulk (early →spastic increased tone and hyperreflexia → pyramidal phase) → atropi (late phase) tract signs and clonus (include Babinski sign).  PERIPHERAL COMPONENTS OF THE MOTOR SYSTEM 1. Motor cranial nerve nuclei of brainstem 4. Cervical & lumbosacral nerve plexus 2. Motor anterior horn cells of spinal cord 5. Peripheral nerves 3. Anterior roots 6. Motor end plates in skeletal muscle ▪ Multipolar → their dendrites receive synaptic contact from a wide variety afferent & efferent system Anterior horn cells (𝛼 and 𝛾 motor neuron) ▪ Cervical level: motor neuron for upper limbs lie in lateral portion of gray matter; truncal muscle lie in medial portion ▪ Lumbar level: lower limb lie laterally; trunk medially ▪ Renshaw cells → interneuron that receive synaptic contact from collateral axon of large 𝛼 motor neuron. Their axon then project back onto anterior horn cells and inhibit their activity (spinal negative feedback loop) Anterior Root ▪ Neurites of motor neurons exit the anterior aspect of the spinal cord as rootlets (fila radicularia) and join together forming anterior roots ▪ Each anterior root join the corresponding posterior root just distal to the dorsal root ganglion→form spinal nerve→exits spinal canal through intervertebral foramen  PERIPHERAL COMPONENTS OF THE MOTOR SYSTEM Peripheral nerve & motor end plate ▪ One pair of spinal nerves for each segment of the body → Afferent somatosensory fibers + efferent somatic motor fibers + efferent autonomic fibers (lateral horn) + afferent autonomic fibers. ▪ Cervical & Lumbosacral levels : spinal nerve join to form nerve plexus → peripheral nerves that innervate musculature of neck and limbs ▪ Synaptic impulse transmission occurs at the neuromuscular junction (motor end plates) Motor Unit ▪ → Anterior horn cells, neurites, muscle fiber ▪ Activity influenced by impulse in a wide variety of motor tract that originate in different areas of the brain, as well as impulses derived from intersegmental reflex neuron of the spinal cord ▪ All movement related impulses integrated in motor unit →transmitted to muscle fibers ▪ Fine differentiated movement→ large number of anterior horn cell with small motor units (5-20 muscle fibers) ▪ Undifferentiated movement from large muscle → few anterior horn cell with large motor unit (100-500 muscle fiber)  CLINICAL SYNDROMES OF MOTOR UNIT LESIONS Pathogenesis of flaccid paralysis Syndrome of flaccid paralysis ▪ Caused by interruption of motor unit at any 1) Diminution of raw strength site 2) Hypotonia or atonia of the musculature ▪ Motor unit damage cuts off the muscle fiber 3) Hyporeflexia or areflexia in the motor unit from both voluntary and reflex innervation. 4) Muscle atrophy ▪ Affected muscles are extremely weak (plegic), diminution of muscle tone If paralisis accompanied by somatosensory (hypotonia), loss reflexes (areflexia) → and autonomic deficits→ lesion presumably Monosynaptic stretch reflex loop distal to nerve roots, located either in nerve interrupted plexus or peripheral nerve ▪ Muscle atropi in few weeks, muscle replaced by connective tissue CENTRAL MOTOR SYSTEM SYNDROME LOCALIZATION OF LESIONS IN THE CENTRAL MOTOR SYSTEM a) Cerebral cortex Clinical sign: -Weakness part of body on opposite side (face & hand / brachiofacial weakness) more frequently -At picture site : predominant distal paresis of upper limb, impaired fine motor control, paresis > plegia, flaccid>spastic -Irritative lesion → focal (jacksonian) seizure Etiology (most common): -Tumor -Infarct -Traumatic injury b) Internal Capsule Clinical sign: -Contralateral flaccid hemiplegia (early) → Spastic (late) -Contralateral facial palsy -Central hypoglossal nerve palsy Etiology (most common): -Stroke (Hemorrhage or ischemia) LOCALIZATION OF LESIONS IN THE CENTRAL MOTOR SYSTEM c) Cerebral peduncle Clinical sign: -Contralateral spastic hemiparesis -Ipsilateral oculomotor nerve palsy (Weber syndrome) Etiology (most common): -Vascular process (hemorrhage/ischemia) -Tumor d) Pontine Lesion Clinical sign: -Contralateral or bilateral hemiparesis -Ipsilateral trigeminal nerve deficit, abducent palsy -Central facial or hypoglossal palsy →rare Etiology (most common): -Tumor -Vascular (brainstem ischemia/hemorrhage) LOCALIZATION OF LESIONS IN THE CENTRAL MOTOR SYSTEM e) Medullary pyramid Clinical sign: -Flaccid contralateral hemiparesis Etiology (most common): -Tumor f) Spinal cord (cervical level) Clinical sign: -Ipsilateral spastic hemiplegia -Quadriparesis / quadriplegia → bilateral lession Etiology (most common): -Tumor, Myelitis, Trauma g) Spinal cord (thoracic level) Clinical sign: -Spastic ipsilateral monoplegia of the lower limb -Paraparesis / paraplegia →bilateral lession Etiology (most common): -Trauma, myelitis SPINAL CORD SYNDROME SPINAL CORD SYNDROMES DORSAL ROOT GANGLION Herpes Zooster Infection (most common in thoracic region) Unpleasant, stabbing pain, paresthesiae in affected area Flaccid paresis, hemiparesis, paraparesis →rare Complication: Post Herpetic Neuralgia POSTERIOR ROOT SYNDROME Sensation in corresponding dermatomes is partial-total loss Incomplete lesion →pain sensation dominant affected Hypotonia, hyporeflexia, areflexia → multiple adjacent roots affected Most common etiology: trauma POSTERIOR COLUMN SYNDROME Secondarily involved by pathological process at dorsal root ganglion and posterior root Impair position and vibration sense, discrimination, stereognosis. Romberg sign (+), spinal ataxia in closed eyes Hypersensitivity to pain Most common etiology: vit B12 deficiency, AIDS associated vacuolar myelopathy, cervical spinal stenosis, tabes dorsalis SPINAL CORD SYNDROMES POSTERIOR HORN SYNDROME Dissociated somatosensory deficit (pain and temperature sensation) Pain and temperature intact below level of the lesion GRAY MATTER SYNDROME Most common etiology : syringomyelia, hematomyelia, intramedullary spinal cord tumor Originated in posterior horn cell, then decussate in the central gray matter, then ascend in the anterior and lateral spinothalamic tract Bilateral dissociated sensory deficit COMBINE POSTERIOR COLUMN + CORTICOSPINAL TRACT SYNDROME Most common etiology : Vit B12 Deficiency Loss of position and vibration sense in lower limbs →spinal ataxia & Romberg sign (+) Spastic paraparesis, hypereflexia, bilateral babinski signs SPINAL CORD SYNDROMES ANTERIOR HORN SYNDROME Most common etiology: poliomyelitis, spinal muscle atrophy (cervical & lumbal) Flaccid paresis, weaknes proximal > distal, atrophic COMBINED ANTERIOR HORN & PYRAMIDAL SYNDROME Most common etiology : Amyotrophic lateral sclerosis (ALS) Combination flaccid & spastic paresis Muscle atrophy (+) in early, general and severe (deep tendon reflexes -) →LMN Reflexes remain elicitable & exaggerated-->UMN Motor cranial nerve→ dysarthria, dysphagia (Progressive bulbar palsy) SYNDROME OF CORTICOSPINAL TRACTS Most common etiology : Primary lateral sclerosis (var. of ALS), spastic spinal paralysis Heaviness and weakness in lower limb Spastic paraparesis, spastic gait disturbance, gradually Reflexes brisker Spastic paresis of upper limb → late SPINAL CORD SYNDROMES COMBINED POSTERIOR COLUMNS, SPINOCEREBELLAR TRACTS, (POSSIBLY) PYRAMIDAL TRACTS Most common etiology: Spinocerebellar ataxia of Friedreich type, axonal form of hereditary neuropathy (HSMN II), other ataxia Impairement position sense, two-point discrimination, stereognosis, spinal ataxia (severe), rombers sign (+). Pain & temperature sense spared Patient gait uncoordinated, festination (+), become spastic over time. Skeletal deformities : Skoliosis / pes cavus SPINAL CORD HEMISECTION SYNDROME / BROWN-SEQUARD SYNDROME Most common etiology : Spinal trauma, cervical disk herniation Interruption descending motor pathways: initially flaccid, ipsilateral paresis below level lesion (spinal shock), later become spastic + hyperreflexia, Babinski signs (+), vasomotor disturbances Interuption posterior coloums: loss of ipsilateral position sense, vibration sense, tactile discrimination below level of lesion. Pain and temperature sensation lost contralaterally below level lesion Simple tactile sentation not impaired Paresthesia (+), radicular pain (+) → irritation posterior roots SPINAL CORD TRANSECTION SYNDROMES Level Cervical Vertebrae (CV) Above 3rd CV : fatal (abolishes breathing bc. Loss function of phrenic and intercostal nerve) Lower CV: Quadriparesis with involvement intercostal muscle Sensory deficits by impaired dermatome Level Thoracic Vertebrae (TV) Upper TV: spares upper limbs, impairs breathing, paralytic ileus (involvement splanchnic nerves), paraparesis Level Lumbar Vertebrae (LV) Severe disturbances, weakness both lower limbs (flaccid paraplegia) Incontinent urin and stool (vesical & anal spincther Sensory deficit on lower limb and power portion of the trunk Epiconus Syndrome (L4-S2) Spastic / flaccid paresis of lower limb (hip external rotation: L4-S1, and extension : L4-L5, knee flexion: L4-S2, Flexion & extension ankles + toes: L4-S2) Achilles reflex (-), Knee-jerk reflex (+) Sensory deficits extend from L4-S5 Bladder and bowel empty disturbance, sexual potency ↓, priapism (+) Transient loss of sweating SPINAL CORD TRANSECTION SYNDROMES Conus Syndrome (below S3) Causes: spinal tumors, ischemia, massive lumbar disk herniation Detrusor areflexia, Urinary retention, overflow incontinence (continual dripping) Fecal incontinence Impotence Saddle anesthesia (S3-S5) Loss of anal reflex Lower limb not paretic, Achiles reflex preserved (L5-S2) Cauda Equina Syndrome Involves lumbar and sacral nerve roots Causes: tumor (ependymoma / lipoma) Radicular pain in sciatic distribution Severe bladder pain, worsens with coughing, sneezing Severe radicular sensory deficits, affecting all sensory modalities, arise at L4 or lower level Lession on upper portion cauda equina : sensory deficit in the leg and saddle area, flaccid paresis with areflexia, incontinence urin and fecal incontinence, impaired sexual function Lession on lower portion cauda equina : sadle anesthesia, lower limb weakness (-), impaired on urination, defecation, sexual function NERVE ROOT SYNDROME (Radicular Syndrome)  NERVE ROOT SYNDROMES (Radicular/perifer Syndrome) ▪ Intervertebral disk→ pulpy inner portion (nucleus pulposus), surrounded by a fibrous ring (annulus fibrosus). ▪ Aging→ disk lose their elasticity& turgor Osteochondrosis: ▪ Degeneration disk, cartilaginous base, end plate of vertebral bodies→ intervertebral disk lose height dan narrowing ▪ Bony overgrowth of facet joints (spondylarthrosis) & vertebral bodies Common causes: Stenosing Processes, Disk (uncovertebral arthrosis) → stenosis of Protrusion, Disk Herniation. intervertebral foramina + compression tissue within them Cervical region: ▪ Saddlelike structure Characteristic Manifestation: ▪ Cervical osteochondrosis most common: ▪ Pain and sensory deficit in corresponding C5-6, C6-7, C3-4, C7-T1 dermatome ▪ Greater impairment of pain sensation Lumbar region: ▪ Weakness in segment-indicating muscle, ▪ intervertebral disks are thick, base & end muscle atrophy plates flat ▪ ↓ Reflex at damaged root ▪ Absence of autonomic deficits (sweating, ▪ Most common affects: L5-S1, L4-L5 piloerection, vasomotor function) in limbs ▪ L5-S1 intervertebral disk narrower than others (bc. Lumbar lordosis) CERVICAL RADICULAR SYNDROME C3, C4 Pain in neck and shoulder, partial diaphragmatic palsy (rare) C5 Pain with/without hypalgesia in C5 dermatome, deltoid & biceps weakness C6 Pain with/without hypagesia in C6 dermatome, biceps & brachioradialis weakness, biceps reflex ↓ C7 Pain with/without paresthesia / hypalgesia in C7 dermatome, triceps and pronator teres weakness, thenar atrophy, triceps reflex ↓ C8 Pain with/without paresthesia/hypalgesia in C8 dermatome, weakness + atrophy hypothenar muscles, triceps & tromner reflexes ↓ LUMBAR RADICULAR SYNDROME L3 Pain with/without paresthesia in L3 dermatome, quadriceps weakness, quadriceps reflex ↓ (Patellar / Knee jerk reflex) L4 Pain with/without paresthesia in L4 dermatome, quadriceps weakness, quadriceps reflex ↓ L5 Pain with/without paresthesia in L5 dermatome, extensor hallucis longus & extensor digitorum brevis weakness, tibialis posterior reflex ↓ S1 Pain with/without paresthesia in S1 dermatome; peronei, gastrocnemius, soleus muscle weakness, gastrocnemius reflex ↓ (Achilles / Ankle-jerk reflex PLEXUS SYNDROME  PLEXUS SYNDROMES Cervical Plexus Brachial Plexus Lumbosacral Plexus (C2-C4) (C5-T1) (L1-S3) ▪ Occupies a relatively Cause: trauma, compression Lumbar Plexus (Lesion L2, L2, L3): sheltered position syndrome, tumors, Less common than brachial plexus (rarely injured) inflamatoric, birth injury (rarely injured) ▪ Unilateral / bilateral Upper: Sacral plexus (Lesion L4, L5, S1, S2, phrenic nerve S3): (cukup sering) ▪ Duchenne-Erb Palsy (Lesion dysfunction (C3, C4, and C5-6): deltoid, biceps, ▪ Peroneal & tibial nerves (join CS) more commonly brachialis, brachioradialis together as sciatic nerve, down caused by a mediastinal muscle. Sensory deficits (+) posterior thigh, separated above process than cervical reg. deltoid muscle, radial the knee) plexus lesion side of arm and hand ▪ Drop Foot (Steppage gait): lesion Lower: peroneal nerve (extensor weak)→more frequent. ▪ Klumpke palsy (Lesion C8- T1): paretic of wrist, finger ▪ Sensoric: lateral leg & dorsum flexor, intrinsic muscle of foot) hand; horner syndrome may ▪ Impaired toe walking: lesion tibial present, trophic nerve (weak plantar flexor) abnormalities hand and ▪ Sensoric: Sole finger PERIPHERAL NERVE SYNDROME  PERIPHERAL NERVE SYNDROMES CARPAL TUNNEL SYNDROME (CTS) ▪ Pain and paresthesiae in affected hand (usually severe at night and may felt in entire upper limb) ▪ Tinnel sign (+) CUBITAL TUNNEL SYNDROME ▪ Injury at Medial side extensor aspect of elbow ▪ Paresthesia + hypesthesia at ulnar portion, atrophy of Wrist Drop (radial Claw hand (ulnar nerve palsy) nerve palsy) hypothenar & adductor pollicis muscle (claw hand) POLYNEUROPATHIES ▪ Multiple peripheral nerve (motor, sensory, autonomic) ▪ Sensoric: stocking and gloves paresthesia) Pope’s blessing Monkey hand (median (median nerve palsy) + ulnar nerve palsy) ▪ Flaccid paresis, sensory deficits, autonomic deficits ▪ Distupted axon→ degeneration myelin sheath begin within hour-days, complete within 15-20 days (Wallerian degeneration) ▪ Most common causes: compression, traumatic injury, ischemia CTS Cubital TS  SYNDROME OF THE NEUROMUSCULAR JUNCTION AND MUSCLE  SYNDROME OF THE NEUROMUSCULAR JUNCTION AND MUSCLE Myasthenia ▪ Exercise dependent weakness: ▪ extraocular muscle →diplopia & ptosis ▪ Dysphagia, proximal weakness of skeletal muscle ▪ Causes: autoimun (body form antibodies Myopathy against acethylcholine receptors or other component of motor end plate) ▪ Slowly progressive, non exercise dependent weakness ▪ Fatty replacement of muscle tissue (liposis / lipomatosis) ▪ No sensory/autonomic disfunction ▪ Fasciculation (+) ▪ Myalgia & muscle spasm → metabolic induced ▪ Type: muscular dystrophies, metabolic myopathies, myotinic dystrophies, myositis  REFERENCES 1. M. Baehr & M Frotscher. Duus’ Topical Diagnosis in Neurology Anatomy, Physiology, Signs, Symptoms. 5th Edition. 2012. Stuttgart, New York: Thieme. 2. M. Baehr & M Frotscher. Diagnosis Topik Neurologi Duus. Anatomi, Fisiologi, Tanda dan Gejala. Edisi 6. 2021. Jakarta: EGC. 3. Splittgerber R. Snell’s Clinical Neuroanatomy. Eight edition. 2018. Walters-Klower 4. Haines D.E. Neuroanatomy An Atlas of Structures, Sections and Systems. Seventh edition. 2011.Lippincott Williams & Wilkins 5. Ngoerah, IGNG. Dasar-Dasar Ilmu Penyakit Saraf. 2017. Denpasar: Udayana University Press. THANK YOU