49
The Neurological Exam Made Simple

Robbins NeuroSyndDiagLasVegas2008

Embed Size (px)

DESCRIPTION

neuro

Citation preview

  • The Neurological Exam Made Simple

  • Syndrome Diagnosis(Anatomical Localization)1.Pattern (syndrome) Recognition2. Nine (Anatomic) syndrome patterns

  • Nine Syndrome PatternsCorticalSub-CorticalBrainstemCerebellumSpinal cordNerve rootPeripheral nerveNeuromuscular junctionMuscle

  • 1. Muscle Proximal symmetric weakness without sensory lossHistoryLower Ext difficulty rising from sitting positionUpper Ext difficulty lifting grocery bags, small children etc.,Normal sensation may have myalgia or cramps

  • 1. Muscle (cont)ExamProximal symmetric weakness without sensory lossMuscles normal size, no atrophy or fasciculations -- Tone and DTRs are normal to slightly decreased

  • Proximal Weakness

  • 2. Neuromuscular Junction Resembles muscle: proximal variable weaknessHistoryFatigability (waxing and waning weakness)Patient fatigues with prolonged activity (myasthenia gravis)Patient strength improves with activity (myasthenia syndrome)

  • 2. Neuromuscular Junction (cont)Exam resembles muscle (proximal weakness)Fatigability of proximal muscles without sensory lossLooses strength after exercise (eg., ptosis after sustained upward gaze)Muscles normal size, no atrophy or fasciculationsNormal tone and DTRs

  • Variable Weakness

  • 3. Peripheral Nerve Distal WeaknessHistoryLower ext trips, drags feet, wears out toes of shoesUpper ext drops objects, problems with gripAsymmetric weakness localized to involved nerve (compression syndromes)Symmetric weakness secondary to metabolic changes (eg., diabetes, renal etc)Muscle atrophy, twitching or quivering (fasciculations)Sensory changes - paresthesias

  • Clinical Findings in Upper and Lower Motor Neuron DefectsUpper motor neuron defectSpastic weaknessNo significant muscle atrophyNo fasciculations and fibrillationsHyperreflexiaBabinskis reflex may be presentLower motor neuron defectFlaccid weaknessSignificant atrophyFasciculations and fibrillationsHyporeflexiaNo Babinskis reflex

  • 3. Peripheral Nerve (cont)ExamDistal often asymmetric weakness Atrophy and Fasciculations Sensory lossMuscle tone normal or slightly decreasedDTRs decreasedAutonomic changesTrophic changes smooth shinny skinVasomotor changes swelling or temperature dysregulation, loss of hair or nails

  • Nerve Hypertrophy

  • 4. Nerve Root *Pain is the hallmarkHistory sharp, stabbing, hot, electric, shooting or radiating painResembles peripheral nerve but weakness may be proximal or distal depending on the involved nerve rootLower ext L5 S1 is most common; distalUpper ext C5-C6 is most common: proximal

  • 4. Nerve Root (cont)ExamDistal often asymmetric weaknessAtrophy and fasciculationsTone normal or decreasedDTR decreased or absent in involved musclesSensory loss (dermatomal)Maneuvers that stretch the nerve root increase pain ( eg., valsalva, SLR etc.,)

  • 5. Spinal Cord - Triad of Symptoms1. Sensory level - Pathognomonic2. Distal symmetric, spastic weakness (UMN) mimics peripheral nerve 3. Bladder and bowel dysfunction due to autonomic fibers in spinal cord

  • 5. Spinal Cord (cont)History Lower ext. weakness drags toes or tripsUpper ext. weakness drops objects or problem with gripSymmetric both legs or both arms and legs equallySensory complaint belt, band, girdle or tightness around trunk or abdomenSphincter dysfunction retention or incontinence of bladder more common than bowel

  • 5. Spinal Cord (cont)ExamSensory level (tested with pinprick)Weakness more common in legs than armsUrinary retention or incontinence Superficial reflexes decreased (anal wink, bulbocavernosus and cremasteric)UMN damage - distal > proximal weakness (weakness of extensor and (anti-gravity muscles greater than flexors)

  • Commissural syndrome

  • Sensory loss with sacral sparing due to the intramedullary lesion shown on the left, involving lateral spinothalamic tracts bilaterally.

  • Brown-Sequard Syndrome

  • 6. Brainstem Ipsilateral cranial nerve and contralateral long tract signs (essentially the spinal cord with embedded cranial nerves)History Long tracts (hemiparesis or hemisensory loss) Cranial nerves (the 6 Ds) DiplopiaDysarthriaDysphagiaDizzinessDeafnessDecreases strength or sensation over the face (crossed signs may be bilateral)

  • Posterior fossa

  • Major nervous system connections

  • 6. Brainstem (cont)ExamCranial nerves Ipsilateral -ptosis, pupillary abnormality, extraocular paralysis, diplopia, nystagmus, decreased corneal and blink reflexes, facial weakness or numbness, deafness, vertigo, dysarthria, dysphagia, weakness or deviation of the palate, decreased gag reflex, weakness of neck, shoulders or tongueLong tracts Contralateral distal extensor (UMN) hemiparesis, increased DTRs, spasticity, Babinski, loss of some and possibly all modalities

  • Distribution of pain and temperature sensation loss characteristic of lesions at the posterior fossa level.

  • Sensory Pathways

  • 7. Cerebellum - In-coordination, clumsiness, intention tremor *(smooths and refines voluntary movements)HistoryClumsiness in lower ext. staggers, drunken walkClumsiness in upper ext. difficulty with targeting movements (such as lighting cigarettes, keys in car ignition) and intention tremorBrainstem symptoms are common with cerebellar disease and vice versa

  • 7. Cerebellum (cont)Exam

    Lower Ext. - Gait (staggering, wide based, ataxic, difficulty with tandem walking, Heel-shin, or tracing patterns on floor with toe

    Upper ext. Intention tremor, difficulty targeting movements (such as finger-nose, heel shin) difficulty with rapid alternating movements (dysdiadochokinesis)

  • 8. Sub-cortical verses 9. CorticalHistory generally diagnosed by

    Specific cortical defectsPattern of motor and sensory defectsThe type of sensory defectsPresence of visual field defects

  • Sub-cortical v Cortical (cont)1.Specific Cortical DefectsLanguage (dominant hemisphere)Speech aphasiaWriting agraphiaReading alexiaComprehension (eg., apraxia)

    Visual-spatial (Non-dominant hemisphere)Denial or neglect of physical signs and symptoms (agnosia)

  • Sub-cortical v Cortical (cont) 2. Patterns of motor & sensory defects (homunculus)Cortical lesions - complete paralysis or sensory loss of face and arm (spares legs)Subcortical lesions complete paralysis or sensory loss of face, arm, trunk and legs

  • Sub-cortical v Cortical (cont) 3. Type of sensory defect *(most primary sensory modalities reach consciousness in the thalamus and do not require the cortex for their perception)

    Cortical lesions patients can still feel pain, touch, vibration and position but have impaired higher sensory processing, ie., graphesthesia or astereognosis)Subcortical defect patient complains of significant numbness

  • Sub-Cortical v Cortical (cont) 4. Visual field defects *(fibers run subcortically)

    Cortical no visual field defect unless occipital lobe involved (cortical blindness-Antons syndrome)

    Sub-cortical has visual field defects

  • Sub-cortical v Cortical (cont) Exam1.Cortical aphasia, visual-spatial dysfunction or seizures

    2.Motor UMN weaknessCortical - Face and arm Sub-cortical - Face, arm, trunk and leg

  • Suprathalamic syndrome

  • Thalamic syndrome

  • Sub-cortical v Cortical (cont) Exam3. SensoryCortical impaired higher sensory processing, (eg.,graphesthesia or astereognosis) with relatively normal sensationSub-cortical decrease primary sensory modalities, (eg., pinprick and touch etc.,)4.VisualCortical no defect unless occipital lobeSub-cortical visual field defects

  • Visual Field Defects

  • Cortical centers related to vision and ocular movement

  • Differential Diagnosis

    Axis levelsAtrophyFascic-ulationsBabinskiHyper-reflexiaPain, severeSensory LossWeaknessCortex + + + +Brainstem + + + +CerebellumCord + + + + Root + + + + +Nerve + + + + +NMJ +Muscle + + + +

  • *Another important point is to realize is that sensory loss and weakness is pervasive throughout the levels. That is why you need to be able to distinguish the patterns innervated by nerve, nerve root, spinal tracts, and cerebral hemispheres. This is where you earn your stripes and the excitement of pinpointing an anatomic level hence the pathology affecting the level.or more precisely .YOU HAVE JUST MADE THE DIAGNOSIS. Lets not get ahead of ourselves because you will need more information in the slides which follows in order to accomplish this. The process in the neurologic diagnosis is an elegant exercise for your brain and will serve you well no matter what field of medicine you enter..remember you have to have the right diagnosis before any treatment can be considered.