APPROACH TO PATIENTS WITH MOTOR AND SENSORY D/O Dr.

Alemani

***Nagsimula na ako sa pinaka-heart ng tranx haha. Dami kasing sinasabi pa sa unahan eh. Yung reference sa baba jan kumuha si Doc Alemani as in parang copy paste and na-double check ko n rin if may discrepancy Reference: Adams and Victor's principles of neurology ebook pages 138-140 and pates 53-56 By Allan H. Ropper, Raymond Delacy Adams, Maurice Victor, Robert H. Brown; Retrieved from http://books.google.com.ph/books?id=uqT4huHvBZ4C&pg=PA50&lpg=PA50&dq=crural+leg+monoplegia&source= bl&ots=nb1-Hmz0v&sig=OuYJXSmFa4u9byFESHpau6p5tmE&hl=en&sa=X&ei=kwRqT82tDqi0iQfznJWhCg&ved=0CCMQ6AEwAQ# v=onepage&q=crural%20leg%20monoplegia&f=false Upper Motor Neuron Signs Hypertonia Marked hypertonic in flexor muscles of the arms Marked hypertonic in extensor muscles of the legs Hyperreflexia (4/4) with or without clonus Upward plantar response (babinzki) Clasp-knife movement Spastic Lower Motor Neuron Signs Hypotonia No voluntary resonse Areflexia Atrophy Fasciculation Fibrillation seen in electromyography

Paralysis/Plegia o Abolition of function o Loss of voluntary response secondary to disrupted motor pathway o Lesion at any point from cerebrum to muscle fiber

Paresis/Palsy o Lesser degree of paralysis o Partial loss of function

***However, as I consulted Google: Paralysis loss of motor function only. Plegia loss of motor and sensory function. Paresis impaired function; meaning it is still there but it doesnt do its work well or as expected. Palsy loss of motor, sensation function; usually localized example face only, forearm and arm as seen in brachial palsy. ***more or less ganun din naman haha Anatomic Consideratios of the Upper Motor Neuron

***Alam nio na yang homunculus Siyempre kung may infarct ka sa Anterior Cerebral Artery, ang affected part ng cerebrum ay yung sinusuplayan ni ACA. Accdg sa homunculus ang manifestation ay sa leg. Make sense d ba? Hahaha

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Paralysis due to lesions of the Upper Motor Neuron The Corticospinal tract may be disrupted anyway along its course producing upper motor neuron signs. The lesions could be in any of the ff sites: o Cortex o Subcotrical white matter o Internal capsule o Brainstem o Spinal cord PATTERNS OF PARALYSIS Monoplegia Weakness or paralysis of all muscles of one arm or leg Should not be isolated muscle that is supplied by a single nerve or motor root. Must not be interpreted as failure to move due to pain Ataxia and sensory disturbances = weakness Other diseases that can manifest this kind of paralysis are: Parkinsons dse Other dse that can cause rigidity and bradykinesia Arthritis Bursitis Fracture Etiology Lesion in cerebral cortex Secondary to ischemia, small tumors or abscess Multiple sclerosis or SC tumor Manifestation Paralayze only half a hand or just the thumb May cause weakness of one limb Nerve conduction studies are normal Monolegia 2ndary to UMN will manifest as UMN signs If monoplegia 2ndary to LMN then therefore will manifest as LMN signs Long continued disuse of one limb may lead to atrophy but it is usually of lesser degree than atrophy due to lower motor neuron disease (denervation atrophy). In disuse atrophy, tendon reflex are retained and nerve conduction studies are normal.

Forms of Monoplegia Monoplegia without atrophy

muscular

Monoplegia with muscular atrophy More frequent than the previous one Examples are complete atrophic brachia monoplegia Crural (leg) monoplegia secondary to letter c etiology

Diseases of Motor neurons Atrophy secondary to disuse of the muscle Trauma of the SC or tumor, myelitis, multiple sclerosis, progressive muscular atrophy, late radiation

Hemiplegia Most frequent form of paralysis Secondary to lesion of the Corticospinal pathway Due to stroke, tumors, infections and vascular anomalies Etiology Disruption of the CST at the midbrain and CN3 Secondary to midbrain infarct Manifestations Ipsilateral CN3 Palsy Contralateral hemiparesis

Form of Hemiplegia Weber Snydrome

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Millard-Gubler pontine lesion)

syndrome

(low

Lesion at low pontine level

Medullary Lesion

Lessions in the medulla (obvious naman haha)

Ipsilateral abducens or facial palsy Contralateral weakness or paralysis of the arm and leg Rationale: Recall ur anatomy, sa pons nalabas c CNV, CNVI, CN7 kaya sila ang greatly affected Tongue Sometimes pharynx and larynx on one side Arm and leg on the other side Medulla, nag eexit sila CNIX, X and XII Example, paralysis of right arm and paralysis of left leg, gets?

Crossed paralyses

Incomplete cervical spinal cord lesion Brown sequard syndrome

Sabi sa past tranx low pontine lesion daw Sabi ng book at sa google, characteristic of brainstem lesion Spinal cord lesion

Ipsilateral hemiparesis that spares the face With loss of vibratory and positon sense on the ipsilateral side Contralateral loss of pain and temperature

Paraplegia Weakness or paralysis of both lower extremities Occurs with the disease of the SC, nerve roots and peripheral nerves Secondary to: o Tumors, acute myelitis, trauma, vascular malformation in the SC, SC infarction o SC infarction is usually due to air embolism that occurs in deep sea divers Difficult to distinguish with peripheral neuropathies because of the element of spinal shock which results in abolition of reflexes and flaccidity In Peripheral neuropathies, motor loss tends to involve distal muscles of the legs more than proximal ones with the exception of Gullain-Bare Syndrome which starts with paraplegia to quadriplegia in ascending pattern of paralysis Etiology Lesion is cervical area rather than thoracic Causes: Fracture dislocation with SC involvement Tumors, myelitis Foramen magnum compression lesions Disc dessication Mscular dystrophies can cause paralysis of all 4 extremities assoc with muscle wasting Autosomal recessive neuromuscular disease Peripheral nerve disease or of the several adjacent nerve roots Manifestations a. Affects all 4 extremities b. Legs are more affected c. Occurs most often as a transitional condition in the devt of partial recovery from quadriplegia

Form of Paraplegia A. Tetraplegia B. Diplegia C. Triplegia

Werdnig Hoffman Disease Pedia group (affects infants 6 mos 1 year old) Isolated paralysis of One or more muscle groups

Tetraplegia Floppy infant upon birth

Weakness or paralysis of a partical muscle of group of muscles

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Non paralytic D/o of movement

Muscular paralysis without visible changes in Motor Neurons, roots and Nerves

No upper of lower motor neuron ds May be due to d/o of position sense or cerebellar coordination or dse of basal ganglia If absence of the d/o mentioned above, apraxia, ataxia should be ruled in Disease due to NMJ dysfunction or intrinsic to the muscles Due to infections and metabolic d/o

Impairment or loss of sensation in the distribution of nerve No lesion in LMN or UMN but certain movements are nonetheless imperfectly performed Apraxia and Ataxia, etc

Hysterical Paralysis malingering patients Do Hoover sign Test o Examiner places his one hand under the heel of paralyzed leg o Ask the patient flex his/her hip (taas paa using his thigh) of the non-paralyzed leg o If you feel downward pressure with your hand below sa paralyzed leg ay naku faker xa! Haha therefore, (+) Hoover sign Try mo itaas ung isa mong leg using your thigh (hip flex) as high as you can, there would be pressure on your other leg True paralysis would be: kahit itaas mo ung paa ng non-paralyzed leg, walang pressure sa true paralyzed leg For better visualization: youtube! Type mo Hoover test! haha

Trip niya lang haha

Examples are: Myasthenia gravis Muscular dystrophies Myotonia congenital Familial periodic paralysis d/o of K, Na, Ca++, Mg metabolism tetanus, botilinium poisoning black widow spider bite thyroid, endocrine, sterioid, statin myopathies Paralysis involving one arm or leg, both legs or all of one side of the body Tendon reflex are retained No atrophy Hysterical gait is often diagnostic When the hysterical patient is asked to move the affected limbs, the movements tend to be slow, hesitant and jerky, often with contraction of agonist and antagonist muscles simultaneously and intermittently Inconsistent on repeated examination and maneuvers

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APROACH TO SENSORY DISORDER Considerations: o o o o Under normal conditions, motor and sensory functions are dependent of each other However, interruption of other sensory pathways and destruction of the parietal cortex also has profound effects on motility To a large extent, motor functions depend on sensory inputs Movement is inextricably dependent on sensation

Sensory Syndromes o o o o Sensory changes due to interruption of single peripheral nerve Depends on whether the nerve involved is predominantly muscular, cutaneous or mixed Localized to its dermatomal distribution if cutaneous Example:Ulnar nerve in the arm patient woud have hyposthesia in the muscles innervated by ulnar nerve (di ko na iisa-isahin kasi marami haha) Sensory Syndromes I. Polyneuropathies a. Myelinopathy b. Axonopathy Sensory Changes due to involvement of Nerve Roots a. Radicular pain Sensory Changes dude to involvement of Sensory Gaglia (Sensory Neuropathy, Gangliopathy) Sensory Spinal Cord Lesions a. Complete SC sensory Sydrome b. Posterior Cord Sydrome c. Brown-Sequard Syndrome (Hemisection of SC) d. Syringomelic Syndrome Hemisensory Loss due to a lesion of the Thalamus a. Thalamic pain syndrome Sensory Loss due to lesions in the parietal Lobe a. Anterior Parietal Lobe syndrome Etiology Causes: 1. 2. 3. 4. 5. Manifestation Purely motor, sensory or mixed; Mostly mixed; Usually starts as sensory then progress to mixed

II. III. IV.

V. VI.

Sensory Syndromes Polyneurophathies Can be classified as demyelinating or axonal (discussed below) Multiple involvement of peripheral nerve a. Myelinopathy

b.

Axonopathy

Metabolic Endocrine Post-infectious Toxic hereditary Lesions primarily affecting myelin or the myelinating Schwann cell Immune mediated attakc on PNS myelin segmental demyelination Metabolic abnormality initially occurs in the cell body or throughout the

Acute onset in hours or days Initially starts in the Lower extremities but not always distally Generalized weakness Mild sensory loss (-) tendon reflex in all extremities Mark slowing conduction velocities Inc CSF protein since myelin is a protein Rapid recovery

Degeneration appears to advance proximally toward the nerve cell body as long as the metab abno is present

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axon Long and large dm fibers are usually affected Sensory Changes due to Involvement of Nerve Roots (Radiculopathy) a. Radicular pain Pain arising from Dorsal root or the dorsal root ganglion Pain to be referred along a portion of the course of the nerve or nerves formed by the affected dorsal root Dermatomal pattern: o Example: if the patient has L1L2 herniated disc in the nucleus pulposus, the patient will experience pain in the dermatomal area of L1-L2.If L4 sciatic pain felt in the back and radiate down to lower extremities Produces same sensory defects as nerve root diseases but is unique because: o Proximal areas of the body also show pronounced sensory sensory (hyposthesia and hypoalgesia) in the face, oral, mucosam scalp, trunk and genitalia o Propioceptions lost which gives rise to ataxia o Reflex are lost -

Sensory Changes due to Involvement of Sensory Ganglia (Sensory neuropathy, Gangliopathy)

Disease of dorsal root ganglia Caused by paraneoplastic syndromes, connective tissue diseases, Sjogren syndromes, toxic exposure

Sensory Spinal Cord Lesions (please refer to the figure in the last page) a. Complete SC Sensory Syndrome b. Posterior cord syndrome

complete transverse disruption of the SC Lesion in the posterior portion of SC Due to interruption to the posterior spinal artery Incomplete spinal cord lesion Due to hemisection of the cord

No motor or sensory function Loss of pain, temperature and touch sensation Paresthesia in the form of tingling and pins and needles sensation or girdle and band like sensation

c.

Brown-sequard syndrome

d. Syringomyelic Syndrome (Lesion of the gray matter) Long fluid spaces are present in the central gray matter of the SC surrounded by thick tissue made of glial cells Involvement of VPL and VPM nuclei of the thalamus Usually due to vascular -

Loss of motor function, proprioception and kinesthesia on the same side of the lesion Loss of pain and temperature on the contralateral side and begins one or two segments below the lesion Example lesion at L1 the loss of pain will be at L2 or L3 and manifestations will be those supplied by L2 and L3 Associated spastic motor paralysis on the same side of the lesion Loss of Pain and temperature sensation depends on extent Tactile sensation is spared

Hemisensory loss due to a lesion of the Thalamus

Loss or dimunition of all forms of sensation on the contraleral side Position sense is affected more frequently than any other sensory function and is usually but not always

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a.

Thalamic pain syndrome Aka Syndrome of DejerineRoussy

lesion and less often due to tumor Damage to the thalamus

Sensory Loss due to lesios in the Parietal Lobe Aka Verger-Dejerine syndrome

profoundly affected than loss of touch and pinprick With partial recovery, some patients may exhibit spontaneous pain or discomfort Example: patient had thalamic stroke, there is still sensory loss but the patient has discomfort/non localizing pain on the affected side Hypersensitivity to pain Disturbances in the discriminative sensory function of the contralateral side without impairment of the primary modalities of sensation unless the damage is profound Loss of position sense and sense of movement Impaired ability to localize touch and pain stimuli (topagnosia) Widening of two point threshold (normal is 4-5 mm) Astereognosis Other Cx Mx Hemineglect Sensory Inattention Example: a patient would dress up only on the normal side Extinction

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